The Role of Optical Coherence Tomography Angiography in Optic Nerve Head Edema: A Narrative Review

Optic nerve head (ONH) edema is a clinical manifestation of many ocular and systemic disorders. Ocular and central nervous system imaging has been used to differentiate the underlying cause of ONH edema and monitor the disease course. ONH vessel abnormalities are among the earliest signs of impaired axonal transportation. Optical coherence tomography angiography (OCTA) is a noninvasive method for imaging ONH and peripapillary vessels and has been used extensively for studying vascular changes in ONH disorders, including ONH edema. In this narrative review, we describe OCTA findings of the most common causes of ONH edema and its differential diagnoses including ONH drusen.


Introduction
Optic nerve head (ONH) edema is a funduscopic feature common to various ocular and central nervous system (CNS) disorders. Altered axonal transport at the level of lamina cribrosa is the core mechanism of ONH edema, regardless of the underlying pathology [1]. ONH edema is clinically characterized by an elevated optic disc with blurred margins. Other fndings may include flling of the physiologic cup, draped retinal vessels over the margin, grayishwhite peripapillary retinal nerve fber layer (RNFL) edema with feathered margins, peripapillary hemorrhages, disc hyperemia, superfcial capillary network dilation of ONH, retinal venous dilation and tortuosity, exudates, or cottonwool spots, and retinal or choroidal folds or macular edema [2].
Although a patient's history and clinical examination may help narrow the diferential diagnosis, ocular and/or CNS imaging are usually required for a defnite diagnosis [3]. Visual feld may reveal characteristic feld defects suggestive of a specifc diagnosis [4]. Magnetic resonance imaging (MRI) of the optic nerve and/or brain may show optic nerved infammation, optic canal lesions, or spaceoccupying lesions [5,6]. Posterior segment ultrasonography [7] as well as autofuorecence and enhanced depth-optical coherence tomography were also useful in detecting optic disc drusen (ODD) [8]. Optical coherence tomography (OCT) of the macula and ONH fndings include spillover subretinal fuid in some patients with NAION and increased RNFL thickness in most patients with ONH edema [9].
Fluorescein angiography has been used to assess vascular changes of the ONH in diferent pathologies, and it is showed to be useful in detecting ONH edema in the presence of ODD [10,11]. OCT angiography (OCTA) is a novel, noninvasive, reproducible, sensitive, contrast-free, 3dimensional ocular imaging technology that provides structural and possibly functional information about superfcial and deep retinal and choroidal vasculature [12][13][14]. Tis article aims to review the OCTA features of diferent causes of ONH edema and implications for its diagnosis and prognosis. Te current literature involving OCTA was reviewed through Google scholar and PubMed.
1.1. Normal ONH and Macular OCTA. A complex vascular system originating from the central retinal artery (CRA) and posterior ciliary artery (PCA) provides the blood supply of ONH. Te peripapillary capillaries are apparent most of the time, even per edema. Tese capillaries, derived from the CRA, are dense and spread to the macular and temporal retinal vessels. At the prelaminar and laminar regions, the papillary capillaries are also evident unless in the presence of remarkable edema. Based on the slab location, the choriocapillaris around the disc could also be visible [15].
Various artifacts may infuence interpreting OCTA. Flow projection artifact from superfcial blood vessels does not allow separate analysis of the fow of deep ONH [16]. Additionally, because both the disc and retinal circulations control the disc fow measurements, OCTA cannot diferentiate between the PCA and retinal circulations [17].
Te main features of optic disc edema in OCTA are (1) tortuosity and dilatation of the surface capillaries including ON and radial peripapillary capillaries; RPC, similar to "tangled ball or bushy"; (2) potential dropout in very severe edema or chronic stages due to compression or becoming undetectable by the slow fow; and (3) increase in sectoral and average RNFL thickness [11,15,18].

