Abstract
Purpose :
Open-angle glaucoma (OAG) is associated with neuroanatomical changes. However, it is unclear whether this indicates that OAG is an eye disease that also affects the brain – due to functional deprivation or transsynaptic degeneration – or if this supports that OAG should be considered part of a neurodegenerative disorder that also affects the eye. In this study, we aim to unravel the underlying mechanism of the association between neuroanatomical changes and OAG. We do so by assessing whether these changes appear in OAG patients with a unilateral visual field defect (unilateral OAG), as functional deprivation is not a priori expected in this group.
Methods :
We included 19 unilateral OAG patients, 15 age-matched controls with non-glaucomatous unilateral blindness (unilaterally blind controls; due to trauma or tumor at least five years ago), and 20 age-matched healthy controls. We acquired T1-weighted magnetic resonance images in all subjects. The images were analyzed using voxel- and surface-based morphometry. Outcome measures were volumes of gray and white matter, cortical thickness, mean curvature and surface area of the gray matter.
Results :
Compared to the healthy controls, the pregeniculate white matter volume was lower in the unilateral OAG patients (optic nerve: p=0.001; optic chiasm: p=0.001); compared to the unilaterally blind controls, it was higher in the unilateral OAG patients (optic nerve: p=0.003; optic chiasm p=0.043). Compared to both the healthy and the unilaterally blind controls, cortical thickness of the visual cortex was lower in the unilateral OAG patients (occipital pole: p=0.006 and p=0.008, respectively; superior lateral occipital cortex: p=0.047 and p=0.004, respectively); compared to the unilaterally blind controls, cortical thickness of the inferior lateral occipital cortex was lower in the unilateral OAG patients (p=0.017).
Conclusions :
We found neuroanatomical changes in unilateral OAG patients that were more widespread than the changes in unilaterally blind subjects, despite the latter group having a more extensive loss of visual input. Furthermore, these changes do not include the entire visual pathways. Therefore, these neuroanatomical changes cannot exclusively be explained by either functional deprivation or transsynaptical degeneration. This indicates that there is a general neurodegenerative brain component to OAG.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.