Gaze-Induced Optic Nerve Head Deformations Are Greater in High Myopia and Strains Increase With Axial Length.

Abstract

<h4>Purpose</h4>To investigate optic nerve head (ONH) deformations caused by horizontal eye movements in high myopia (HM) using in vivo optical coherence tomography (OCT) imaging and finite-element (FE) modeling, and to identify factors influencing these deformations.<h4>Methods</h4>A total of 28 HM eyes and 28 non-HM eyes were imaged at baseline, 20° adduction, and 20° abduction positions using OCT. Lamina cribrosa (LC) effective strains were quantified using a three-dimensional tracking algorithm. A baseline FE model of an emmetropic eye with an axial length of 23.5 mm and normal tissues structures and a HM model with elongated axial length and thinner sclera were developed. The effects of varying scleral stiffness and the eye movement center on gaze-induced ONH deformations were explored.<h4>Results</h4>In vivo measurement showed that LC strains were significantly greater in HM eyes than in non-HM eyes during adduction (5.95% ± 3.52% vs. 3.65% ± 1.85%; P = 0.002) and abduction (3.35% ± 1.94% vs. 2.29% ± 1.65%; P = 0.016). Strains correlated positively with axial length. FE modeling demonstrated greater gaze-induced LC strains in the HM model compared to the emmetropic model, in both adduction and abduction. A softer sclera reduced LC strains in the HM model, whereas a forward shift in the eye movement center (relative to the geometric center, as seen in HM eyes) increased strain.<h4>Conclusions</h4>This study demonstrates that gaze-induced ONH deformations increase with axial elongation. The findings highlight the role of scleral stiffness and eye movement center position in modulating ONH biomechanics, contributing to the understanding of glaucomatous, glaucoma-like, and non-glaucomatous optic neuropathy in HM.