Optic Nerve Head Strain Differences Suggest Distinct Glaucoma Pathophysiologies

Normal-tension glaucoma may have a different pathophysiology than high tension glaucoma.

Optic nerve head strain is caused by different biomechanical processes in patients with normal-tension glaucoma (NTG) than those with high-tension glaucoma (HTG), a report published in the British Journal of Ophthalmology shows. Patients with NTG experience higher gaze-induced optic nerve head strain, while those with HTG  experience higher intraocular pressure (IOP)-induced strain, according to research. The differing biomechanical responses to these external loads indicate distinct pathophysiologies between the groups.

Researchers conducted a clinic-based cross-sectional study to assess IOP-induced and gaze-induced optic nerve head strain in patients with HTG and NTG.

The study included the ONH of 228 eyes of 228 participants. There were 114 patients with HTG (mean age, 69±5 years; 68% men, 32% women) and 114 patients with NTG (mean age, 67±6 years; 55% men, 45% women). 

All patients underwent imaging with optical coherence tomography (OCT) under various gaze conditions, including OCT primary gaze, 20° adduction from OCT primary gaze, 20° abduction from OCT primary gaze, and OCT primary gaze with acute IOP elevation (approximately 33 mm Hg). The researchers mapped in vivo 3-dimensional deformations of the ONH tissues using digital volume correlation analysis and compared IOP-induced and gaze-induced deformations and optic nerve head strain between the groups.

We suspect that if adduction is going to cause long-term damage to the [optic nerve head] tissues, it should come from a repetitive movement pattern that occurs in an eye with prior biotechnical susceptibilities (eg, shorter and/or stiffer optic nerve) to the [optic nerve head] strains induced by adduction.

The study shows, among all patients, adduction and IOP elevation generated similarly high effective optic nerve head strain (4.4% vs 4.5%; P =.80) in the lamina cribrosa, and abduction generated significantly lower effective strain (3.1%) than both IOP elevation and adduction (P <.01 for both). 

Researchers also demonstrated that the lamina cribrosa underwent significantly higher effective strain under IOP elevation in patients with HTG than those with NTG (4.6% vs 4.1%; P <.05), and the lamina cribrosa exhibited significantly higher effective strain under adduction in patients with NTG than those with HTG (4.9% vs 4.0%; P <.05).

“We suspect that if adduction is going to cause long-term damage to the [optic nerve head] tissues, it should come from a repetitive movement pattern that occurs in an eye with prior biotechnical susceptibilities (eg, shorter and/or stiffer optic nerve) to the [optic nerve head] strains induced by adduction,” the researchers explain. “This effect could also be cumulative over several years.”

Limitations of the study included uncertainties related to the method of IOP elevation (via ODM), a study population of all Chinese patients older than 50 years, poor OCT resolution and signal quality of the posterior portion of the eye beyond the lamina cribrosa, differing glaucoma severity and RNFL thickness among the patients with NTG and HTG, and an offset primary gaze position.

Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.  

References:

Chuangsuwanich T, Tun TA, Braeu FA, et al. Adduction induces large optic nerve head deformations in subjects with normal-tension glaucoma. Br J Ophthalmol. Published online April 3, 2023. doi:10.1136/bjo-2022-322461