Experimental Glaucoma

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Claude F. Burgoyne - One of the best experts on this subject based on the ideXlab platform.

  • Comparing three different modes of electroretinography in Experimental Glaucoma: diagnostic performance and correlation to structure.
    Documenta ophthalmologica. Advances in ophthalmology, 2017
    Co-Authors: Laura J Wilsey, Claude F. Burgoyne, Grant Cull, Christy Hardin, Sowjanya Gowrisankaran, Brad Fortune
    Abstract:

    Purpose To compare diagnostic performance and structure–function correlations of multifocal electroretinogram (mfERG), full-field flash ERG (ff-ERG) photopic negative response (PhNR) and transient pattern-reversal ERG (PERG) in a non-human primate (NHP) model of Experimental Glaucoma (EG).

  • In Vivo Detection of Laminar and Peripapillary Scleral Hypercompliance in Early Monkey Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Kevin M. Ivers, Stuart K. Gardiner, Hongli Yang, Brad Fortune, Lirong Qin, Luke Reyes, Claude F. Burgoyne
    Abstract:

    PURPOSE To compare optical coherence tomography (OCT) detected, optic nerve head (ONH) compliance within control and Experimental Glaucoma (EG) eyes of 15 monkeys at EG onset. METHODS Intraocular pressure (IOP) was chronically elevated in one eye of each animal using a laser. Experimental Glaucoma onset was identified using confocal scanning laser tomography (CSLT). Optical coherence tomography ONH imaging (40 radial B-scans) was performed at 10 mm Hg before and after laser. At EG onset, OCT scans were obtained at IOP 10 and 30 mm Hg. Optical coherence tomography landmarks within the IOP 10/30 images were delineated to quantify IOP 10/30 differences (compliance) for anterior lamina cribrosa surface depth (ALCSD) relative to Bruch's membrane opening (BMO) (ALCSD-BMO), ALCSD relative to peripheral BM (ALCSD-BM), and BMO depth relative to peripheral BM (BMOD-BM). A linear mixed effects model assessed for acute IOP elevation effects, control versus EG eye effects, and their interaction. RESULTS Effects of IOP elevation were greater in EG versus control eyes for ALCSD-BMO (-46 ± 45 vs. -8 ± 13 μm, P = 0.0042) and ALCSD-BM (-92 ± 64 vs. -42 ± 22 μm, P = 0.0075). Experimental Glaucoma eye-specific ALCSD-BMO and ALCSD-BM compliance exceeded the range of control eye compliance in 9 and 8 of the 15 EG eyes, respectively. Post-laser peak IOP (R2 = 0.798, P < 0.0001) and post-laser mean IOP (R2 = 0.634, P < 0.0004) most strongly correlated to EG versus control eye differences in ALCSD-BMO compliance. CONCLUSIONS Laminar (ALCSD-BMO) and peripapillary scleral (ALCSD-BM) hypercompliance are present in most monkey eyes at the onset of EG.

  • Lamina Cribrosa Microarchitecture in Monkey Early Experimental Glaucoma: Global Change.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Juan Reynaud, Howard Lockwood, Stuart K. Gardiner, Galen Williams, Hongli Yang, Claude F. Burgoyne
    Abstract:

