Optic nerve head tissue deformations and stresses are thought to be major contributing factors to the development and progression of glaucomatous neuropathy. These biomechanical insults are often presumed to be associated with elevated IOP. However, many patients suffer from glaucoma despite a normal IOP, and thus there are important pathogenic factors that act at normal IOP or that are independent of IOP. Over the last few years, a couple of groups, including the one led by Dr. Demer, have explored the hypothesis that eye movements, particularly adduction, can cause optic nerve tension and traction of the posterior pole. The authors hypothesize that this posterior pole traction may cause substantial insult to the tissues of the optic nerve head, and thus be an IOP-independent factor for glaucoma. This is an intriguing hypothesis that has great potential to enable a more comprehensive understanding of how the biomechanical environment within the optic nerve head is affected by intra and extraocular factors.
In this study, the authors use MRI to measure how optic nerve traction in adduction varied with factors such as race and gender, paying particular attention to the patient IOPs. The images in the manuscript are compelling. Taken together with those in previous reports, the evidence is strong that gaze changes can cause major deformations of the optic nerve, including straightening, and what looks like tethering and traction of the posterior globe. This is the case even in control, non-glaucomatous, eyes. The optic nerve and posterior pole deformations are large and clearly discernible, even though the resolution of patient MRIs is low compared with that of other techniques typically used to visualize the optic nerve head. The large optic nerve head deformations caused by gaze changes have also been observed using optical coherence tomography and numerical modeling. The authors also found that in patients with open-angle glaucoma, increased adduction was associated with abnormally large globe retraction, and that this was independent of the level of IOP. This is consistent with the authors hypothesis that optic nerve traction is an independent pathogenic factor in the neuropathy, but there are other possible explanations. For instance, altered the tissue properties, due to remodeling, as has been reported in glaucoma, could change the deformations of the optic nerve or the optic nerve head.
Even if gaze-induced deformations are proven to cause or contribute to a neuropathy, it remains to be shown that this is a glaucomatous neuropathy
It is important to consider that it remains be demonstrated that optic nerve tethering caused by gaze changes can actually cause or contribute to the neuropathy. The observed large scale deformations of the optic nerve head are consistent with the idea, but they are not yet proof. Since tethering during adduction appears common, it would also be important to understand why only some people seem to be affected. Further, even if gaze-induced deformations are proven to cause or contribute to a neuropathy, it remains to be shown that this is a glaucomatous neuropathy. Of course, any neuropathy is important to the patient, and thus clinically relevant, but the mechanism does matter.