IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Downs, J. C.
Right arrow Articles by Burgoyne, C. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Downs, J. C.
Right arrow Articles by Burgoyne, C. F.
(Investigative Ophthalmology and Visual Science. 2001;42:3202-3208.)
© 2001 by The Association for Research in Vision and Ophthalmology, Inc.

Posterior Scleral Thickness in Perfusion-Fixed Normal and Early-Glaucoma Monkey Eyes

J. Crawford Downs1, Michael E. Ensor1, Anthony J. Bellezza1, Hilary W. Thompson2, Richard T. Hart1 and Claude F. Burgoyne1,2

1 From the Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana; and the 2 LSU Eye Center, Louisiana State University Health Sciences Center, New Orleans.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
PURPOSE. To characterize posterior scleral thickness in the normal monkey eye and to assess the effects of acute (15- to 80-minute) and short-term chronic (3- to 7-week) intraocular pressure (IOP) elevations.

METHODS. Both eyes of four normal monkeys (both eyes normal) and four monkeys with early glaucoma (one eye normal and one eye with induced chronic elevation of IOP) were cannulated. In each monkey, IOP was set to 10 mm Hg in the normal eye and 30 or 45 mm Hg in the contralateral eye (normal or early glaucoma) for 15 to 80 minutes. All eight monkeys were perfusion fixed, yielding eight low IOP–normal eyes, four high IOP–normal eyes, and four high IOP–early glaucoma eyes. Posterior scleral thickness was measured histomorphometrically at 15 measurement points within each eye, and the data were grouped by region: foveal, midposterior, posterior-equatorial, and equatorial.

RESULTS. Overall, posterior scleral thickness was significantly different in the various regions and among the treatment groups (P < 0.0001). In the low IOP–normal eyes, the posterior sclera was thickest in the foveal region (307 µm) and thinner in the midposterior (199 µm), posterior-equatorial (133 µm), and equatorial (179 µm) regions. In the high IOP–normal and high IOP–early glaucoma eyes, the posterior sclera was thinner both overall and within specific regions, compared with the low IOP–normal eyes.

CONCLUSIONS. The posterior sclera in the perfusion-fixed normal monkey eye thins progressively from the fovea to the equator and is thinnest just posterior to the equator. Acute and short-term chronic IOP elevations cause regional thinning within the posterior sclera of some monkey eyes, which significantly increases stresses in the scleral wall.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Scleral thickness is a critical component in determining the stresses (force/cross-sectional area) and strains (deformation under load) in the scleral shell due to intraocular pressure (IOP). For a given level of IOP, stress and strain in the scleral wall increase proportionally with a decrease in scleral thickness, according to the standard formula governing pressure vessel theory.1

In glaucoma, thinning of the sclera may occur in response to chronic elevation of IOP.2 In this circumstance, scleral wall stress that is already increased due to elevated IOP is further increased in those regions of glaucomatous scleral thinning. This suggests that not only the initial thickness but also the behavior (response to chronic IOP elevation) of the peripapillary sclera may contribute to the susceptibility of an individual optic nerve head (ONH) to a given level of IOP.

As part of an ongoing attempt to study the ONH as a biomechanical structure, we are building finite element models of the load-bearing connective tissues of the perfusion-fixed monkey lamina cribrosa, scleral canal wall, and peripapillary sclera. Finite element modeling is a computational technique that is used to estimate the stresses and strains within a complex, load-bearing structure. We have previously used this technique to describe IOP-related stress in models of an idealized human posterior scleral shell and ONH.3 We are currently constructing three-dimensionally accurate models to characterize the manner in which the load-bearing connective tissues of the lamina cribrosa and scleral canal wall are influenced and then damaged by a given level of IOP.