    PURPOSE The purpose of this study was to characterize Experimental Glaucoma (EG) versus control eye differences in lamina cribrosa (LC), beam diameter (BD), pore diameter (PD), connective tissue volume fraction (CTVF), connective tissue volume (CTV), and LC volume (LV) in monkey early EG. METHODS Optic nerve heads (ONHs) of 14 unilateral EG and 6 bilateral normal (BN) monkeys underwent three-dimensional reconstruction and LC beam segmentation. Each beam and pore voxel was assigned a diameter based on the largest sphere that contained it before transformation to a common cylinder with inner, middle, and outer layers. Full-thickness and layer averages for BD, PD, CTVF, CTV, and LV were calculated for each ONH. Beam diameter and PD distributions for each ONH were fit to a gamma distribution and summarized by scale and shape parameters. Experimental Glaucoma and depth effects were assessed for each parameter by linear mixed-effects (LME) modeling. Animal-specific EG versus control eye differences that exceeded the maximum intereye difference among the six BN animals were considered significant. RESULTS Overall EG eye mean PD was 12.8% larger (28.2 ± 5.6 vs. 25.0 ± 3.3 μm), CTV was 26.5% larger (100.06 ± 47.98 vs. 79.12 ± 28.35 × 106 μm3), and LV was 40% larger (229.29 ± 98.19 vs. 163.63 ± 39.87 × 106 μm3) than control eyes (P ≤ 0.05, LME). Experimental Glaucoma effects were significantly different by layer for PD (P = 0.0097) and CTVF (P < 0.0001). Pore diameter expanded consistently across all PDs. Experimental Glaucoma eye-specific parameter change was variable in magnitude and direction. CONCLUSIONS Pore diameter, CTV, and LV increase in monkey early EG; however, EG eye-specific change is variable and includes both increases and decreases in BD and CTVF.

  • expansions of the neurovascular scleral canal and contained optic nerve occur early in the hypertonic saline rat Experimental Glaucoma model
    Experimental Eye Research, 2016
    Co-Authors: Marta Pazos, Stuart K. Gardiner, Hongli Yang, William O Cepurna, Elaine C Johnson, John C Morrison, Claude F. Burgoyne
    Abstract:

    Purpose To characterize early optic nerve head (ONH) structural change in rat Experimental Glaucoma (EG).

  • The Non-Human Primate Experimental Glaucoma Model
    Experimental eye research, 2015
    Co-Authors: Claude F. Burgoyne
    Abstract:

    The purpose of this report is to summarize the current strengths and weaknesses of the non-human primate (NHP) Experimental Glaucoma (EG) model through sections devoted to its history, methods, important findings, alternative optic neuropathy models and future directions. NHP EG has become well established for studying human Glaucoma in part because the NHP optic nerve head (ONH) shares a close anatomic association with the human ONH and because it provides the only means of systematically studying the very earliest visual system responses to chronic intraocular pressure (IOP) elevation, i.e. the conversion from ocular hypertension to Glaucomatous damage. However, NHPs are impractical for studies that require large animal numbers, demonstrate spontaneous Glaucoma only rarely, do not currently provide a model of the neuropathy at normal levels of IOP, and cannot easily be genetically manipulated, except through tissue-specific, viral vectors. The goal of this summary is to direct NHP EG and non-NHP EG investigators to the previous, current and future accomplishment of clinically relevant knowledge in this model.

Harry A. Quigley - One of the best experts on this subject based on the ideXlab platform.

  • Scleral fibroblast response to Experimental Glaucoma in mice.
    Molecular vision, 2016
    Co-Authors: Ericka Oglesby, Gülgün Tezel, Elizabeth Cone-kimball, Matthew R. Steinhart, Joan L. Jefferys, Mary Ellen Pease, Harry A. Quigley
    Abstract:

    Purpose To study the detailed cellular and molecular changes in the mouse sclera subjected to Experimental Glaucoma.

  • Changes in scleral collagen organization in murine chronic Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2014
    Co-Authors: Jacek K. Pijanka, Mary Ellen Pease, Harry A. Quigley, Elizabeth C. Kimball, Ahmed Abass, Thomas Sorensen, Thao D. Nguyen, Craig Boote
    Abstract:

