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Lirong Qin, Galen Williams, Stuart Gardiner, Brad Fortune, J Crawford Downs, Claude Burgoyne, Hongli Yang; Spectral Domain Optical Coherence Tomography (SDOCT) Detected Lamina Cribrosa Compliance Change in Non-human Primate (NHP) Early Experimental Glaucoma (EEG). Invest. Ophthalmol. Vis. Sci. 2013;54(15):53.
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To compare optic nerve head (ONH) SDOCT morphology change due to acute IOP elevation from 10 to 30 mmHg (SDOCT compliance) within the contralateral normal (N) and EEG eyes of 13 NHPs at the onset of unilateral EEG.
BBoth eyes of each NHP (3-23 y.o.) underwent ONH SDOCT and Confocal Scanning Laser Tomography (CSLT) (both Heidelberg Engineering) ONH imaging 30 minutes after manometric IOP lowering to 10 mmHg and again 30 minutes after elevation to 30 mmHg prior to and every two weeks following the onset of unilateral, laser-induced, chronic IOP elevation. EEG was defined as the onset of CSLT surface change confirmed on two occasions. Within the 40 radial B-scans of the 30 degree SD-OCT volumes from the second EEG confirmation session, masked operators delineated the retinal and ONH landmarks necessary to quantify: anterior lamina cribrosa surface depth (ALCSD) relative to a Bruch’s Membrane Opening (BMO) reference plane (ALCSD-BMO), ALCSD and BMO depth relative to a peripheral BM reference plane (ALCSD-BM and BMOdepth), neuroretinal rim width, BMO area, and prelaminar tissue thickness. Mixed effects models were used to assess the effects of IOP (i.e. compliance), disease status, and the interaction between them. A significant interaction was taken as evidence of a change in compliance.
ALCSD-BMO and ALCSD-BM change due to acute IOP elevation was significantly greater in the EEG compared to normal eyes (ALCSD-BMO: 44±42 μm (mean±s.d.) in EEG eyes vs 5±14 μm in N eyes, p=0.0046; ALCSD-BM: 86±63 in EEG eyes vs 37±19 in N eyes, p=0.0141). Significant compliance was observed for all eyes between IOP 10 and 30 for BMO depth, prelaminar tissue thickness and rim width (p<0.0001), but no significant difference in compliance was observed between N and EEG eyes for these parameters. EEG eye compliance (ALCSD-BMO and ACSD-BM change) was significantly predicted by cumulative IOP difference and peak IOP (maximum IOP of the EEG eye).
In a pooled analysis, NHP EEG eyes cross-sectionally exhibit significantly more SDOCT-measured lamina cribrosa compliance than their contralateral normal eyes as quantified by ALCSD-BMO or ALCSD-BM. This compliance is predicted by the IOP exposure and may be a manifestation of EEG-induced alterations in lamina cribrosa and peripapillary scleral structural stiffness.
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