July 2018

GLAUCOMA

Research highlight
Normal tension glaucoma: The result of repetitive strain?


by Maxine Lipner EyeWorld Senior Contributing Writer


Optic nerve tethering in adduction in a case of advanced normal tension glaucoma with progressive visual field loss at low-normal IOP. Colorized, high resolution MRI shows that while amply long in abduction, the optic nerve is not long enough to allow adduction without damaging traction on the optic nerve head. Coronal MRI shows large areas of optic atrophy on the left.
Source: Joseph Demer, MD


“If this proves to be true, reducing the angle of adduction and/or the force of the medial rectus muscle that’s causing the adduction would reduce the force exerted by the optic nerve against this very susceptible junction with the eyeball.”
—Joseph Demer, MD

A closer look at the impact of eye movements

For patients with normal tension glaucoma, recent research suggests that the culprit may be common eye movements, according to Joseph Demer, MD, PhD, Arthur L. Rosenbaum Professor of Pediatric Ophthalmology, Stein Eye Institute, and professor of neurology, University of California, Los Angeles. The research explored whether repetitive strain from eye movements could damage the optic nerve and lead to vision loss.
This theory was an outgrowth of Dr. Demer’s earlier work to better understand strabismus with the aid of MRI scanning. “We have been working on optimizing this technique so that we can see the function of the eye muscles by MRI,” Dr. Demer said. “By making these MRI pictures in different gaze positions, it became obvious that the optic nerve was getting pulled tight in some positions.” In some cases, the tugging of the optic nerve on the eye was sufficient to retract this back into the socket. It occurred to Dr. Demer that the part of the eye that was being pulled on the hardest was the temporal edge of the optic nerve as it exits the eye wall, which is an area where peripapillary atrophy develops.

Studying eye movement

Dr. Demer thought that the tension on the optic nerve during these eye movements may produce damage to the peripapillary region. With this in mind, investigators built a finite element analysis computer model out of thousands of tiny three-dimensional virtual pyramidal elements.
Using this computer model, investigators then had the eyeball to rotate into the position where they found the optic nerve gets tethered and calculate the stress in each part. “It turns out that there’s a lot of stress and strain in this area at the temporal edge of the optic nerve where the peripapillary atrophy happens, and the distribution of it would cause the optic nerve head to tilt temporally,” Dr. Demer said. Such temporal tilting is not present in children but is very common in adults, especially those with nearsightedness. “You could easily imagine that this is a repetitive strain injury because we make tens of thousands of these eye movements every day,” he said.
In the study, investigators looked at several groups of people including those with normal tension glaucoma who were losing their sight and age-matched controls without glaucoma. Patients underwent both MRI and OCT scanning. Their results were then compared to those of young, healthy people without glaucoma, as well as those with strabismus who have misaligned eyes with differing amounts of eye movements.
Investigators found that for those with normal tension glaucoma there was a tightening when they rotated the eye toward the nose beyond an angle of about 26 degrees, Dr. Demer noted. “When that occurs, the eyeball gets pulled back significantly into the socket in a way that we do not see in any other group,” he said. The only other group this was noticed in was those with high pressure glaucoma.
In building the computer model, investigators noted that the optic nerve and the sheath that surrounds it start out in youth thin and pliable, but this changes with age. Dr. Demer pointed out that open angle glaucoma is much more prevalent in older people. “It may simply be a coincidence, but it’s certainly a strong coincidence that as people get older and the risk of chronic open angle glaucoma goes up, their optic nerves and sheaths get thicker and stiffer,” he said.
Dr. Demer theorized that with age the area becomes vulnerable to damage. “There’s a vast amount of compelling data that the damage produced by the optic nerve occurs at the junction between the optic nerve and the eyeball in glaucoma, that the pattern of visual loss is consistent with that,” Dr. Demer said. “Our theory also proposes this is where the damage occurs because our calculations suggest from the computer model that this is where the damage will be.”
The impact that such repetitive movements have on the eye should not be underestimated. “We think that this may be a major cause of visual loss in glaucoma,” Dr. Demer said, adding that it may also be a factor in myopia. The force concentration on the back of the eye seems to be occurring in an area where the eye gets elongated in myopia. “All of the forces that we calculate to be exerted by the optic nerve on the back of the eye match the distribution of eyeball stretching that occurs in nearsightedness,” he said. This is particularly true for severe axial myopia, he stressed.

Clinical strategies

In the case of glaucoma, if such repetitive eye movements prove to be pivotal, there are several clinical strategies that could be easily implemented. “If this proves to be true, reducing the angle of adduction and/or the force of the medial rectus muscle that’s causing the adduction would reduce the force exerted by the optic nerve against this very susceptible junction with the eyeball,” Dr. Demer said. One way to do this would be with eye muscle surgery to weaken the range of the adduction eye movement.
Another possibility would be to increase the relative length of the optic nerve so that there is greater slack here. To do that, physicians could perform orbital decompression surgery, drilling out some of the wall of the orbit, to make the eye sink back into the socket. Or they could use liposuction to remove some of the fat in the eye socket to accomplish this. Yet another possibility might be to use a medication to cause atrophy of some of this fat, such as a prostaglandin analog drug, Dr. Demer said.
Dr. Demer hopes that practitioners come away from the study with the realization that this is a plausible theory about normal tension open angle glaucoma. “If this theory is sufficiently supported to motivate change in clinical practice, it could dramatically alter the way glaucoma is diagnosed and treated for a large number of patients,” he said. “Also, this may have implications for an even bigger disease, which is the worldwide epidemic of myopia.”

Reference

1. Demer JL, et al. Magnetic resonance imaging of optic nerve traction during adduction in primary open-angle glaucoma with normal intraocular pressure. Invest Ophthalmol Vis Sci. 2017;58:4114–4125.

Editors’ note: Dr. Demer has no financial interests related to his comments.

Contact information

Demer: jld@jsei.ucla.edu

Normal tension glaucoma: The result of repetitive strain? Normal tension glaucoma: The result of repetitive strain?
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