    Purpose: The organization of scleral collagen helps to determine the eye's biomechanical response to intraocular pressure (IOP), and may therefore be important in Glaucoma. This study provided a quantitative assessment of changes in scleral collagen fibril organization in bead-induced murine Experimental Glaucoma. Methods: Wide-angle x-ray scattering was used to study the effect of bead-induced Glaucoma on posterior scleral collagen organization in one eye of 12 CD1 mice, with untreated fellow eyes serving as controls. Three collagen parameters were measured: (i) the local preferred fibril directions, (ii) the degree of collagen anisotropy and (iii) the total fibrillar collagen content. Results: The mouse sclera featured a largely circumferential orientation of fibrillar collagen with respect to the optic nerve head canal. Localized alteration to fibril orientations was evident in the inferior peripapillary sclera of bead-treated eyes. Collagen anisotropy was significantly (p < 0.05) reduced in bead-treated eyes in the superior peripapillary (Treated: 43 ± 8%; Control: 49 ± 6%) and mid-posterior (Treated: 39 ± 4%; Control: 43 ± 4%) sclera, and in the peripapillary region overall (Treated: 43 ± 6%; Control: 47 ± 3%). No significant differences in total collagen content were found between groups. Conclusions: Spatial changes in collagen fibril anisotropy occur in the posterior sclera of mice with bead-induced chronic IOP elevation and axonal damage. These results support the idea that dynamic changes in scleral form and structure play a role in the development of Experimental Glaucoma in mice, and potentially in human Glaucoma.

  • retinal ganglion cell morphology after optic nerve crush and Experimental Glaucoma
    Investigative Ophthalmology & Visual Science, 2012
    Co-Authors: G Kalesnykas, Ericka Oglesby, Matthew R. Steinhart, Mary Ellen Pease, Donald J Zack, Frances E Cone, Jing Tian, Harry A. Quigley
    Abstract:

    Purpose. To study sequential changes in retinal ganglion cell (RGC) morphology in mice after optic nerve crush and after induction of Experimental Glaucoma.

  • Calibration of the TonoLab Tonometer in Mice with Spontaneous or Experimental Glaucoma
    Investigative ophthalmology & visual science, 2011
    Co-Authors: Mary Ellen Pease, Frances E Cone, Scott Gelman, Janice L. Son, Harry A. Quigley
    Abstract:

    It is essential to measure intraocular pressure (IOP) accurately in Experimental Glaucoma research. Mouse models permit genetic manipulations in the elucidation of Glaucoma pathogenesis and treatment, but the tiny size of the mouse's eye presents a challenge to accurate tonometry. Various solutions have been devised for IOP measurement in the mouse, including needle cannulation through the cornea, use of existing commercial tonometers such as the pneumatonograph and TonoPen (Reichert, Inc., Depew, NY), and modifications of other commercial tonometers.1–10 The validity of noninvasive tonometry in the mouse eye has been confirmed in several strains under anesthesia.11–14 McKinnon et al.15 concluded: “TonoLab tonometry is technically easier than TonoPen tonometry, and has become the IOP measurement technique of choice” for Experimental Glaucoma in the mouse. In the DBA/2J mouse, spontaneous increase in IOP occurs, and many experiments have been conducted, often with needle cannulation used for tonometry. It may be preferable not to puncture the cornea repeatedly to monitor IOP, but it has not been shown that tonometry accurately reflects IOP in spontaneous or induced Glaucoma in the mouse. Continuous IOP monitoring with implantable devices is under development, but has not been reported for mouse eyes. Sappington et al.16 have recently published a mouse model of Glaucoma involving injection of beads into the anterior chamber. We have modified this model by first injecting beads (of 6 μm diameter) followed by viscoelastic injection. In a companion report, we confirm that the mouse eye enlarges significantly with chronic IOP elevation, as was first documented in the DBA/2J mouse. Enlargement of the eye could alter tonometric accuracy. Hence, we performed calibration studies in mouse eyes with bead/viscoelastic Experimental Glaucoma and their fellow eyes, studying younger and older mice of three different strains, as well as DBA/2J mice after development of spontaneous Glaucoma. One previous study compared TonoLab (TioLat, Helsinki, Finland) IOP measures with needle cannulation, but without testing a range of IOP.17 To our knowledge, this is the first extensive calibration study of tonometry in both spontaneous and induced mouse Glaucoma.