To construct a finite element model of the scleral canal wall and lamina cribrosa requires a model of the larger posterior scleral shell, to establish boundary conditions for the connective tissues of the peripapillary sclera. The response of a model of the ONH is not only determined by the level of applied IOP, but is also greatly influenced by the stresses and strains transmitted to the edge (boundary) of the ONH and peripapillary sclera by the adjacent posterior sclera. The purpose of this investigation was to characterize the thickness of the posterior sclera within perfusion-fixed normal monkey eyes and then to assess whether acute and/or short-term chronic elevations of IOP influence that thickness.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Animals
All animals were treated in accordance with the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research. Scleral specimens from eight male rhesus monkeys (estimated age, 5–11 years) killed as part of another study were obtained (Table 1) . Four of these monkeys, with two normal eyes, were perfusion fixed using buffered, hypertonic aldehyde solutions, with one eye set to low IOP (10 mm Hg) and one eye set to high IOP (either 30 or 45 mm Hg) for 15 to 80 minutes before fixation. In the other four monkeys, chronic elevated IOP had been induced in one eye 1 to 2 months earlier. Each of these monkeys was perfusion fixed with the normal eye set to low IOP (10 mm Hg) and the early experimental glaucomatous eye set to high IOP (either 30 or 45 mm Hg) 15 to 80 minutes before perfusion (Table 1) . Spontaneous IOPs were measured using an applanation tonometer (Tonopen XL; Bio-Rad, Glendale, CA), and axial length measurements were made with an A-scan ultrasonometer (A-1500 A-Scan; Sonomed, Lake Success, NY).


View this table:
[in this window]
[in a new window]
  		Table 1. Animal Data

 
Early Experimental Glaucoma
In both eyes of four monkeys, ONH surface compliance testing4 was performed on three separate occasions to characterize normal ONH surface position and compliance. Early experimental glaucoma was then induced in one eye of each animal by lasering the trabecular meshwork every 2 weeks until a statistically significant elevation in IOP was observed (Table 1) . Each lasered eye was then compliance tested every 2 weeks to detect the onset of early glaucomatous damage to the ONH tissues. Early glaucomatous damage was defined as the onset of fixed posterior deformation of the ONH surface and/or the onset of ONH surface hypercompliance within the data from two consecutive compliance tests.5 All four monkeys were perfusion fixed within 2 weeks of the onset of early glaucomatous damage.

Scleral Specimen Preparation
After perfusion fixation, the scleral tissues of the various monkeys were stored for different lengths of time in 5% glutaraldehyde solution before processing. However, both scleral shells of a given monkey were always processed for scleral specimen generation on the same day, as follows.

A 10-0 polypropylene suture was placed through the sclera to mark the position of the fovea, and the ONH and peripapillary sclera were then removed with a 6-mm trephine. The clean scleral shell was placed on a fixed polyethylene ball corresponding to the diameter of the shell, with the fovea at the apex. Vinyl stencils were then pinned at the fovea and the equator along the superior, inferior, nasal, and temporal axes. The stencils established the positions of the eight 2-mm-wide scleral strips, which were cut with a scalpel: four cardinal strips, which extended from the fovea to the equator along the nasal, temporal, superior, and inferior axes, and four equatorial strips, which divided the clinical equator of the posterior scleral shell into four quadrants: inferonasal, superonasal, inferotemporal, and superotemporal (Fig. 1A) . The foveal end of each cardinal strip was cut with a pointed end and marked with a 10-0 polypropylene suture passed 3 mm from the tip. The eight scleral strips for each eye were then dehydrated, infiltrated, and embedded in historesin (Technovit 7100; Kulzer, Wehrheim, Germany) perpendicular to the face of the embedding block to allow for serial sagittal sectioning.



View larger version (23K):
[in this window]
[in a new window]
  		Figure 1. (A) Diagram of a posterior scleral shell showing the orientation of the scleral strips and the locations of the scleral thickness measurement points. (B) Diagram of a posterior scleral shell showing the regionalization of the scleral thickness measurement points according to their location relative to the fovea. S, superior; N, nasal; I, inferior; T, temporal; SN, superonasal; IN, inferonasal; IT, inferotemporal; ST, superotemporal.

 
Scleral Specimen Sampling
A preliminary study determined that a single group of eight sagittal sections was adequate to characterize scleral thickness throughout the entire 2-mm width of a scleral specimen (data not shown). For each scleral specimen, a microtome (model RM2165; Leica, Bensheim, Germany) was used to cut 200 µm into the embedded tissues. Eight serial, sagittal, 3-µm-thick sections were then cut, mounted on glass slides, and stained with Van Gieson stain.