Anterior Ischemic Optic Neuropathy.
Anterior ischemic optic neuropathies (AION) are classifed as arteritic (AAION) and nonarteritic (NAION). AAION is frequently associated with giant cell arteritis, a systemic, visual, and lifethreatening vasculitis [19]. NAION mainly threatens patients with cardiovascular risk factors and those with small, crowded cupless optic discs known as "disc-at risk" [20]. Essentially, the primary vascular pathology of NAION is thought to be the ischemia of the anterior lamina cribrosa and small vessels of the posterior ciliary vessels, resulting in a local infarct of the optic disc afecting small-caliber vessels.
In a study by Luisa Pierro et al., OCTA quantitative analysis demonstrated signifcant diferences between representative cases of AAION and NAION, particularly in terms of vessel density (VD) values for RPC and SCP (p < 0.01), while DCP and CC were nonsignifcant. On the contrary, vessel tortuosity (VT) values were remarkably reduced in AAION than NAION for SCP, DCP, and RPC (p < 0.01). VD and VT values were signifcantly lower both in AAION and NAION eyes compared to fellow and control eyes (p < 0.01). Furthermore, no signifcant changes were detected when comparing contralateral eyes comparing with controls. Hence, quantitative analysis in OCTA has demonstrated more vascular abnormality in AAION than NAION, which may be justifed by more swelling of the optic disc characterizing AAION [20]; however, further studies are warranted to determine quantitative values as possible cutof to diferentiate between AAION from NAION [21].
Some authors described a diference in vessel density or the fow index between NAION eyes and unafected fellow eyes [22,23,26]. Studies comparing NAION, fellow eyes, and normal eyes are summarized in Table 1. 1.3. ONH OCTA. Te most consistent changes in OCTA of patients with NAION are the morphological changes in the ONH vessels. OCTA has revealed tortuous capillaries inside or nearby the optic disc in NAION, which clinically is known as pseudoangiomatous hyperplasia [65]. Vessel tortuosity is a sensitive parameter for quantifying perfusion impairment occurring at the early phase of AAION and NAION and a good prognostic factor in patients with AION [20]. Moreover, irregularity, twisting, and focal loss of the superfcial RPC vasculature have been reported in NAION [42].
Diferent studies have noted the change of the RPC visualization, vascular dropout, and fading of the regular peripapillary pattern in the acute phase of NAION (Table 1) [21,22,26,35,65]. Temporal [22] and superior [23] peripapillary sectors are mostly afected. Disc edema or hemorrhage may infuence signal attenuation and may cause peripapillary vasculature dropout as a masking artifact, so it is emphasized that a decrease of the fow density at diferent layers in patients with NAION may not necessarily suggest a primary ischemic process but may result from compressive edema or imaging artifacts (signal attenuation by blood or imaging artifacts or edema).
Two distinct patterns of vasculature loss in NAION have been illustrated: (1) difuse loss of microvasculature network around the optic disc and (2) additional sectoral choroidal vasculature dropout extending from the disc [66]. Lower metabolic requirements following NAION lead to the decrease of retinal blood fow as an autoregulatory response. Tis mechanism can be quantifed through the analysis of vessel density and fow index [23,26,36,67]. Vessel density is the proportion of the total measured area occupied by the vessel area. It has been well demonstrated that vessel density reduction is secondary to the loss of attributing layers of the neural tissue in the progression course of NAION [23,36,38,39]. A recent meta-analysis recruiting fourteen published studies showed signifcantly lower vessel density in RPC, the whole enface, RPC inside the disc, and RPC peripapillary measured by OCTA in patients with NAION compared to healthy subjects. Te axoplasm blockage and subsequent RNFL edema leading to impedance in the fow of RPC and retina predominate in the peripapillary region [40].
Interestingly, vessel density changes can be reversible. Te superfcial vessel density is reduced due to the swelling of RNFL and early thinning of the underlying RNFL layers [68,69]. So, it should be kept in mind that part of this vascular density reduction and its reversibility is a result of the artifact caused by optic disc edema during the acute phase of disease. Vessel density might also have prognostic value in AION patients [20].
Te fow index is calculated as the average fow signal in the area measured. A signifcant decline has been shown in the adjusted fow index at the ONH and RPC in the NAION eyes [70]. Te vessel length density and the number of vessel intersections could be signifcantly decreased at the ONH,     RPC, and vitreous layers. Peripapillary microvasculature damage is reported in both ONH and RPC layers in patients with NAION [70]. Both thinning and pachychoroid in these patients have suggested that choroidal architecture might play a role in the pathogenesis of NAION [71,72]. While there is no diference in the vessel density at the level of the choriocapillaris, increased choriocapillaris perfusions have been noted [38,41]. Increased signal penetration due to the atrophy of overlying RNFL and ganglion cell complex-inner plexiform layer (GCC-IPL) might explain this fnding. Moreover, it may be a compensatory mechanism for the peripapillary vascular impairment in NAION.

