NDLI: Relating Retinal Ganglion Cell Function and Retinal Nerve Fiber Layer (RNFL) Retardance to Progressive Loss of RNFL Thickness and Optic Nerve Axons in Experimental Glaucoma

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Relating Retinal Ganglion Cell Function and Retinal Nerve Fiber Layer (RNFL) Retardance to Progressive Loss of RNFL Thickness and Optic Nerve Axons in Experimental Glaucoma

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cull, Grant Wang, Lin Reynaud, Juan Burgoyne, Claude F. Fortune, Brad
Abstract	PURPOSE: To relate changes in retinal function and retinal nerve fiber layer (RNFL) retardance to loss of RNFL thickness and optic nerve axon counts in a nonhuman primate (NHP) model of experimental glaucoma (EG). METHODS: Bilateral longitudinal measurements of peripapillary RNFL thickness (spectral-domain optical coherence tomography, SDOCT; Spectralis), retardance (GDxVCC), and multifocal electroretinography (mfERG; VERIS) were performed in 39 NHP at baseline (BL; median, 5 recordings; range, 3-10) and weekly after induction of unilateral EG by laser photocoagulation of the trabecular meshwork. Multifocal ERG responses were high-pass filtered (>75 Hz) to measure high- and low-frequency component (HFC and LFC) amplitudes, including LFC features N1, P1, and N2. High-frequency component amplitudes are known to specifically reflect retinal ganglion cell (RGC) function. Complete (100%) axon counts of orbital optic nerves were obtained in 31/39 NHP. RESULTS: Postlaser follow-up was 10.4 ± 7.9 months; mean and peak IOP were 18 ± 5 and 41 ± 11 mm Hg in EG eyes, 11 ± 2 and 18 ± 6 mm Hg in control (CTL) eyes. At the final available time point, RNFL thickness had decreased from BL by 14 ± 14%, retardance by 20 ± 11%, and the mfERG HFC by 30 ± 17% (P < 0.0001 each). Longitudinal changes in retardance and HFC were linearly related to RNFL thickness change (R2 = 0.51, P < 0.0001 and R2 = 0.22, P = 0.002, respectively); LFC N2 was weakly related but N1 or P2 (N1: R2 = 0.07, P = 0.11; P1: R2 = 0.04, P = 0.24; N2: R2 = 0.13, P = 0.02). At zero change from BL for RNFL thickness (Y-intercept), retardance was reduced by 11% (95% confidence interval [CI]: -15.3% to -6.8%) and HFC by 21.5% (95% CI: -28.7% to -14.3%). Relative loss of RNFL thickness, retardance, and HFC (EG:CTL) were each related to axon loss (R2 = 0.66, P < 0.0001; R2 = 0.42, P < 0.0001; R2 = 0.42, P < 0.0001, respectively), but only retardance and HFC were significantly reduced at zero relative axon loss (Y-intercept; retardance: -9.4%, 95% CI: -15.5% to -3.4%; HFC: -10.9%, 95% CI: -18.6% to -3.2%; RNFL thickness: +1.8%, 95% CI: -4.9% to +5.4%). CONCLUSIONS: Retinal nerve fiber layer retardance and RGC function exhibit progressive loss from baseline before any loss of RNFL thickness or orbital optic nerve axons occurs in NHP EG. These in vivo measures might serve as potential biomarkers of early-stage glaucomatous damage preceding axon loss and RGC death.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.15-16548
Journal	Investigative Opthalmology & Visual Science
Issue Number	6
Volume Number	56
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2015-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Glaucoma Physiopathology Nerve Fibers Pathology Optic Nerve Diseases Retinal Ganglion Cells Physiology Animals Axons Disease Models, Animal Electroretinography Intraocular Pressure Macaca Mulatta Optic Disk Tomography, Optical Coherence Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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