  • obstructed axonal transport of bdnf and its receptor trkb in Experimental Glaucoma
    Investigative Ophthalmology & Visual Science, 2000
    Co-Authors: Mary Ellen Pease, Harry A. Quigley, S J Mckinnon, Lisa A Kerriganbaumrind, Donald J Zack
    Abstract:

    PURPOSE. In both animal model systems and in human Glaucoma, retinal ganglion cells (RGCs) die by apoptosis. To understand how RGC apoptosis is initiated in these systems, the authors studied RGC neurotrophin transport in Experimental Glaucoma using acute intraocular pressure (IOP) elevations in rats and chronic IOP elevation and unilateral optic nerve transections in monkeys. Moons. Eyes were studied in masked fashion by light and electron microscopy and by immunohistochemistry with antibodies directed against the tyrosine kinase receptors (TrkA, B, and C) and against brain-derived neurotrophic factor (BDNF), as well as by autoradiography to identify retrograde axonal transport of 125 I-BDNF injected into the superior colliculus. RESULTS. With acute Glaucoma in the rat, RGC axons became abnormally dilated, accumulating vesicles presumed to be moving in axonal transport at the optic nerve head. Label for TrkB, but not TrkA, was relatively increased at and behind the optic nerve head with IOP elevation. Abnormal, focal labeling for TrkB and BDNF was identified in axons of monkey optic nerve heads with chronic Glaucoma. With acute IOP elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer at less than half the level of control eyes. CONCLUSIONS. Interruption of BDNF retrograde transport and accumulation of TrkB at the optic nerve head in acute and chronic Glaucoma models suggest a role for neurotrophin deprivation in the pathogenesis of RGC death in Glaucoma.

Hongli Yang - One of the best experts on this subject based on the ideXlab platform.

  • In Vivo Detection of Laminar and Peripapillary Scleral Hypercompliance in Early Monkey Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Kevin M. Ivers, Stuart K. Gardiner, Hongli Yang, Brad Fortune, Lirong Qin, Luke Reyes, Claude F. Burgoyne
    Abstract:

    PURPOSE To compare optical coherence tomography (OCT) detected, optic nerve head (ONH) compliance within control and Experimental Glaucoma (EG) eyes of 15 monkeys at EG onset. METHODS Intraocular pressure (IOP) was chronically elevated in one eye of each animal using a laser. Experimental Glaucoma onset was identified using confocal scanning laser tomography (CSLT). Optical coherence tomography ONH imaging (40 radial B-scans) was performed at 10 mm Hg before and after laser. At EG onset, OCT scans were obtained at IOP 10 and 30 mm Hg. Optical coherence tomography landmarks within the IOP 10/30 images were delineated to quantify IOP 10/30 differences (compliance) for anterior lamina cribrosa surface depth (ALCSD) relative to Bruch's membrane opening (BMO) (ALCSD-BMO), ALCSD relative to peripheral BM (ALCSD-BM), and BMO depth relative to peripheral BM (BMOD-BM). A linear mixed effects model assessed for acute IOP elevation effects, control versus EG eye effects, and their interaction. RESULTS Effects of IOP elevation were greater in EG versus control eyes for ALCSD-BMO (-46 ± 45 vs. -8 ± 13 μm, P = 0.0042) and ALCSD-BM (-92 ± 64 vs. -42 ± 22 μm, P = 0.0075). Experimental Glaucoma eye-specific ALCSD-BMO and ALCSD-BM compliance exceeded the range of control eye compliance in 9 and 8 of the 15 EG eyes, respectively. Post-laser peak IOP (R2 = 0.798, P < 0.0001) and post-laser mean IOP (R2 = 0.634, P < 0.0004) most strongly correlated to EG versus control eye differences in ALCSD-BMO compliance. CONCLUSIONS Laminar (ALCSD-BMO) and peripapillary scleral (ALCSD-BM) hypercompliance are present in most monkey eyes at the onset of EG.