Section Image Acquisition
A digital color image of each section was acquired under a light microscope (Optiphot-2; Nikon, Tokyo, Japan) fitted with a three-charge-coupled device (CCD) color camera (HV-C20; Hitachi, Tokyo, Japan), along with a companion image of a slide-mounted micrometer scale to allow calibration of the exact pixel size. All images were generated at a resolution of approximately 5 µm/pixel (Fig. 2) .



View larger version (22K):
[in this window]
[in a new window]
  		Figure 2. Image of a histologic sagittal section of a cardinal scleral strip showing the location of the pairs of marks used to determine scleral thickness. 0, orientation suture. The foveal marks (1 and 2) were placed 1 mm toward the fovea from the orientation suture, the posterior-equatorial marks (3 and 4) were placed at the equatorial end, and the midposterior marks (5 and 6) were placed equidistant between the foveal and posterior-equatorial marks.

 
Scleral Thickness Measurements within Each Image
A total of 1024 section images (16 eyes with 8 scleral strips per eye and 8 sections per strip) were processed as follows. First, the exact pixel size was calculated using the companion slide-mounted micrometer image. For each cardinal strip image, three pairs of opposing marks (foveal, midposterior, and posterior-equatorial) were placed on the anterior and posterior scleral surfaces (Figs. 1A 2) . For the equatorial section images, one pair of opposing marks was made on the anterior and posterior surfaces at the midpoint of the scleral section. Thus, scleral thickness was measured at 15 measurement points in each eye (Fig. 1A) .

Each image was marked by an operator who was masked to treatment group. After marking, the coordinates of each pair of points were output to a custom routine (Mathematica software; Wolfram Research, Champaign, IL) that calculated the Cartesian distance between the points.

Assignment to Treatment Groups
Data from each eye were assigned to one of three treatment groups: low IOP–normal eyes (n = 8), high IOP–normal eyes (n = 4), and high IOP–early glaucoma eyes (n = 4), where low IOP and high IOP signify acute IOP settings, and early glaucoma indicates chronic IOP elevation.

Analysis of Variance Testing to Assess the Effects of Treatment, Region, and Monkey
A nested analysis of variance (ANOVA) was used to assess the effects of treatment and region on the dependent variable, scleral thickness. Within this ANOVA, overall effects of acute elevation of IOP were first assessed by comparing the pooled data from the low IOP–normal and high IOP–normal treatment groups. The effects of acute IOP elevation were secondarily assessed in individual monkeys by comparing the low IOP–normal eye with the high IOP–normal eye in monkeys 1, 2, 3, and 4.

The overall effect of chronic IOP elevation (early glaucoma) was assessed by comparing the pooled data from the high IOP–normal and high IOP–early glaucoma treatment groups.

Finally, the combined effects of both acute and chronic IOP elevation were first assessed by comparing the pooled data from the low IOP–normal and high IOP–early glaucoma treatment groups, and secondarily assessed by comparing the low IOP–normal eye with the high IOP–early glaucoma eye in monkeys 5, 6, 7, and 8.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Reproducibility of Scleral Thickness Measurements
The results of three separate measurements of scleral thickness made on different days by a single observer at four measurement points on scleral strips from each of the two eyes of two monkeys are reported in Table 2 . By ANOVA, the effect of measurement day was not significant overall or within the data from monkey 8, but was significant in the data from monkey 1 (P < 0.001). Even in the face of the variability due to measurement day, the effects of monkey, eye (treatment), measurement point, and region remained significant (P < 0.0001). Additionally, the measurement day differences in monkey 1, although statistically significant, were small relative to the magnitude of the significant differences observed between eyes, measurement points, and regions (Figs. 3 4 and 5 ; Table 3 ).


View this table:
[in this window]
[in a new window]
  		Table 2. Reproducibility Study: Posterior Scleral Thickness at Four Measurement Points in Both Eyes of Two Monkeys

 


View larger version (32K):
[in this window]
[in a new window]
  		Figure 3. Diagrams of posterior scleral shells showing mean posterior scleral thickness (in micrometers) at each measurement point, both overall (A) and for each treatment group (B, C, D).