Macular OCTA.
Controversial results on alterations of macular vessel density have been reported. Liu et al. showed a gradual decline in the whole GCC and the corresponding whole superfcial vessel density in NAION after 1-2 weeks, which deteriorated at 1-2 and 3-6 months of follow-ups along with the exacerbating superior hemifeld defect [44]. Aghsaei Fard and coworkers reported a signifcant decline in superfcial but not deep macular vessel density in NAION compared with control eyes [37]. Unlike peripapillary capillary density, progressive loss of vessel density in chronic NAION was not observed in the macular area [45]. Early decline of superfcial and deep vessel density but not GCC was observed in the acute phase of NAION within two weeks of presentation [48]. Moreover, an early decrease of the whole deep vessel density has been reported in acute NAION. It is presumed that the deep capillary vortexes [73] may compensate earlier for the lower blood fow and the hypoxic/ischemic alterations of the macula, as previously explained in patients with diabetes mellitus and hypertension [74,75].
A 6 × 6 mm scan has limited ability to discriminate vascular depth and may overestimate the parameters due to the blending of superfcial and deep vessel density changes in NAION [69,76]. Contrary to previous studies using 6 × 6 scan, evaluation with a 3 × 3 mm scan showed insignifcant change in the whole deep vessel density with time. Tis fnding can be explained by enhanced visibility of deep retinal vessels due to aggravated thinning of inner layers [44]. Nevertheless, despite the high accuracy of the 3 × 3 mm scans, its limited scanning area could miss changes outside the scanned area and underestimate the measurements [44].
OCTA has been suggested as a helpful tool for monitoring NAION progression [21,43]. Initial data suggest that OCTA may show spontaneous, partial recovery of peripapillary vascular fow densities as the natural course of NAION in accordance with the partial improvement of the visual function. [22]. Te whole vessel density of the ONH might be signifcantly lower in the chronic NAION compared with the acute NAION [26]. While there was no signifcant change in the microcirculation of the superfcial peripapillary retina, the vessel density of the deep optic disc may decline signifcantly [26,42]. Of note, a greater loss of superfcial RPC was demonstrated suggesting a sectoral reduction of RPC as the optic disc edema subsided [44].
Although there is a signifcant reduction in RPC density in acute and chronic NAION compared to healthy eyes, peripapillary capillary density decreases signifcantly from the acute to the chronic phase of NAION [45]. Moreover, there might be no remarkable diference in optic disc blood fow area, outer vessel density, and fow index in chronic AION compared to normal eyes [77].
Contrary to these fndings, Song et al. [26] and Rebolledo et al. [46] have reported no signifcant diference in declined peripapillary vessel density in the acute and chronic NAION. However, the evaluations were performed with a smaller scanning area [46]. It seems that longer follow-up intervals corresponding to the resolution stage can discover a signifcant decrease in capillary density [44]. Various degrees of axonal loss may be better demonstrated in the chronic stage when the masking artifact of edema is resolved because an artifact promoted by the edema might reduce the peripapillary vascular fow impairment [47,78]. Also, there might be a vicious cycle of neural-vascular interaction that leads to reduced vascular supply demand in the atrophic stage of the NAION [78,79].

