Recently, Lee et al. suggested that development of γPPA and a focal LC defect during axial elongation are mainly caused by nasal shifting of the LC and vulnerability on the opposite side of the LC shift from subsequent scleral expansion and LC damage.
22–24 Further, their recent study showed that eyes with a mild shift of the LC had larger angular deviation of vascular trunk against the horizontal midline and a higher prevalence of a focal LC defect than did those with moderate or severe shift.
23 These findings correspond well with the current results showing that eyes with focal γPPA had a higher prevalence of a focal LC defect and a maximal EOBT located farther from the fovea-BM-opening axis than did eyes with conventional γPPA.
23 When the axis of LC shift is highly deviated from the horizontal axis, it collides easily with the radially oriented collagen fiber of the scleral tissue,
23,25 and, as such, might lead to high susceptibility to focal LC damage and concurrent development of focally extended scleral flange. On the other hand, it is also possible that mechanisms other than axial elongation play a role in the development of focal γPPA.
5 The present focal γPPA group was older and had a shorter AXL than the conventional γPPA group, and their age and AXL were comparable to those of the no γPPA group. Therefore, the development of small exposed border tissue in aged patients with relatively short AXL might not be fully explained by an LC shift incurred by axial elongation. In these circumstances, morphological LC change incurred by sustained vertical force related to IOP could serve as a potential mechanism of adjacent-border-tissue dragging. This process, moreover, might be facilitated by altered biomechanical properties of the LC and border tissue as well as by increased IOP. In this respect, the current observations that focal γPPA group had thinner RNFL than no γPPA group in the TI sector, an area in which focal LC defect and maximal focal γPPA frequently develop add to the literature.
14 Because focal LC defects are known to be closely associated with functional and structural damage to RGC axons,
11,26,27 development of an EOBT, glaucomatous RNFL defect, and focal LC defect may share a common pathway. Similarly, eyes with a focal LC defect had significantly thinner RNFL in the TI sector in all three subgroups of γPPA. However, the present study is limited in such speculations due to its cross-sectional nature and lack of differences in the VF parameters according to the presence of focal γPPA and focal LC defect. Lack of the VF differences may be because the disease severity of the current study population was relatively mild (average VF MD, -7.08 dB) compared with that of a previous study (average VF MD, -11.64 dB), which showed the relationship between the focal LC defect and VF severity.
27 Another recent study on eyes having early to moderate glaucoma (average VF MD, −4.19 dB) showed that VF severity did not differ according to the presence of a LC defect.
28 Further, longitudinal studies on patients with glaucoma with various disease severities are warranted to elucidate the causal relationships among axial elongation, morphological change of LC, and border tissue, as well as glaucomatous VF and RNFL damage.