  • Lamina Cribrosa Microarchitecture in Monkey Early Experimental Glaucoma: Global Change.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Juan Reynaud, Howard Lockwood, Stuart K. Gardiner, Galen Williams, Hongli Yang, Claude F. Burgoyne
    Abstract:

    PURPOSE The purpose of this study was to characterize Experimental Glaucoma (EG) versus control eye differences in lamina cribrosa (LC), beam diameter (BD), pore diameter (PD), connective tissue volume fraction (CTVF), connective tissue volume (CTV), and LC volume (LV) in monkey early EG. METHODS Optic nerve heads (ONHs) of 14 unilateral EG and 6 bilateral normal (BN) monkeys underwent three-dimensional reconstruction and LC beam segmentation. Each beam and pore voxel was assigned a diameter based on the largest sphere that contained it before transformation to a common cylinder with inner, middle, and outer layers. Full-thickness and layer averages for BD, PD, CTVF, CTV, and LV were calculated for each ONH. Beam diameter and PD distributions for each ONH were fit to a gamma distribution and summarized by scale and shape parameters. Experimental Glaucoma and depth effects were assessed for each parameter by linear mixed-effects (LME) modeling. Animal-specific EG versus control eye differences that exceeded the maximum intereye difference among the six BN animals were considered significant. RESULTS Overall EG eye mean PD was 12.8% larger (28.2 ± 5.6 vs. 25.0 ± 3.3 μm), CTV was 26.5% larger (100.06 ± 47.98 vs. 79.12 ± 28.35 × 106 μm3), and LV was 40% larger (229.29 ± 98.19 vs. 163.63 ± 39.87 × 106 μm3) than control eyes (P ≤ 0.05, LME). Experimental Glaucoma effects were significantly different by layer for PD (P = 0.0097) and CTVF (P < 0.0001). Pore diameter expanded consistently across all PDs. Experimental Glaucoma eye-specific parameter change was variable in magnitude and direction. CONCLUSIONS Pore diameter, CTV, and LV increase in monkey early EG; however, EG eye-specific change is variable and includes both increases and decreases in BD and CTVF.

  • expansions of the neurovascular scleral canal and contained optic nerve occur early in the hypertonic saline rat Experimental Glaucoma model
    Experimental Eye Research, 2016
    Co-Authors: Marta Pazos, Stuart K. Gardiner, Hongli Yang, William O Cepurna, Elaine C Johnson, John C Morrison, Claude F. Burgoyne
    Abstract:

    Purpose To characterize early optic nerve head (ONH) structural change in rat Experimental Glaucoma (EG).

  • Age-related differences in longitudinal structural change by spectral-domain optical coherence tomography in early Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2014
    Co-Authors: Hongli Yang, Juan Reynaud, Stuart K. Gardiner, Galen Williams, Brad Fortune, Christy Hardin, Nicholas G. Strouthidis, J. Crawford Downs, Claude F. Burgoyne
    Abstract:

    Purpose. To characterize age-related differences in the magnitude of spectral-domain optical coherence tomography (SD-OCT) structural change in early Experimental Glaucoma (EG).

  • Longitudinal Detection of Optic Nerve Head Changes by Spectral Domain Optical Coherence Tomography in Early Experimental Glaucoma
    Investigative ophthalmology & visual science, 2014
    Co-Authors: Hongli Yang, Stuart K. Gardiner, Galen Williams, Brad Fortune, Christy Hardin, Nicholas G. Strouthidis, Claude F. Burgoyne
    Abstract:

    Purpose. We determined if the detection of spectral-domain optical coherence tomography (SDOCT) optic nerve head (ONH) change precedes the detection of confocal scanning laser tomography (CSLT) ONH surface, SDOCT retinal nerve fiber layer (RNFL), scanning laser perimetry (SLP), and multifocal electroretinography (mfERG) change in eight Experimental Glaucoma (EG) eyes.

