Adduction-Induced Strain on the Optic Nerve in Primary Open Angle Glaucoma at Normal Intraocular Pressure

ABSTRACT

Purpose/Aim

The optic nerve (ON) becomes taut during adduction beyond ~26° in healthy people and patients with primary open angle glaucoma (POAG), but only retracts the globe in POAG. We used magnetic resonance imaging (MRI) to investigate this difference.

Materials and Methods

MRI was obtained in 2-mm quasi-coronal planes in central gaze, and smaller (~23-25°) and larger (~30-31°) adduction and abduction in 21 controls and 12 POAG subjects whose intraocular pressure never exceeded 21 mmHg. ON cross-sections were analyzed from the globe to 10 mm posteriorly. Area centroids were used to calculate ON path lengths and changes in cross-sections to calculate elongation assuming volume conservation.

Results

For both groups, ON path was nearly straight (<102.5% of minimum path) in smaller adduction, with minimal further straightening in larger adduction. ON length was redundant in abduction, exceeding 103% of minimum path for both groups. For normals, the ON elongated 0.4 ± 0.5 mm from central gaze to smaller adduction, and 0.4 ± 0.5 mm further from smaller to larger adduction. For POAG subjects, the ON did not elongate on average from central gaze to smaller adduction and only 0.2 ± 0.4 mm from smaller to larger adduction (P = .045 vs normals). Both groups demonstrated minimal ON elongation not exceeding 0.25 mm from central gaze to smaller and larger abduction. The globe retracted significantly more during large adduction in POAG subjects than normals (0.6 ± 0.7 mm vs 0.2 ± 0.5 mm, P = .027), without appreciable retraction in abduction. For each mm increase in globe axial length, ON elongation in large adduction similarly increased by 0.2 mm in each group.

Conclusions

The normal ON stretches to absorb force and avert globe retraction in adduction. In POAG with mild to severe visual field loss, the relatively inelastic ON tethers and retracts the globe during adduction beyond ~26°, transfering stress to the optic disc that could contribute to progressive neuropathy during repeated eye movements.

KEYWORDS:

• Biomechanics
• normal tension glaucoma
• optic nerve
• optic nerve strain

Acknowledgments

This work was supported by the US Public Health Service, Washington, DC, under NEI Grants EY008313 and EY00331, and by an unrestricted grant to the Department of Ophthalmology from Research to Prevent Blindness, New York, NY. The funding organizations had no role in the design or conduct of this research.

Disclosure statement

None of the authors has a financial interest in any material related to this paper.

Additional information

Funding

This work was supported by the US Public Health Service, Washington, DC, under NEI Grants [EY008313 and EY000331] and by an unrestricted grant from Research to Prevent Blindness, New York, NY. The funding organizations had no role in the design or conduct of this research.