Deformation of the lamina cribrosa and anterior scleral canal wall in early experimental glaucoma.

PURPOSE To test the hypothesis that pathophysiologic deformation of the lamina cribrosa and anterior scleral canal wall underlies the onset of confocal scanning laser tomography (CSLT)-detected optic nerve head (ONH) surface change in early experimental glaucoma. METHODS Both eyes of four normal (two normal eyes) monkeys and four with early glaucoma (one eye with laser-induced IOP elevation, observed until the onset of CSLT-detected ONH surface change) were enucleated immediately after death and immersion fixed at IOP 0 mm Hg. In an additional four normal monkeys and five with early glaucoma, both eyes were cannulated, and IOP set to 10 mm Hg in one normal eye and either 30 or 45 mm Hg in the other (normal or early-glaucoma) eye. After 15 to 80 minutes of acute IOP elevation, these nine monkeys were perfusion-fixed. Within images of serial sagittal sections of the ONH tissues in all 17 monkeys, anterior lamina cribrosa position, laminar thickness, and scleral canal diameter were measured. For each parameter, differences between the two eyes of each monkey and between treatment groups were assessed by ANOVA. RESULTS Within the eyes of the eight monkeys with IOP 0 mm Hg, the lamina cribrosa was posteriorly displaced and thicker and the scleral canal was enlarged at Bruch's membrane and at the anterior laminar insertion in the early-glaucoma eyes compared with the contralateral normal eyes (plastic deformation). Within the high-IOP normal eyes, the lamina cribrosa was posteriorly displaced compared with that in the low-IOP normal eyes, but there were no significant differences in laminar thickness or scleral canal diameter (normal compliance). Within the high-IOP early-glaucoma eyes, the lamina cribrosa was posteriorly displaced and thicker and the scleral canal enlarged, compared with both low-IOP normal eyes and high-IOP normal eyes (hypercompliant deformation). Differences in laminar position between the high-IOP early-glaucoma eyes and the contralateral low-IOP normal eyes (hypercompliant plus plastic deformation) were more than eight times greater than the differences between the high-IOP normal eyes and the contralateral low-IOP normal eyes (normal compliance). CONCLUSIONS Both plastic (permanent) and hypercompliant deformation of the lamina cribrosa and anterior scleral canal wall are present in young adult monkey eyes with early experimental glaucoma. These findings suggest that damage to the ONH connective tissues occurs early in the monkey model of experimental glaucoma.

[1]  J C Morrison,et al.  The anatomy and pathophysiology of the optic nerve head in glaucoma. , 2001, Journal of glaucoma.

[2]  H. Thompson,et al.  Optic Disc Surface Compliance Testing Using Confocal Scanning Laser Tomography in the Normal Monkey Eye , 2001, Journal of glaucoma.

[3]  M. Wax,et al.  In vitro evaluation of reactive astrocyte migration, a component of tissue remodeling in glaucomatous optic nerve head , 2001, Glia.

[4]  C. S. Ricard,et al.  Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human optic nerve head astrocytes , 2001, Glia.

[5]  R. T. Hart,et al.  The optic nerve head as a biomechanical structure: initial finite element modeling. , 2000, Investigative ophthalmology & visual science.

[6]  M. Wax,et al.  Matrix metalloproteinases and tumor necrosis factor α in glaucomatous optic nerve head , 2000 .

[7]  D. Easty,et al.  Age related compliance of the lamina cribrosa in human eyes , 2000, The British journal of ophthalmology.

[8]  T. Fukuchi,et al.  Collagen fibrillar network in the optic nerve head of normal monkey eyes and monkey eyes with laser-induced glaucoma--a scanning electron microscopic study. , 1999, Current eye research.

[9]  M. Hernandez,et al.  Astrocyte Responses in Human Optic Nerve Head With Primary Open‐Angle Glaucoma , 1997, Journal of glaucoma.

[10]  David J. Sheskin,et al.  Handbook of Parametric and Nonparametric Statistical Procedures , 1997 .

[11]  H A Quigley,et al.  Change in the Optic Disc and Nerve Fiber Layer Estimated with the Glaucoma‐Scope in Monkey Eyes , 1996, Journal of glaucoma.

[12]  R. Varma,et al.  Early changes in optic disc compliance and surface position in experimental glaucoma. , 1995, Ophthalmology.

[13]  C. R. Ethier,et al.  Deformation of the lamina cribrosa by elevated intraocular pressure. , 1994, The British journal of ophthalmology.

[14]  M. Hernandez Ultrastructural immunocytochemical analysis of elastin in the human lamina cribrosa. Changes in elastic fibers in primary open-angle glaucoma. , 1992, Investigative ophthalmology & visual science.

[15]  H. Quigley,et al.  Alterations in elastin of the optic nerve head in human and experimental glaucoma. , 1991, The British journal of ophthalmology.

[16]  G. Dunkelberger,et al.  Optic nerve head extracellular matrix in primary optic atrophy and experimental glaucoma. , 1990, Archives of ophthalmology.

[17]  W. Andrzejewska,et al.  Changes in the extracellular matrix of the human optic nerve head in primary open-angle glaucoma. , 1990, American journal of ophthalmology.

[18]  Y. Ogura,et al.  The relation between glaucomatous damage and optic nerve head mechanical compliance. , 1989, Archives of ophthalmology.

[19]  Jost B. Jonas,et al.  Optic disc morphometry in chronic primary open-angle glaucoma , 1988, Graefe's Archive for Clinical and Experimental Ophthalmology.

[20]  J M Miller,et al.  Videographic measurements of optic nerve topography in glaucoma. , 1988, Investigative ophthalmology & visual science.

[21]  J. M. Miller,et al.  Quantitative evaluation of the optic nerve head in patients with unilateral visual field loss from primary open-angle glaucoma. , 1987, Ophthalmology.

[22]  N. Levy,et al.  Displacement of optic nerve head in response to short-term intraocular pressure elevation in human eyes. , 1984, Archives of ophthalmology.

[23]  R. Massof,et al.  Morphologic changes in the lamina cribrosa correlated with neural loss in open-angle glaucoma. , 1983, American journal of ophthalmology.

[24]  H. Quigley,et al.  Chronic experimental glaucoma in primates. II. Effect of extended intraocular pressure elevation on optic nerve head and axonal transport. , 1980, Investigative ophthalmology & visual science.

[25]  H. Quigley,et al.  An analysis of visual acuity, visual fields, and disk cupping in childhood glaucoma. , 1979, American journal of ophthalmology.

[26]  A. H. Bunt,et al.  Orthograde and retrograde axoplasmic transport during acute ocular hypertension in the monkey. , 1977, Investigative ophthalmology & visual science.

[27]  H. Quigley,et al.  The dynamics and location of axonal transport blockade by acute intraocular pressure elevation in primate optic nerve. , 1976, Investigative ophthalmology.

[28]  A. Hendrickson,et al.  Effect of intraocular pressure on rapid axoplasmic transport in monkey optic nerve. , 1974, Investigative ophthalmology.

[29]  J. Craig,et al.  The lamina cribrosa in normal and glaucomatous human eyes. , 1974, Transactions - American Academy of Ophthalmology and Otolaryngology. American Academy of Ophthalmology and Otolaryngology.

[30]  H. Quigley Childhood glaucoma: results with trabeculotomy and study of reversible cupping. , 1982, Ophthalmology.