Optic nerve head injury and optical coherence tomography angiography.

We wrote this letter to discuss the microvascular abnormalities related to optic nerve head (ONH) injury visualized by optical coherence tomography angiography (OCTA). With the advent of OCTA, different fundus vasculature levels in the macular region can be displayed precisely and noninvasively to investigate its mechanisms. OCTA is a promising diagnostic approach for detecting in f l ammatory, i s chemic , and compres s i ve opt i c neuropathies (1). However, the potential relationship between parapapillary microvascular dysfunction and ONH injury is still unclear and should be investigated by combined structural and functional OCT. The macula and the ONH’s different microvasculature results in a weaker association of the vascular density (VD) of the macula with tissue thickness compared to ONH VD (2). Anatomically, the optic disc’s surface (i.e., the superficial nerve fiber layer) is supplied by superficial ONH capillaries derived from the central retinal artery (3). The retinal ganglion cell axons in the peripapillary nerve fiber layer are fed by distinct capillary networks originating from adjacent retinal arterioles (4). It has been reported that both global and sectoral circumpapillary VD on the ONH surface, excluding the papillomacular bundle area, decreases significantly with age (5). Moreover, the anterior lamina cribrosa is supplied by short posterior ciliary arteries, the Zinn-Haller arterial circle, and partially by the peripapillary choroidal vasculature (3,6). Finally, the posterior lamina cribrosa is supplied through various sources, mainly the peripheral pia arteries and short posterior ciliary arteries of the Zinn-Haller arterial circle (3). Peripapillary OCTA vessel parameters have greater intrasession repeatability than intersession reproducibility in both non-glaucomatous and glaucomatous eyes (7). Previous studies have compared the flow pattern using OCTA in the peripapillary region in normal eyes, glaucomatous eyes, and acute nonarteritic anterior ischemic optic neuropathy (NAION) eyes. Normal subjects showed VD’s steepest slopes in the nasal superior and inferior circumpapillary sectors (−0.098%/year and −0.096%/year, respectively) (5). Conversely, in patients with NAION, OCTA revealed decreased peripapillary VD and peripapillary vascular dilatation and tortuosity (8). Similarly, patients with papilledema have dilated and tortuous capillaries at the ONH surface (9). In contrast, glaucoma-related decreased peripapillary retinal perfusion can be detected as a focal defect pattern using OCTA (10). ONH perfusion detected by optical microangiography showed significant differences between glaucomatous eyes and normal controls and was significantly correlated with disease severity and structural defects in glaucomatous eyes (11). Furthermore, glaucomatous eyes with focal lamina cribrosa defects are usually accompanied by peripapillary microvasculature dropout (12). Our clinical practice has identified blood flow signals in the deep anterior lamina cribrosa via both spectral-domain OCTA and swept-source OCTA (Figures 1,2), providing a new biomarker for assessing the blood supply of the optic disc. Numa et al. reported blood flow signals visualized on or immediately adjacent to lamina beams, outside of lamina pores, using en face OCTA (13). Letter to the Editor