A focal lamina cribrosa (LC) defect is defined as a laminar surface irregularity that interrupts the smooth curvilinear contour of the anterior LC surface, which is usually observed on cross-sectional optic nerve imaging by optical coher-ence tomography.1,2 Since focal LC defects were first described in 2012 in glaucomatous eyes,1 studies have characterized the structure2-4 and associated clinical features2,5,6 of these defects in glaucoma, and suggested its pathogenic and clinical significance as a marker of progressive glaucomatous damage.6-8
In this longitudinal cohort study, Moghimi et al. showed that the mean rate of retinal nerve fiber layer (RNFL) thinning was two-fold faster in eyes with than without LC defects, with the most noticeable RNFL thinning observed at the location of the LC defect. These findings were comparable to those of a previous study, which showed a significant topographic relationship between the optic disc pit and the location of future RNFL thinning.6 The authors concluded that the LC defects could be an independent factor for rapid RNFL thinning, and that glaucoma progression might correspond to the location of the LC defect.
The mechanism underlying the LC defect and its association with glaucoma are poorly understood. The LC defect may indicate a localized susceptibility of the LC to the damaging effects of elevated intraocular pressure (IOP).3,6 It is also possible that structural alterations in the LC affects the axonal flow of the nearby axons.5 Alternatively, vascular insufficiency in eyes with LC defects may increase their susceptibility to glaucoma progression.9
The authors hypothesized that the importance of each risk factor might differ between eyes with and without LC defects. They therefore assessed the role of each factor in eyes with LC defects. Interestingly, IOP, which was significantly associated with faster RNFL thinning in eyes without LC defects, was NOT significantly associated with faster RNFL thinning in eyes with LC defects. Such finding may indicate that factors other than mechanical stress are more important in eyes LC defects. It remains unclear, however, whether the pathogenesis of glaucoma differs in eyes with and without LC defects.
A more pronounced IOP reduction may be required in eyes with LC defects, because these eyes may be more susceptible to glaucoma progression
Without providing a conclusive answer to this question, Moghimi et al. cited another study showing regional microvasculature dropout at the locations of LC defects,9 suggesting that these microvascular alterations may increase the rate of glaucoma progression in these regions. However, the authors also emphasized that further reduction in IOP may slow glaucoma progression in eyes with LC defects. Thinner cornea, rather than increased IOP, was significantly associated with faster RNFL loss in eyes with LC defects in their study. Corneal thickness may reflect the biomechanical properties of the optic nerve head that is susceptible to glaucoma. In this regard, a more pronounced IOP reduction may be required in eyes with LC defects, because these eyes may be more susceptible to glaucoma progression.