Focal Lamina Cribrosa Defects Associated With Glaucomatous Rim Thinning and Acquired Pits

Abstract

Considering the potential clinical importance of focal lamina cribrosa (LC) defects as a characteristic structural feature in glaucoma and a risk factor for glaucomatous visual field progression, it may be helpful to know the structure of focal LC defects and the spatial relationship between them and glaucomatous optic disc changes such as neuroretinal rim thinning/ notching and acquired pits of the optic nerve (APON). Objective: To investigate structural and spatial relationships between focal LC defects and glaucomatous neuroretinal rim thinning/notching and APON. Design: In a cross-sectional analysis of data from an ongoing, prospective, longitudinal study, serial enhanceddepth imaging (EDI) optical coherence tomographic (OCT) images of the optic nerve head were obtained from patients with glaucoma and reviewed for focal LC defects (laminar holes or disinsertions). Anterior laminar insertion points and edges of laminar holes or disinsertions were marked in EDI-OCT images, reconstructed 3-dimensionally, and superimposed on optic disc photographs. Setting: A glaucoma referral practice. Participants: Two hundred thirty-nine eyes (120 patients) were examined. Fifty-four eyes were excluded because of an incomplete horizontal or vertical set of serial EDI-OCT images or poor-quality EDI-OCT images owing to media opacity, irregular tear film, or poor patient cooperation. Among the remaining 185 eyes, 40 (from 31 patients) had laminar holes or disinsertions and were included for analysis. Main Outcome Measures: Presence, extent, and location of laminar holes or disinsertions. Results: Among 185 eyes, 11 laminar holes and 36 laminar disinsertions were found in 40 eyes. Superimposed images of the 3-dimensionally reconstructed focal LC defects and disc photographs showed that the outline of the LC defect corresponded almost precisely to that of clinical APON for 6 laminar holes and that the LC defect was much larger than and enclosed APON for 10 laminar disinsertions. The remaining 5 laminar holes and 26 laminar disinsertions corresponded to focal neuroretinal rim loss, with no evidence of APON in disc photographs. Conclusions and Relevance: Focal LC defects (laminar holes or disinsertions) are associated with neuroretinal rim loss and APON. The extent of LC defects can be visualized more effectively on EDI-OCT images than by clinical examination.

Three-Dimensional Imaging of Lamina Cribrosa Defects in Glaucoma Using Swept-Source Optical Coherence Tomography

“…However, the same research group included hole-like defects (laminar holes) and prominently altered laminar insertions (laminar disinsertions) to assess the association between lamina cribrosa defects and neuroretinal rim loss and APON because they aimed to avoid misclassification of normal anatomical variations and artifacts as real glaucomatous focal lamina cribrosa defects by using stricter criteria. 27 Our strategy is consistent with this approach, and the lamina cavity and lamina disinsertion on 3D SS-OCT in the current study appear to correspond to the hole-like defects and altered laminar insertions, respectively, in the earlier study. In order to interpret the findings of the earlier and present studies, it must be taken into consideration that only eyes with full-thickness lamina cribrosa defects were included for further analysis.…”

“…Most of the full-thickness lamina cribrosa defects were located at or near the superior optic disc margin, consistent with earlier studies. 21,27 Histopathological studies revealed the following regional variations of the lamina cribrosa in presumably healthy human eyes: the superior and inferior portions, compared to the nasal and temporal regions, had larger single pore areas and summed pore areas, thinner connective tissue, and less glial cell support. [37][38][39] These regional variations, which are thought to account for the greater susceptibility to early glaucomatous damage in the superior and inferior portions, may be responsible for the frequent detection of full-thickness lamina cribrosa defects in these susceptible locations.…”

The Connective Tissue Components of Optic Nerve Head Cupping in Monkey Experimental Glaucoma Part 1: Global Change

“…First, using current OCT imaging, it may be linked to nerve fiber layer (NFL) hemorrhages, 16 NFL defects, 34 visual field progression, 35 and the development of acquired optic disc pits. 36 Second, it may confirm the relative timing of its direction (i.e., inward during initial deformation, outward as deformation progresses) suggested by our cross-sectional findings. Regarding posterior laminar insertion migration, we propose that outward posterior laminar insertion migration is a prominent component of laminar remodeling in response to chronic IOP elevation in the monkey eye.…”

Effect of Focal Lamina Cribrosa Defect on Disc Hemorrhage Area in Glaucoma

“…Although the etiology of DH is unclear, both mechanical 13,23 and vascular theories 24,25 having been hypothesized, these results suggest that a localized structural LC defect might be a factor predisposing to the disruption of the microvascular structure passing through the damaged sector. Focal LC defects occur mostly on the far periphery of the LC at or near the laminar insertion point, 21,26 and similarly, DH occurs preferentially at the disc margin. 1,27 In the same context, several studies have demonstrated that, in glaucomatous eyes, FLCD is spatially correlated not only with neuroretinal rim loss, 26 visual field defects, 21 and RNFL defects, 28 but also with DH.…”