Dataset Information

Comparison of Optic Nerve Head Microvasculature Between Normal-Tension Glaucoma and Nonarteritic Anterior Ischemic Optic Neuropathy.

ABSTRACT:

Purpose

To compare the microvasculature of the optic nerve head (ONH) and peripapillary tissues in eyes with normal-tension glaucoma (NTG) and nonarteritic anterior ischemic optic neuropathy (NAION) using optical coherence tomography angiography (OCTA).

Methods

Thirty-eight eyes with treatment-naïve NTG, 38 eyes with NAION matched for retinal nerve fiber layer (RNFL) thickness in each superior and inferior quadrant, and 38 healthy eyes matched by age were included. ONH and peripapillary retinal microvasculature was evaluated in en face images obtained using OCTA. Vessel density (VD) was calculated as the percent area occupied by vessels in the measured region in each layer segmented into the prelaminar tissue (PLT), lamina cribrosa (LC), and peripapillary retina (PR).

Results

VDs in the PLT and LC were lower in NTG eyes than in both NAION and healthy eyes (P ≤ 0.008), and did not differ between the NAION and healthy eyes. VDs in the PR did not differ between the NTG and NAION eyes. In intersectoral comparisons, VDs in the PLT (P = 0.030) and LC (P = 0.028) were lower in the affected than in the unaffected sector of eyes with NTG, but the differences did not occur in eyes with NAION. VD in the PR was lower in the affected than in the unaffected sector in both NTG and NAION eyes (both P < 0.001).

Conclusions

Despite similar degrees of RNFL loss and VD decreases in the PR, VDs in the ONH differed between eyes with NTG and NAION, indicating different mechanisms of vascular impairment and ONH damage in each condition.

SUBMITTER: Kim JA

PROVIDER: S-EPMC8374994 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Anterior ischemic optic neuropathy (AION) can be divided into nonarteritic (NAION) and arteritic (AAION) forms. NAION makes up ~85% of all cases of AION, and until recently was poorly understood. There is no treatment for NAION, and its initiating causes are poorly understood, in part because NAION is not lethal, making it difficult to obtain fresh, newly affected tissue for study. In-vivo electrophysiology and post-mortem studies reveal specific responses that are associated with NAION. New models of NAION have been developed which enable insights into the pathophysiological events surrounding this disease. These models include both rodent and primate species, and the power of a 'vertically integrated' multi-species approach can help in understanding the common cellular mechanisms and physiological responses to clinical NAION, and to identify potential approaches to treatment. The models utilize laser light to activate intravascular photoactive dye to induce capillary vascular thrombosis, while sparing the larger vessels. The observable optic nerve changes associated with rodent models of AION (rAION) and primate NAION (pNAION) are indistinguishable from that seen in clinical disease, including sectoral axonal involvement, and in-vivo electrophysiological data from these models are consistent with clinical data. Early post-infarct events reveal an unexpected inflammatory response, and changes in intraretinal gene expression for both stress response, while sparing outer retinal function, which occurs in AAION models. Histologically, the NAION models reveal an isolated loss of retinal ganglion cells by apoptosis. There are changes detectable by immunohistochemistry suggesting that other retinal cells mount a brisk response to retinal ganglion cell distress without themselves dying. The optic nerve ultimately shows axonal loss and scarring. Inflammation is a prominent early histological feature. This suggests that clinically, specific modulation of inflammation may be a useful approach to NAION treatment early in the course of the disease.