Early Macular Vessel Density Loss in Acute Ischemic Optic Neuropathy Compared to Papilledema: Implications for Pathogenesis

Abstract

PurposeThis study compares macular and parafoveal vasculature in patients with optic disc swelling.MethodsTwenty eyes with acute nonarteritic anterior ischemic optic neuropathy (NAION), 39 eyes with papilledema at first presentation, and 22 eyes of normal subjects were imaged using optical coherence tomography angiography (OCT-A). Macular ganglion cell complex (GCC) and peripapillary retinal nerve fiber layer thicknesses were measured in addition to macula and parafovea superficial and deep vasculature.ResultsAge- and gender-mixed models showed that the macular and parafoveal superficial and deep vasculature density values were significantly lower in NAION eyes than control eyes (P ≤ 0.0001 for all comparisons). All vessel density values were not statistically different between papilledema eyes and control eyes. Whole superficial and deep macula vasculature in the NAION eyes (45.9% ± 4.2%, 50.9% ± 6.5%) were significantly lower than in papilledema eyes (50.5% ± 4.6%, 57.3% ± 6.1%) (P = 0.03 and P = 0.01, respectively). No significant differences in GCC thickness were observed among NAION, papilledema, and control eyes. Whole superficial and deep macular vasculatures, but not macular GCC thickness, were significantly correlated with visual field mean deviation (r = 0.39, P = 0.001 and r = 0.41, P < 0.001, respectively).ConclusionsMacular OCT-A is able to show early macular vasculature abnormalities associated with optic nerve damage; this change occurs before detectable macular GCC atrophy.Translational RelevanceMacular vessel density measurement offers an opportunity to evaluate the optic nerve damage at initial presentation, but further longitudinal studies are needed.

Early Macular Vessel Density Loss in Acute Ischemic Optic Neuropathy Compared to Papilledema: Implications for Pathogenesis

“…Focusing on NAION eyes, we would like to clarify these findings based on prior published data,3,4 which, however, have not been mentioned by the authors. In contrast to the studies of Fard et al1 and Akbary et al,2 we previously reported that NAION eyes had a significant thinning of the ganglion cell inner plexiform layer minimum (GCIPL min) as early as 2.2 days after symptoms onset ( P = 0.017). In fact, the GCIPL min was abnormally thinned in more than 50% of eyes (56.3%) within a week of symptom onset 3…”

“…We read with great interest the article by Fard et al1 comparing macular and parafoveal vasculature in 20 eyes with acute nonarteritic anterior ischemic optic neuropathy (NAION), 39 eyes with papilledema at first presentation, and 22 healthy eyes. They found that superficial and deep vasculature density values were significantly lower in NAION eyes compared to control and papilledema eyes.…”

“…First, different OCT devices and combinations of macular inner layers were used: Avanti SD-OCT (Optovue, Inc., Fremont. CA) to map the GCC by Fard et al,1 and Cirrus OCT (Carl Zeiss Meditec) to quantify the GCIPL thickness by De Dompablo et al3 and Rebolleda et al4 This point is relevant because a significant macular RNFL thickening develops almost immediately in NAION, which may be an extension of peripapillary edema 5. Considering that GCC analysis includes the combined thickness of the GCIPL and macular RNFL, the macular RNFL thickening could mask the neuronal loss at the acute phase, which would be better detected by the analysis only focused on GCIPL.…”

Follow-up of nonarteritic anterior ischemic optic neuropathy with optical coherence tomography angiography

“…And the axonal swelling or RNFL edema resulting from the blocked axoplasm and leading to impedance in ow of RPC and retinal vessels might be severer in the site closer to the optic disc. While, Fard et al 26 have reported an early reduction of SVD and DVD in 6 × 6 mm scans but not of GCC at the acute stage within 2 weeks of onset. It might be that we missed the changes outside 3 × 3 mm scanning area in the early stage.…”

“…There are several limitations in our study, including its retrospective nature, the small number of subjects, and some loss to follow-up at 3-6 months. Here, we focused on ow alterations with time, yet visual eld loss of threshold was not analyzed in detail as previous studies showed a corresponding loss of structure and capillary density in the location of the visual eld loss 9,13,26 . Additionally, vasculature in prelaminar and laminar slabs was not evaluated due to the current limits of the technology, which may be more related to the ischemia mechanism of PCA.…”