 


View larger version (16K):
[in this window]
[in a new window]
  		Figure 4. Diagrams of posterior scleral shells showing the location and direction of significant changes in mean posterior scleral thickness in pair-wise treatment group comparisons at each measurement point (P < 0.05). (-), thinner; (+), thicker. Remaining abbreviations are as in Figure 1 .

 


View larger version (24K):
[in this window]
[in a new window]
  		Figure 5. Diagrams of posterior scleral shells showing the location and direction of significant changes in mean posterior scleral thickness (A) in the high IOP–normal eye compared with the contralateral low IOP–normal eye in normal monkeys 1, 2, 3, and 4 and (B) in the high IOP–early glaucoma eye compared with the contralateral low IOP–normal eye in monkeys 5, 6, 7, and 8 (P < 0.05). Symbols and abbreviations are as in Figures 4 and 1 , respectively.

 

View this table:
[in this window]
[in a new window]
  		Table 3. Scleral Thickness Overall and by Region and Treatment and Calculated Increase in Scleral Wall Stress Due to Scleral Thinning

 
Mean Posterior Scleral Thickness by Measurement Point
The mean posterior scleral thickness at each measurement point is displayed for all 16 eyes (overall) and for each treatment group in Figure 3 . Because the effect of treatment was significant by ANOVA (P < 0.0001), the data for each treatment group are emphasized throughout the remainder of this report.

Mean Posterior Scleral Thickness by Region
The mean posterior scleral thicknesses for the four regions (foveal, midposterior, posterior-equatorial, and equatorial; Fig. 1B ) were significantly different for virtually all comparisons within the data for each of the three treatment groups by ANOVA testing (Table 3) . Within the low IOP–normal eyes, the sclera was thickest near the fovea (mean, 307 µm), thinner in the midposterior and equatorial regions (199 and 179 µm, respectively), and thinnest in the posterior-equatorial regions (133 µm). The same pattern of scleral thickness was present in all treatment groups (Table 3) and in each of the 16 eyes considered individually (data not shown).

Effect of Acute IOP Elevation on Posterior Scleral Thickness
Overall, mean scleral thickness was significantly less in the high IOP–normal eyes (186 µm), compared with the low IOP–normal eyes (204 µm; Table 3 ). By region, scleral thickness was indistinguishable in three of the four regions; however, in the foveal region, the sclera was significantly thinner in the high IOP–normal eyes (265 µm), compared with the low IOP–normal eyes (307 µm; P < 0.0001, ANOVA). Within the four normal monkeys (monkeys 1, 2, 3, and 4) considered individually, the mean posterior scleral thickness was significantly greater in the normal eye fixed at low IOP than in the contralateral normal eye fixed at high IOP in monkeys 1 and 2, but not in monkeys 3 and 4 (data not shown). Finally, scleral thickness was significantly less at 6 of the 15 measurement points in the high IOP–normal treatment group, compared with the low IOP–normal group (Fig. 4A) . Statistically significant differences in scleral thickness between the low IOP–normal eyes and the contralateral high IOP–normal eyes of monkeys 1 to 4 individually are shown for each measurement point in Figure 5A . Although the pooled data in Figure 4A show a trend toward posterior scleral thinning in the high IOP–normal treatment group, the individual monkey data, as shown in Figure 5A , are equivocal.

Effect of Short-Term Chronic IOP Elevation (Early Glaucoma) on Posterior Scleral Thickness
Overall and within three of the four regions, mean posterior scleral thicknesses in the high IOP–normal eyes and high IOP–early glaucoma eyes were indistinguishable (Table 3) . In the midposterior region, however, mean scleral thickness was significantly less in the high IOP–early glaucoma eyes (168 µm) than in the high IOP–normal eyes (189 µm; Table 3 ). Mean scleral thickness was significantly less at 4 of the 15 measurement points and significantly greater at 2 of the 15 measurement points in the high IOP–early glaucoma eyes than in the high IOP–normal eyes (Fig. 4B) .

