In this paper, Haykal and co-workers report findings from diffusion-weighted MRI scans of the optic tracts and optic radiations in 12 primary open angle glaucoma (POAG) patients from 2017- 2018. The same patients had been recruited to earlier MRI studies in 2008-2009 and 2013- 2014 and these served as the initial MRI scans to which the latter ones in this study were compared. The mean time interval between scans was 6.1 ± 2.4 years and 4.8 ± 1.7 years in glaucoma and control group
White matter density differences were measured by fiber density (FD), fiber bundle cross-section (FC) and their combination (FDC), and were compared to 14 age-matched controls. Retinal nerve fiber layer (RNFL) changes were evaluated by laser polarimetry. Visual fields in the glaucoma group were assessed by HVF with early to advanced stages of loss noted. The control group was evaluated by FDT. The average of right and left eye RNFL and visual field parameters were used to assess clinical changes.
In this pilot study, no significant correlation of MRI with clinical findings was observed and thus the relationship of MRI findings to glaucoma disease progression is uncertain. The authors reported a significant decrease in FD in the right optic tract and both optic radiations, however no significant changes to the left optic tract were noted. Studies of the lateral geniculate nucleus (LGN), the relay station between these tracts and radiations, may add context to the findings, given that earlier neuroimaging studies have shown significant LGN neural degeneration in glaucoma patients.1,2
Future studies with increased sample size, more sensitive RNFL assessment with OCT, measurement of visual field damage at multiple time points, and information regarding glaucoma treatment received may allow more accurate assessment of glaucoma progression. Longitudinal MRI assessment with optimized methods at additional time points may also help to understand central visual system findings in relation to the clinical course of disease.
The concept of a lag of transsynaptic degeneration lends itself to a discussion of potential neuroprotective drugs to protect against visual system degeneration
Transsynaptic degeneration of the central visual system is well described in experimental primate glaucoma.3,4,5 The concept of a lag of transsynaptic degeneration lends itself to a discussion of potential neuroprotective drugs to protect against visual system degeneration. Indeed, memantine has been shown to attenuate both neuron atrophy6 and dendritic shrinkage in this model.7 At this time, lowering intraocular pressure remains the cornerstone of treatment to reduce the risk of progressive visual system degeneration in glaucoma.8