Deformation of Optic Nerve Head and Peripapillary Tissues by Horizontal Duction

Abstract

Purpose To ascertain deformation of the optic nerve head (ONH) and peripapillary tissues caused by horizontal duction. Design Prospective, experimental study. Methods Optical coherence tomography of the ONH region was performed in 23 eyes of twelve normal volunteers in central gaze and increasing (10, 20, and 30°) adduction and abduction. Main outcome measures were changes from central gaze in the configuration of the ONH and peripapillary tissues in eccentric gazes. Results Adduction but not abduction was associated with significant, progressive relative posterior displacement of the temporal peripapillary retinal pigment epithelium (tRPE) from its position in central gaze reaching 49±10 μm in 30° adduction (standard error of mean, p<0.0001). Absolute (anterior or posterior) optic cup displacement (OCD) averaged 41±7 μm in 30° adduction. Linear regression showed significant effect of adduction on absolute OCD (slope 1.09±0.36 μm/degree, p=0.0037). In 20° and 30° adduction, all eyes exhibited significant progressive temporal ONH tilting reaching 3.1±0.4° in 30° adduction (p<0.0001). Abduction was not associated with significant peripapillary RPE displacement, OCD, or ONH tilt. Both nasal and temporal peripapillary choroid averaged 9 to 19 μm thinner in adduction and abduction than in central gaze (p<0.02). Conclusions Adduction temporally tilts and displaces the prelaminar ONH and peripapillary tissues. Both adduction and abduction compress the peripapillary choroid. These effects support MRI and biomechanical evidence that adduction imposes strain on the ONH and peripapillary tissues. Repetitive strain from eye movements over decades might in susceptible individuals lead to optic neuropathies such as normal tension glaucoma.

Predictions of Optic Nerve Traction Forces and Peripapillary Tissue Stresses Following Horizontal Eye Movements

“…Other independent studies also concluded that ONH deformation was more affected by adduction. 13,15 Additionally, a higher ppS stress in adduction also was consistent with a larger optic nerve sheath traction force predicted in this study. We speculated that the overall higher stresses in ppS and higher traction forces in adduction were because of a more elongated optic nerve in adduction than in abduction for the same magnitude of eye rotation.…”

“…41 The shearing deformation observed in this study (Fig. 2) and other OCT observations [13][14][15] might be able to explain the optic disc rotation about the vertical axis (axis along the superior-inferior direction) observed in myopic eyes. 42 It is plausible that continuous stretching of peripapillary tissues following repeated eye movements might contribute to the development of rotated optic discs and peripapillary zones simultaneously through a tissue remodeling process.…”

“…This deformation pattern is in agreement with that observed in three recent OCT studies. [13][14][15] Furthermore, LC strains (see Supplementary Material SC) in this study were on the same order of magnitude as those measured in vivo.…”

“…13 Recently, there has been renewed interest in the effects of eye movements on the optic nerve and ONH deformations and their possible links to optic neuropathies. Specifically, studies that used optical coherence tomography (OCT), [13][14][15] finite element (FE) modeling, 16 and magnetic resonance imaging (MRI), 17 all converge to the single fact that horizontal eye movements considerably deform the ONH tissues (through the ''strong'' optic nerve [including its sheath] traction imposed on the ONH), and that these deformations can be as large (or significantly larger) than those induced by a substantial IOP elevation. 14,16 Because eye movements appear to have a strong impact on the ONH tissues, and can even alter the axial length of the eye, 18 we aimed to understand if there could exist a link between eye movements and the development of peripapillary zones.…”

Gaze-evoked deformations of the optic nerve head in thyroid eye disease

“…Thyroid eye disease (TED) is an autoimmune disorder where activated orbital fibroblasts 63 differentiate into adipocytes or myofibroblasts and have increased hyaluronan production (1). These 64 processes often involve expansion and infiltration of the orbital fat and the extraocular muscles (2,3). 65…”