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Editors Selection IGR 24-1

Pathogenesis: Eye Movements and Optic Nerve Traction

Comment by Michael Girard on:

84276 Optic Nerve Traction During Adduction in Open Angle Glaucoma with Normal versus Elevated Intraocular Pressure, Demer JL; Clark RA; Suh SY et al., Current Eye Research, 2020; 45: 199-210

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Recently, there has been renewed interest in the effects of eye movements on the optic nerve head (ONH) and their possible links to optic neuropathies including glaucoma. Specifically, studies that used optical coherence tomography (OCT),^1-3 finite element (FE) modelling,⁴ and magnetic resonance imaging (MRI),⁵ all converge to the single fact that during horizontal eye movements, the optic nerve (the 'cable' linking the eye to the brain) can exert a traction force on the eye globe to deform the ONH tissues; surprisingly these deformations can be as large (or significantly larger) than those induced by a substantial IOP elevation to 40-50 mmHg.¹

The proposed study is one of several that aims to shed some light on whether such mechanical forces could be responsible for axonal loss in glaucoma. While a controversial topic, it could potentially explain an alternate pathway for axonal loss that is independent of intraocular pressure, and such a theory may be of high interest to explain the development of normal tension glaucoma (NTG). Specifically, in the proposed study, the authors imaged glaucoma subjects (NTG and high-tension glaucoma [HTG]) and healthy controls in both abduction and adduction using MRI. They found that in both healthy controls and glaucoma subjects, the optic nerve was straight in adduction. Furthermore, abnormal globe retraction was observed in adduction in glaucoma subjects (but not in healthy controls), which may suggest the presence of a high traction force within the optic nerve and its sheath that is transmitted to the ONH connective tissues. The authors further made 2 important observations: (1) globe retraction in glaucoma occurred regardless of the IOP level; (2) Globe retraction in glaucoma eyes was more prominent in Asians (rather than in Caucasians) ‐ a population that is more prone to NTG.

However, it is worth mentioning that the authors would benefit from reproducing their results in much larger cohorts, as they only recruited 35 glaucoma subjects (NTG and HTG) that covered 3 ethnic groups. As wide biomechanical variations are known to exist in ocular tissues, conclusions from this study would require independent validations. The study would also benefit from additional biomechanical measurements. For instance, ONH strains (i.e. deformations) in adduction can be mapped from OCT images,¹ and optic nerve traction forces can be estimated using a prediction tool known as finite element modelling.⁶ The use of such biomechanical metrics are important because the simple observation of a straight optic nerve does not necessarily translate to the presence of a very large traction force and/or large ONH deformations (as could occur in the presence in a soft dura and a stiff sclera). In all, the fact that optic nerve traction could contribute to axonal loss in glaucoma is thought provoking and should not be discarded that easily. Optic nerve traction may well be the largest force that is acting on the back of the eye,⁶ the implications of which could be considerable in both myopia and glaucoma. Further studies should be carried out, and they would fit nicely under a new field, named 'orbital tissue biomechanics', that remains poorly explored. Importantly, the impact of optic nerve traction does not stop here. Since a large force acts on the back of the eye, it could explain several eye disorders that currently have an unknown cause,⁷ including the development of: (1) peripapillary atrophy in glaucoma and myopia; (2) staphylomas in myopia; (3) tilted discs in myopia; and (4) intrachoroidal cavitations.

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