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H. Yang, G. Williams, J. Downs, I. Sigal, M. Roberts, J. Grimm, H. Thompson, C. Burgoyne; Optic Nerve Head (ONH) Lamina Cribrosa Insertion Migration and Pialization in Early Non-Human Primate (NHP) Experimental Glaucoma. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1631.
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To geometrically characterize the lamina cribrosa insertion into the scleral canal wall in normal and early experimental glaucoma (EEG) NHP ONH to test whether regional posterior (outward) migration of the lamina cribrosa insertion occurs in NHP EEG leading to pialization (laminar beam insertion into the pia instead of the sclera).
Trephinated ONHs from both eyes of 12 normal (N) and 9 unilateral EEG NHPs were perfusion fixed, serial sectioned, 3D reconstructed and delineated. Regional and overall values for the following distances were calculated for each ONH: anterior scleral canal opening to anterior laminar insertion distance(ASCO-ALI); anterior to posterior laminar insertion distance (ALI-PLI); and posterior scleral canal opening to posterior laminar insertion distance (PSCO-PLI). The outward ALI and PLI migrations were defined to be statistically significant changes in ASCO-ALI and PSCO-PLI distances in the outward direction. Data were pooled into 4 groups based on perfusion IOP and eye status: N10/10 (n=6); N 10/30or45 (n=6); EEG 10/10 (n=3) and EEG 10/30or45 (n=6). Treatment and region effects were accessed within each NHP and overall by ANOVA.
ALI was outwardly migrated in the EEG 30/45 group (P<0.0001). PLI was outwardly migrated in EEG 10/10 (22 µm) and EEG 30/45 (44 µm) (P<0.0001) groups. Laminar insertion thickening (ALI-PLI expansion) was significant (32 µm in both EEG groups). These changes of EEG eyes held true in a majority of EEG monkeys. Regionally, 3 of the 9 EEG eyes demonstrated outward PLI migration to the degree of posterior lamina pialization (Fig 1) in at least 2 adjacent regions.
Outward migration of the ALI may be the result of physical trauma and/or remodeling of the anterior laminar beams. Outward migration of the PLI may be the result of laminar remodeling that includes retrolaminar septal recruitment (Roberts et al, IOVS, 2009). The implications of these findings on the pathogenesis of ONH splinter hemorrhages, cupping, blood flow alterations and axon loss will be discussed.
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