Structure-Function Correlation.
Tere is a good correlation between the perfusion and the visual acuity, visual feld defect, and structural OCT repercussions [42]. Correlation between the decrease of the peripapillary vessel density and the location of visual feld defects as well as peripapillary RNFL thinning has been reported. Te whole and temporal peripapillary vessel density strongly correlated with visual acuity and temporal peripapillary superfcial retinal microvasculature dropout on the ONH mode was associated with visual acuity loss [23]. Tis was in agreement with the previous knowledge that the extent of papillomacular bundle damage is responsible for the severity of loss of visual acuity following an episode of NAION [80]. Of note, the whole and temporal vessel density at the optic disc on the RPC mode was not correlated with visual acuity, while the whole and temporal vessel density of the peripapillary superfcial retina was signifcantly associated with logMAR visual acuity [26].
Despite previous dye angiographic studies, OCTA revealed a hypoperfusion in the RPC and PPC following NAION, especially at the level of choroid, corresponding to both functional and structural impairments. Of note, a 100% correlation was detected between hypoperfusion at the level of the RPC and atrophy of the GCC, and a 90% correlation was detected between RPC hypoperfusion and visual feld defcits. Te authors hypothesized that RPC hypoperfusion is most likely to be a downstream result of the ischemic event rather than the initial component of ischemia. Hypoperfusion at the level of the peripapillary choriocapillaris was strongly correlated (80%) with GCC atrophy much like at the level of the RPC. Moreover, global peripapillary choriocapillaris hypoperfusion was more frequent than discrete, localized hypoperfusion. [24].
Irreversible vascular damage may lead to profound perfusion decrease, not afecting the overall ONH but in selective quadrants. Tis irreversible damage might have a role in vessel density decrease in the early stages and then RNFL loss and visual feld defects in later stages [20]. Temporal peripapillary vessel density was correlated with fnal VA and VF outcomes in the acute NAION. In the chronic NAION, both peripapillary and superfcial macular vessel densities were positively associated with visual outcomes. Te reduced nasal perifoveal vessel density in superfcial capillary plexus also signifcantly correlated with the poor visual outcomes for acute and chronic stages [81]. Temporal [22] and superior quadrants [24] have shown the most reduction in vessel density, which is compatible with the commonly identifed inferonasal feld defect [82]. Te presence of a watershed area in temporal site of the ONH makes this part prone to ischemic injury.

ONH OCTA.
In the setting of papilledema, the determination of disc swelling onset is imprecise, which can cause a bias toward OCTA features of papilledema. A "tangled ball of vessels" at the surface of the ONH has been explained [35], whilst there was no change at the level of the RPC. Te visibility of the peripapillary vasculature might be enhanced in chronic papilledema as a result of increased vessel diameter and density [65].
Te main diferentiating feature of papilledema from NAION on ONH OCTA is the vascular dropout observed in NAION [17]. In a retrospective study investigating microvasculature changes in eyes with disc edema, peripapillary capillary network changes were noted in NAION and papillitis, whilst superfcial optic disc vessel dilation and tortuosity without any peripapillary network pattern alteration were reported in patients with papilledema. [35]. Te difuse loss of microvasculature cuf without focal defcit or hypoperfusion in eyes with papilledema suggests a reduced peripapillary capillary network visibility secondary to disc edema rather than the actual ischemic process [66]. A possible role for autoregulatory vascular mechanisms has also been proposed [77].
Inaccurate autosegmentation, difculty in recognizing the scleral canal boundaries, and inability to separate large vessels from capillaries are some of the limitations of OCTA angio analytics software when evaluating papilledema. Fell et al. developed a custom digital subtraction analysis software that successfully separated large vessels from capillaries and calculated mean perfused large vessel density and perfused capillary density in RPC, ONH, and vitreous layers. Customized OCTA postprocessing software showed a remarkable decrease in perfused capillary density in highgrade papilledema and subsequent optic atrophy. Large vessel analysis of ONH and vitreous layers may exhibit alterations in the visibility secondary to changes in ppRNFL thickness [83].
Aghsaei Fard et al. showed signifcantly lower peripapillary vasculature measures in papilledema and pseudopapilledema eyes than in healthy eyes and comparable measures between papilledema and pseudopapilledema. However, peripapillary "capillary" density of papilledema eyes was not signifcantly diferent from healthy subjects, whilst pseudopapilledema eyes had substantially lower capillary values than control eyes. In pseudopapilledema eyes, capillary density was considerable lower in the whole image and nasal sector peripapillary of the inner retina than in papilledema eyes. Te whole image and nasal peripapillary sector capillary densities may have a diagnostic value for distinguishing actual and pseudo-disc swelling using OCTA [50].
In another study, Aghsaei Fard et al. using commercial software showed that NAION eyes had lower peripapillary total vasculature density values, followed by papilledema eyes and control eyes. Te customized software showed substantially lower perfused capillary density of NAION eyes than papilledema eyes, but there were no signifcant diferences between papilledema and control subjects. Moreover, eyes with optic neuritis had a signifcantly lower whole image and perfused capillary density than papilledema. However, NAION and optic neuritis were comparable using the customized software. Te area under the receiver operating curves for diferentiating NAION from papilledema eyes and optic neuritis from papilledema eyes gave the highest values for the whole image capillary density with the customized software, followed by peripapillary total vasculature with commercial software.