Donald J Zack - One of the best experts on this subject based on the ideXlab platform.

  • retinal ganglion cell morphology after optic nerve crush and Experimental Glaucoma
    Investigative Ophthalmology & Visual Science, 2012
    Co-Authors: G Kalesnykas, Ericka Oglesby, Matthew R. Steinhart, Mary Ellen Pease, Donald J Zack, Frances E Cone, Jing Tian, Harry A. Quigley
    Abstract:

    Purpose. To study sequential changes in retinal ganglion cell (RGC) morphology in mice after optic nerve crush and after induction of Experimental Glaucoma.

  • obstructed axonal transport of bdnf and its receptor trkb in Experimental Glaucoma
    Investigative Ophthalmology & Visual Science, 2000
    Co-Authors: Mary Ellen Pease, Harry A. Quigley, S J Mckinnon, Lisa A Kerriganbaumrind, Donald J Zack
    Abstract:

    PURPOSE. In both animal model systems and in human Glaucoma, retinal ganglion cells (RGCs) die by apoptosis. To understand how RGC apoptosis is initiated in these systems, the authors studied RGC neurotrophin transport in Experimental Glaucoma using acute intraocular pressure (IOP) elevations in rats and chronic IOP elevation and unilateral optic nerve transections in monkeys. Moons. Eyes were studied in masked fashion by light and electron microscopy and by immunohistochemistry with antibodies directed against the tyrosine kinase receptors (TrkA, B, and C) and against brain-derived neurotrophic factor (BDNF), as well as by autoradiography to identify retrograde axonal transport of 125 I-BDNF injected into the superior colliculus. RESULTS. With acute Glaucoma in the rat, RGC axons became abnormally dilated, accumulating vesicles presumed to be moving in axonal transport at the optic nerve head. Label for TrkB, but not TrkA, was relatively increased at and behind the optic nerve head with IOP elevation. Abnormal, focal labeling for TrkB and BDNF was identified in axons of monkey optic nerve heads with chronic Glaucoma. With acute IOP elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer at less than half the level of control eyes. CONCLUSIONS. Interruption of BDNF retrograde transport and accumulation of TrkB at the optic nerve head in acute and chronic Glaucoma models suggest a role for neurotrophin deprivation in the pathogenesis of RGC death in Glaucoma.

  • Obstructed axonal transport of BDNF and its receptor TrkB in Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2000
    Co-Authors: Mary Ellen Pease, Harry A. Quigley, S J Mckinnon, Lisa A. Kerrigan-baumrind, Donald J Zack
    Abstract:

    Purpose In both animal model system and in human Glaucoma, retinal ganglion cells (RGCs) die by apoptosis. To understand how RGC apoptosis is initiated in these systems, the authors studied RGC neurotrophin transport in Experimental Glaucoma using acute intraocular pressure (IOP) elevations in rats and chronic IOP elevation and unilateral optic nerve transections in monkeys. Methods Eyes were studied in masked fashion by light and electron microscopy and by immunohistochemistry with antibodies directed against the tyrosine kinase receptors (TrkA, B, and C) and against brain-derived neurotrophic factor (BDNF), as well as by autoradiography to identify retrograde axonal transport of 125I-BDNF injected into the superior colliculus. Results With acute Glaucoma in the rat, RGC axons became abnormally dilated, accumulating vesicles presumed to be moving in axonal transport at the optic nerve head. Label for TrkB, but not TrkA, was relatively increased at and behind the optic nerve head with IOP elevation. Abnormal, focal labeling for TrkB and BDNF was identified in axons of monkey optic nerve heads with chronic Glaucoma. With acute IOP elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer at less than half the level of control eyes. Conclusions Interruption of BDNF retrograde transport and accumulation of TrkB at the optic nerve head in acute and chronic Glaucoma models suggest a role for neurotrophin deprivation in the pathogenesis of RGC death in Glaucoma.

