Correlation Between Ischemic Retinal Accidents and Radial Peripapillary Capillaries in the Optic Nerve Using Optical Coherence Tomographic Angiography: Observations in 6 Patients

Abstract

Background:Perfusion of the optic nerve has been widely studied using fluorescein angiography (FAG), which is currently regarded as the criterion standard. However, FAG has adverse effects associated with intravenous contrast administration and is limited in its capacity to characterize and stratify the different vascular layers of the optic nerve and retina. The use of new imaging techniques, such as optical coherence tomographic angiography (Angio-OCT), is therefore important.Aim:A qualitative description is made of the vascular layers of the optic nerve and of how vascular events affect radial peripapillary capillaries (RPC). Two patients with central retinal artery occlusion (CRAO), 1 with arteritic anterior ischemic optic neuropathy (AAION), and 3 healthy subjects were studied.Results:The Angio-OCT imaging afforded better visualization of the depth of the RPC and rest of the vascular layers of the retina compared with FAG. Optic nerve surface perfusion was affected in AAION and proved normal in CRAO.Conclusions:Our results indicate that perfusion of the papilla and RPC mainly arises from the papillary plexus that depends on the posterior ciliary artery.

Peripapillary Retinal Vascular Involvement in Early Post-COVID-19 Patients

“…Moreover, a reduction in RPCP density has been demonstrated to be an early sign of glaucoma [ 35 , 36 ]. RPCP density and flow index reduction are also correlated to visual acuity and visual field loss in non-arteritic ischemic optic neuropathy [ 37 , 38 ]. On the contrary, a RPCP flow and density impairment can be the consequence of retinal neural remodeling secondary to optic nerve axonal degeneration [ 39 ].…”

Evaluation of optical coherence tomography angiography changes in nonarteritic anterior ischemic optic neuropathy

“…[ 3 - 9 ] The RPC layer, as described by Michaelson[ 15 ] and Henkind,[ 16 ] is derived primarily from Parapapillary retinal arterioles and forms a network within the RNFL layer that runs parallel to the axons and acts as the primary supply to the axons. As reported in a few studies,[ 17 , 18 ] central retinal vasculature is not the sole contributor to the RPC layer and short posterior ciliary arteries do contribute via anastomosis. As the primary insult in NAION is a transient hypoperfusion of posterior ciliary arteries, this may contribute to the RPC density reduction.…”

Association of Neuroretinal Thinning and Microvascular Changes with Hypertension in an Older Population in Southern Italy

“…This opposite distribution could be due to the activity-vascular related mechanism by which denser temporal RPC exists to fulfill the highly metabolic requirements of photoreceptors, ganglion cells, and retinal pigment epithelial cells within the macular area [28], despite the reported association between RNFL thickness and peripapillary VD [29] supports the idea that the perfusion of RPC may be proportional to the quantity of RNFL supplied [12]. The peripapillary plexus is considered to be crucial for the homeostasis and function of the ganglion cells and their axons in the RNFL [30], and a reduced VD has been observed in early glaucoma [31] and non-arteritic ischemic optic neuropathy [32], associated with a reduced RNFL and GCC thickness [33]. Therefore, we may hypothesize that in the hypertensive condition the reduced thickness of GCC and RNFL could be related to the vascular rarefaction in a peripapillary sector with a high metabolic requirement.…”