Macular OCTA. Macular and parafoveal vessel densities
showed no signifcant diference between patients with papilledema and healthy controls. Te whole superfcial and deep macula vasculature were signifcantly lower in eyes with NAION compared with eyes with papilledema. Regarding GCC thickness, no signifcant diferences were observed among NAION, papilledema, and control eyes. Whole superfcial and deep macular vasculatures were correlated with visual feld mean deviation but not macular GCC thickness [48]. However, the stage (acute or chronic) and/or severity of the disease play key roles in macular OCTA fndings in these conditions. Further studies with a quantitative analysis of perfusion density may aid in determining the role of vascular changes in the progression of papilledema.

Pseudopapilledema, Optic Nerve Head Drusen, and
Papillitis. Tere are reports that morphologic characteristics and peripapillary RNFL thickness on SD-OCT can help diferentiate ONH drusen and edema [84,85]. However, SD-OCT mainly illustrates the presence of ONH drusen and cannot rule out the concurrent disc swelling. Fluorescein leakage from the optic disc diferentiates true disc edema in these cases [11].
Studies using OCTA have reported focal capillary attenuation [18] and signifcantly lower vessel density in ONHD compared with normal eyes [52]. Qualitative assessment of ONH microvasculature was fruitless in precise diferentiation of mild disc edema (NAION) from pseudoedema (ONH drusen) due to poor intergrader agreement on grading for vessel dilation and tortuosity. Using en face images, a signifcant reduction in ONH VD values was noted in eyes with acute NAION compared with ONHD and healthy eyes [17]. Additionally, in the study by Cennamo et al. [52], vessel density in ONHD was signifcantly lower than the normal eyes. Te reduction could be attributed to the lower RNFL in the adjacent area. However, this decrease was not consistently seen in the parameters of RPC layer. Terefore, the quantitative OCTA of disc microvasculature, particularly in the optic nerve head slab, may diferentiate optic disc edema due to NAION from pseudo disc edema due to ONH drusen [17].
Te only study investigating RPC in the acute phase of papillitis concluded that the most useful diferentiating feature of papillitis from NAION was the lack of vascular dropout in papillitis. Even in the presence of signifcant edema that may mask the peripapillary network, they reappear beyond the edema. Quantitative studies noted vascular dilation as a consequence of infammatory processes, which may be helpful in the diagnosis of papillitis [35].

Optic Neuritis.
Optic neuritis (ON) is unilateral or bilateral infammation of the optic nerve due to various causes, including multiple sclerosis (MS), optic neuritis associated with neuromyelitis optica (NMO), infectious, or isolated. In patients with MS, ON is the presenting symptom in 25% and occurs in 75% of cases during the disease course [86]. Atrophy of the RNFL occurs after episodes of ON. Since the choroid supplies blood to the retina and optic nerve, the evaluation of peripapillary choroidal thickness and vascular perfusion can be helpful in the diagnosis of optic nerve diseases [87]. Radial peripapillary capillary and choroidal slabs are two acceptable slabs to assess perfusion of the RNFL layer vessels and choroidal vessels [88].
Wang et al. used OCTA to measure the ONH fow index (defned as the average fow signal within the whole ONH) in 52 eyes of MS patients, 14 eyes with a history of ON, and 21 eyes of healthy control. Tey classifed the fow index based on standard deviation (SD) into three categories: normal (<1.65 SDs under average), borderline (1.65 to 2.33 SDs under average), and abnormal (>−2.33 SDs lower the average). Te ONH fow index was signifcantly reduced in patients with MS with a history of ON than healthy controls (43% vs. 5%, p < 0.01). 21% of patients with MS without a history of ON eyes had a reduction in fow index compared to HCs (p � 0.198). In the parafovea zone, there was no diference between the three groups. Tey concluded that OCTA can be used to detect and monitor ONH perfusion in MS patients [29].
Similarly, Spain et al. investigated 68 eyes from MS patients and 55 healthy eyes with OCT and OCTA to assess the structural and vascular change in the peripapillary area. Eyes from MS patients, whether they had a history of ON or not, showed a decrease in the ONH fow index and OCT structure parameters like NFL thickness than healthy control. Tese parameters were decreased more in patients with ON than without ON. Tey compared the results with their previous study in which the ONH fow index did not have any reduction in MS without the ON group, and so due to the larger sample in this study, there was a 5.5% reduction in MS without ON compared to healthy control and 14.7% reduction in MS with ON than healthy control eyes. In conclusion, OCTA can detect optic nerve hypoperfusion and fow index decline in MS eyes. Combining these data with structural OCT parameters may increase the accuracy of the assessment of the nerve damage [89].