Combined Effect of Acute and Short-Term Chronic IOP Elevation on Posterior Scleral Thickness
Overall, the posterior sclera was significantly thinner in the high IOP–early glaucoma eyes (182 µm) compared with the low IOP–normal eyes (204 µm; Table 3 ). By region, scleral thickness was indistinguishable between the two groups in the equatorial region, but was significantly less in the foveal, midposterior, and posterior-equatorial regions in the high IOP–glaucoma eyes (Table 3) . Within the four monkeys with early glaucoma (monkeys 5, 6, 7, and 8) considered individually, the posterior sclera was significantly thinner in the high IOP–early glaucoma eye in three of the four monkeys (data not shown).

Finally, scleral thickness was significantly less at 9 of the 15 measurement points and significantly greater at 1 of the 15 measurement points in the high IOP–early glaucoma eyes, compared with the low IOP–normal eyes (Fig. 4C) . Statistically significant scleral thickness differences between the high IOP–early glaucoma eyes and low IOP–normal eyes of monkeys 5, 6, 7, and 8 are shown in Figure 5B . Within these data, the overwhelming trend is toward thinning of the sclera in the high IOP–early glaucoma eyes compared with their contralateral low IOP–normal control eyes.


   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The purpose of this study was to characterize the thickness of the posterior sclera in normal (perfusion-fixed) monkey eyes and secondarily to assess whether acute and short-term chronic elevations of IOP induce detectable posterior scleral thinning. The principal findings of this report are as follows. First, in the low IOP–normal eyes, the posterior sclera was thickest in the foveal region (307 µm) and thinner in the midposterior (199 µm), posterior-equatorial (133 µm), and equatorial (179 µm) regions. Second, compared with the low IOP–normal eyes, the posterior sclera in both the high IOP–normal eyes and the high IOP–early glaucoma eyes was thinner, both overall and in specific regions. Third, although scleral thinning appeared to be greater in the high IOP–early glaucoma eyes than in the high IOP–normal eyes, the differences were not clear enough to separate the effects of acute IOP elevations and short-term chronic IOP elevations (early glaucoma) on posterior scleral thickness in the monkey eye.

The central feature of our data is the profound thinning of the sclera, when moving anteriorly from the fovea toward the equator, with the posterior sclera being thinnest just posterior to the equator. This trend is present within the data from all 16 eyes combined (overall), the data for each of the three treatment groups, and the data for each of the 16 eyes considered individually. A similar pattern has been reported for the posterior sclera in human eyes.6 7 8 Olson et al.6 reported scleral thickness in humans of 900 to 1000 µm in the foveal region and 390 µm near the equator. Fine and Yanoff7 reported human scleral thicknesses of 1000 and 400 to 500 µm in the foveal and equatorial regions, respectively. Although our data indicate that perfusion-fixed monkey sclera is thinner in all regions than human sclera, the relative decrease (approximately 57%) in scleral thickness from the foveal region to the posterior equatorial region is comparable to that reported in human eyes (approximately 60% in the study by Olson et al.6 and 50% to 60% in the study by Fine and Yanoff7 ).

Comparison of the high IOP–normal data (n = 4) with the low IOP–normal data (n = 8) suggests that thinning of the posterior sclera can be detected after acute (15–80 minutes) elevation of IOP in some monkey eyes. This effect can be seen in the overall and regional data (Table 3) and at some of the individual measurement points, principally within the foveal region (Fig. 4) . However, in the four normal monkeys considered individually, scleral thinning was not consistently present in the high-IOP eye (Fig. 5A) . These findings suggest that acute IOP elevations induce posterior scleral thinning in some, but not all, normal monkey eyes.

By contrast, scleral thinning resulting from the combined effects of acute and short-term chronic IOP elevation was clearly present within both the pooled and individual monkey data of the four early glaucoma monkeys. Nemeth2 used B-scan ultrasonography to detect thinning of the posterior coat volume (total tissue volume of the retina-choroid-sclera) in human glaucomatous eyes. However, that study is limited by the relatively small number of patients (n = 15), a questionable statistical strategy, and the inability of B-scan ultrasonography to isolate scleral thickness within its measurement of posterior coat thickness.