  • retinal ganglion cell death in Experimental Glaucoma and after axotomy occurs by apoptosis
    Investigative Ophthalmology & Visual Science, 1995
    Co-Authors: Harry A. Quigley, Mary Ellen Pease, Robert W Nickells, L A Kerrigan, D Thibault, Donald J Zack
    Abstract:

    PURPOSE: To investigate whether retinal ganglion cell death in Experimental Glaucoma and after axotomy occurs by apoptosis. METHODS: Chronic elevated eye pressure was produced in 20 monkey eyes, and the optic nerve was transected unilaterally in the orbit of 10 monkeys and 14 rabbits. Sixteen monkey and 14 rabbit eyes were studied as normal controls. Analytic methods included light and electron microscopy, histochemistry for DNA fragmentation (TUNEL method), and DNA electrophoresis in agarose gels. RESULTS: Dying ganglion cells in the Experimental retinas exhibited morphologic features of apoptosis, including chromatin condensation and formation of apoptotic bodies. Cells with a positive reaction for DNA fragmentation were observed in eyes subjected to axotomy and Experimental Glaucoma but were only rarely encountered in control eyes. No evidence of internucleosomal fragmentation was detected electrophoretically, possibly because of the small proportion of cells that were dying at any given time. CONCLUSION: Some retinal ganglion cells injured by Glaucoma and by axotomy die by apoptosis.

Stuart K. Gardiner - One of the best experts on this subject based on the ideXlab platform.

  • In Vivo Detection of Laminar and Peripapillary Scleral Hypercompliance in Early Monkey Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Kevin M. Ivers, Stuart K. Gardiner, Hongli Yang, Brad Fortune, Lirong Qin, Luke Reyes, Claude F. Burgoyne
    Abstract:

    PURPOSE To compare optical coherence tomography (OCT) detected, optic nerve head (ONH) compliance within control and Experimental Glaucoma (EG) eyes of 15 monkeys at EG onset. METHODS Intraocular pressure (IOP) was chronically elevated in one eye of each animal using a laser. Experimental Glaucoma onset was identified using confocal scanning laser tomography (CSLT). Optical coherence tomography ONH imaging (40 radial B-scans) was performed at 10 mm Hg before and after laser. At EG onset, OCT scans were obtained at IOP 10 and 30 mm Hg. Optical coherence tomography landmarks within the IOP 10/30 images were delineated to quantify IOP 10/30 differences (compliance) for anterior lamina cribrosa surface depth (ALCSD) relative to Bruch's membrane opening (BMO) (ALCSD-BMO), ALCSD relative to peripheral BM (ALCSD-BM), and BMO depth relative to peripheral BM (BMOD-BM). A linear mixed effects model assessed for acute IOP elevation effects, control versus EG eye effects, and their interaction. RESULTS Effects of IOP elevation were greater in EG versus control eyes for ALCSD-BMO (-46 ± 45 vs. -8 ± 13 μm, P = 0.0042) and ALCSD-BM (-92 ± 64 vs. -42 ± 22 μm, P = 0.0075). Experimental Glaucoma eye-specific ALCSD-BMO and ALCSD-BM compliance exceeded the range of control eye compliance in 9 and 8 of the 15 EG eyes, respectively. Post-laser peak IOP (R2 = 0.798, P < 0.0001) and post-laser mean IOP (R2 = 0.634, P < 0.0004) most strongly correlated to EG versus control eye differences in ALCSD-BMO compliance. CONCLUSIONS Laminar (ALCSD-BMO) and peripapillary scleral (ALCSD-BM) hypercompliance are present in most monkey eyes at the onset of EG.