Toxic/Nutritional, Traumatic Optic Neuropathy.
Toxic optic neuropathy is an optic nerve damage due to a variety of toxins. Te toxins are derived from foods, drugs, metals, and carbon dioxide. Tere are various signs and symptoms like bilateral visual loss, color vision reduction, and central and cecocentral scotoma due to damage to the optic nerve, retina, and chiasma. More important toxins are methanol, quinines, isoniazid, ethambutol, linezolid, tobacco, vincristine, cyclosporine, and amiodarone. Systemic conditions like diabetes and thyroid disease can make toxic substances and afect the optic nerve [91,92]. Several modalities have been used for the diagnosis and follow-up of the patients. OCT is used to detect the thickening of the RNFL in the acute phase and thinning and atrophy in the late stage [93]. Fluorescein angiography can also evaluate retinal vascularity in toxic neuropathies but is not always accessible because of various side efects of dye-like anaphylaxis, nausea, and renal impairment.
Abri Aghdam et al. evaluated patients with NAION, traumatic optic neuropathy (TON), methanol induced optic neuropathy, compressive optic neuropathy, and healthy controls. Te authors measured disc area, cup/disc ratio and cup volume, RPC vessel density inside the disc, peripapillary RPC vessel density, and peripapillary RNFL thickness. Tey found a signifcant positive correlation between RPC vessel density and RNFL thickness, and both parameters reduced in patients of all groups compared to controls. RPC vessel density can be considered as a marker of axonal energy demands and its implication for RNFL thickness reduction. Inside RPC vessel density and peripapillary RPC vessel density showed signifcant correlation only in NAION (r � 0.36, p � 0.042) and methanol-induced optic neuropathy (r � 0.42, p � 0.018). Disc area and the cup size were larger in methanol-induced optic neuritis, and RNFL thickness was lower in traumatic optic neuritis compared to other groups. Since they did not fnd specifc vascular changes which can diferentiate between groups, they concluded that structural assessment might be superior to vascular parameters in diferentiating toxic and traumatic optic neuropathies [56].
Montorio et al. found no diferences in vessel density of superfcial capillary plexus in the macula of patients with traumatic optic neuropathy 48 hr after trauma, but a signifcant reduction happened in the 1st and 3rd-month, which was stable at the sixth month. Te RPC area declined in the third month and was stable in the sixth month. Deep capillary plexus VD decreased 48 hr after trauma and then increased in the frst month of follow-up. In the third and sixth months, the result was similar to the control group.
BCVA had slightly decreased 48 hr after the trauma, but it was not signifcant, and follow-up examinations showed no signifcant diference between traumatic eyes and control. Hence, OCTA may be useful for monitoring the course of vascular changes in traumatic optic neuropathy, even in patients with stable BCVA [57]. Studies on the efect of venom envenomation [53] and iron defciency anemia [54] on vascular changes in ONH OCTA are summarized in Table 1.

Leber Hereditary Optic
Neuropathy. Leber hereditary optic neuropathy (LHON) is a mitochondrial disorder. Symptoms mainly occur in the second and third decade of life with vision loss and optic disc hyperemia, followed by the pallor of optic disc and atrophy in chronic phases. Studies using OCTA showed that reduction in vessel density precedes structural changes and increases from subacute to chronic phases of LHON [58,60,64].

Conclusion
Briefy, despite the limitations of OCTA, it is recommended as the initial test for the vascular assessment in NAION. If OCTA did not confrm the diagnosis, more invasive modalities like FA could be performed. Moreover, OCTA could be a helpful tool for quantifying and monitoring ischemia in NAION. So far, prelaminar and laminar vasculature has not been assessed due to the limitations of the technology, which may be more associated with the ischemia of PCA. It seems that the current role of OCTA in NAION is more supportive rather than diagnostic. Future research could potentially enable the diagnostic capability of quantitative measures. OCTA is helpful in diferentiating NAION and papillitis from papilledema. Te most signifcant diagnostic accuracy is related to whole-image capillary density for diferentiating disc swelling. [51].
In the future, longitudinal studies with more cases will provide standard values for diferential diagnostic and therapeutic goals.
OCTA can be a valuable modality to evaluate the vascular changes in ON patients to monitor and distinguish disease severity.