The histologic data in our study suggest that short-term chronic (mean of 4.3 weeks) IOP elevations of moderate magnitude (mean maximum measured IOP, 27.3 mm Hg) cause detectable thinning of the posterior sclera in a majority of monkey eyes. Two distinct phenomena may underlie these findings. In the first scenario, the material properties of early glaucomatous sclera in the monkey are unaltered, and scleral thinning is due either to the Poisson effect (thinning of the wall due to expansion of the shell) or radial compression of the sclera (which squeezes out fluid, causing a loss in scleral tissue volume), or a combination of the two. In the second scenario, the extracellular matrix of the posterior sclera is damaged or remodeled in early-glaucoma monkey eyes. In this case, the scleral thinning we detected in early-glaucoma eyes was due to an abnormal response to the acute IOP elevation that preceded fixation. Quigley et al.9 reported a decrease in collagen fibril density within the lamina cribrosa and peripapillary sclera in human eyes with glaucomatous damage. Although the same study did not detect this effect in monkeys, it is possible that extracellular matrix alterations within the posterior sclera occur early in response to chronic elevation of IOP. In this connection, initial results from ongoing studies in our laboratory suggest that the viscoelastic material properties of the peripapillary sclera are fundamentally altered in early-glaucoma eyes.10 11

Our present study is limited by several considerations. First, we used perfusion fixation to best ensure that the connective tissues of the scleral shell and ONH were captured in their in vivo state at controlled levels of IOP. Panda-Jonas et al.12 reported 12.5% linear shrinkage in the optic disc after fixation. In a recent study of human sclera, thickness did not change significantly in response to fixation.6 There is also some evidence to suggest that acellular collagenous tissues swell with fixation.13 14 Regardless of the degree of shrinkage or swelling, assuming that it occurs evenly over all specimens, our scleral thickness measurements should still legitimately model the relative variation in scleral thickness by location and treatment that would be present in nonfixed monkey eyes.

Second, our perfusion conditions did not allow us to have a group of monkeys in which both normal eyes were perfusion fixed at an IOP of 10 mm Hg. Such a group of monkeys would have allowed us to characterize the magnitude of scleral thickness differences between the two eyes of a normal monkey—overall, regionally, and at each measurement point—because of physiologic differences alone. Also, we did not have monkeys with low IOP–normal and low IOP–early glaucoma eyes; this comparison would have enabled us to isolate the effect of short-term, chronic IOP elevation from that of acute IOP elevation immediately preceding fixation. In addition, we did not have monkeys with low IOP– and high IOP–early glaucoma eyes, which would have allowed evaluation of the effect of acute IOP elevation in early-glaucoma eyes.

Finally, perfusion of the scleral vessels (and therefore fixation) may have been inhibited in the high-IOP eyes. To ensure good fixation at high pressure, animals were left undisturbed (with high IOP maintained) for 1 hour before dissection. However, after enucleation, the vortex and retinal veins were partially filled with blood in a subset of the high-IOP eyes. In addition, when serial sagittal sections of the ONH of these same monkey eyes were viewed as part of another study, the choroid also was intermittently filled with blood. Taken together, these findings suggest that in some high-IOP eyes, scleral thickness may not have been captured at the time of initial perfusion (at high IOP), but instead may include some degree of artifactual scleral swelling that occurred between perfusion, enucleation, and placement of the posterior globes into fixative. If such swelling is present, it suggests that our study may underestimate the effect of acute and short-term chronic IOP elevation on posterior scleral thickness in the normal and early-glaucoma monkey eye.

IOP-induced alterations in scleral thickness are important because stress and strain in the scleral wall increase proportionally with a decrease in scleral thickness. Thus, if the sclera thins in response to chronic IOP elevations, the increases in scleral wall stresses due to the elevated IOP are further exacerbated by the increases in stress due to scleral thinning.

Spherical thin-walled pressure vessel theory states that circumferential scleral wall stress equals IOP multiplied by the internal radius of the scleral shell, divided by two times the wall thickness.1 As a result, a decrease in scleral thickness of a certain percentage induces approximately the same percentage increase in scleral wall stress. Although the scleral shell is not exactly spherical and the material properties of scleral tissue are viscoelastic and anisotropic, pressure vessel theory can be used to approximate the increases in scleral wall stress induced by scleral thinning. Thus, on the basis of our observed differences in scleral thickness, estimated scleral wall stress was increased approximately 11% in the foveal region and 9% overall in the high IOP–normal group; and 11%, 16%, and 13% in the foveal, midposterior, and posterior equatorial regions and 11% overall in the high IOP–early glaucoma group (Table 3) . These data are for scleral regions away from the ONH; similar data for the peripapillary sclera will be the subject of a future report.15


   Acknowledgements
 
The authors thank Stephanie Hager, Bud Hirons, Juan Reynaud, and Lindell Skinner for technical assistance.