  • Lamina Cribrosa Microarchitecture in Monkey Early Experimental Glaucoma: Global Change.
    Investigative ophthalmology & visual science, 2016
    Co-Authors: Juan Reynaud, Howard Lockwood, Stuart K. Gardiner, Galen Williams, Hongli Yang, Claude F. Burgoyne
    Abstract:

    PURPOSE The purpose of this study was to characterize Experimental Glaucoma (EG) versus control eye differences in lamina cribrosa (LC), beam diameter (BD), pore diameter (PD), connective tissue volume fraction (CTVF), connective tissue volume (CTV), and LC volume (LV) in monkey early EG. METHODS Optic nerve heads (ONHs) of 14 unilateral EG and 6 bilateral normal (BN) monkeys underwent three-dimensional reconstruction and LC beam segmentation. Each beam and pore voxel was assigned a diameter based on the largest sphere that contained it before transformation to a common cylinder with inner, middle, and outer layers. Full-thickness and layer averages for BD, PD, CTVF, CTV, and LV were calculated for each ONH. Beam diameter and PD distributions for each ONH were fit to a gamma distribution and summarized by scale and shape parameters. Experimental Glaucoma and depth effects were assessed for each parameter by linear mixed-effects (LME) modeling. Animal-specific EG versus control eye differences that exceeded the maximum intereye difference among the six BN animals were considered significant. RESULTS Overall EG eye mean PD was 12.8% larger (28.2 ± 5.6 vs. 25.0 ± 3.3 μm), CTV was 26.5% larger (100.06 ± 47.98 vs. 79.12 ± 28.35 × 106 μm3), and LV was 40% larger (229.29 ± 98.19 vs. 163.63 ± 39.87 × 106 μm3) than control eyes (P ≤ 0.05, LME). Experimental Glaucoma effects were significantly different by layer for PD (P = 0.0097) and CTVF (P < 0.0001). Pore diameter expanded consistently across all PDs. Experimental Glaucoma eye-specific parameter change was variable in magnitude and direction. CONCLUSIONS Pore diameter, CTV, and LV increase in monkey early EG; however, EG eye-specific change is variable and includes both increases and decreases in BD and CTVF.

  • expansions of the neurovascular scleral canal and contained optic nerve occur early in the hypertonic saline rat Experimental Glaucoma model
    Experimental Eye Research, 2016
    Co-Authors: Marta Pazos, Stuart K. Gardiner, Hongli Yang, William O Cepurna, Elaine C Johnson, John C Morrison, Claude F. Burgoyne
    Abstract:

    Purpose To characterize early optic nerve head (ONH) structural change in rat Experimental Glaucoma (EG).

  • Age-related differences in longitudinal structural change by spectral-domain optical coherence tomography in early Experimental Glaucoma.
    Investigative ophthalmology & visual science, 2014
    Co-Authors: Hongli Yang, Juan Reynaud, Stuart K. Gardiner, Galen Williams, Brad Fortune, Christy Hardin, Nicholas G. Strouthidis, J. Crawford Downs, Claude F. Burgoyne
    Abstract:

    Purpose. To characterize age-related differences in the magnitude of spectral-domain optical coherence tomography (SD-OCT) structural change in early Experimental Glaucoma (EG).

  • Longitudinal Detection of Optic Nerve Head Changes by Spectral Domain Optical Coherence Tomography in Early Experimental Glaucoma
    Investigative ophthalmology & visual science, 2014
    Co-Authors: Hongli Yang, Stuart K. Gardiner, Galen Williams, Brad Fortune, Christy Hardin, Nicholas G. Strouthidis, Claude F. Burgoyne
    Abstract:

    Purpose. We determined if the detection of spectral-domain optical coherence tomography (SDOCT) optic nerve head (ONH) change precedes the detection of confocal scanning laser tomography (CSLT) ONH surface, SDOCT retinal nerve fiber layer (RNFL), scanning laser perimetry (SLP), and multifocal electroretinography (mfERG) change in eight Experimental Glaucoma (EG) eyes.

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