   Footnotes
 
Presented in part at the Association for Research in Vision and Ophthalmology annual meeting, Fort Lauderdale, Florida, May 2000.

Supported in part by National Eye Institute Grants R01EY11610 (CFB) and P30EY02377 (departmental core grant), National Institutes of Health, Bethesda, Maryland; a grant from The Whitaker Foundation, Rosslyn, Virginia (CFB); and a Career Development Award (CFB) and an unrestricted departmental grant (LSU Eye Center) from Research to Prevent Blindness, Inc., New York, New York.

Submitted for publication May 17, 2001; revised August 23, 2001; accepted September 20, 2001.

Commercial relationships policy: N.

The publication costs of this article were defrayed in part by page charge payment. This article must therefore be marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Corresponding author: Claude F. Burgoyne, LSU Eye Center, 2020 Gravier Street, Suite B, New Orleans, LA 70112. cburgo{at}lsuhsc.edu


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Timoshenko, S, Goodier, JN (1934) Theory of Elasticity McGraw-Hill New York.
  2. Nemeth, J. (1990) Changes in the posterior eye segment in glaucoma Fortschr Ophthalmol 87,138-139[Medline][Order article via Infotrieve]
  3. Bellezza, AJ, Hart, RT, Burgoyne, CF (2000) The optic nerve head as a biomechanical structure: initial finite element modeling Invest Ophthalmol Vis Sci 41,2991-3000[Abstract/Free Full Text]
  4. Burgoyne, CF, Quigley, HA, Thompson, HW, Vitale, S, Varma, R. (1995) Measurement of optic disc compliance by digitized image analysis in the normal monkey eye Ophthalmology 102,1790-1799[Medline][Order article via Infotrieve]
  5. Burgoyne, CF, Quigley, HA, Thompson, HW, Vitale, S, Varma, R. (1995) Early changes in optic disc compliance and surface position in experimental glaucoma Ophthalmology 102,1800-1809[Medline][Order article via Infotrieve]
  6. Olsen, TW, Aaberg, SY, Geroski, DH, Edelhauser, HF (1998) Human sclera: thickness and surface area Am J Ophthalmol 125,237-241[Medline][Order article via Infotrieve]
  7. Fine, BS, Yanoff, M. (1979) Ocular Histology. A Text and Atlas 2nd ed. ,186-193 Harper & Row New York.
  8. Friedman, B. (1966) Stress upon the ocular coats: effects of scleral curvature scleral thickness, and intra-ocular pressure Eye Ear Nose Throat Monthly 45,59-66
  9. Quigley, HA, Dorman-Pease, ME, Brown, AE (1991) Quantitative study of collagen and elastin of the optic nerve head and sclera in human and experimental monkey glaucoma Curr Eye Res 10,877-888[Medline][Order article via Infotrieve]
  10. Downs, JC, Thomas, KA, Hart, RT, Burgoyne, CF (2000) Quadrant-dependent elastic and viscoelastic material properties of normal monkey and rabbit eyes (Biomed Eng Soc Abstract nr T-5.2) Ann Biomed Eng 28,S44
  11. Downs, JC, Thomas, KA, Hart, RT, Burgoyne, CF (2001) Elastic and viscoelastic material properties of peripapillary sclera in normal and early glaucomatous monkey eyes [ARVO Abstract] Invest Ophthalmol Vis Sci 42(4),S831Abstract nr 4461
  12. Panda-Jonas, S, Jonas, JB, Jakobczyk, M, Schneider, U. (1994) Retinal photoreceptor count, retinal surface area, and optic disc size in normal human eyes Ophthalmology 101,519-523[Medline][Order article via Infotrieve]
  13. Hopwood, D. (1969) Fixatives and fixation: a review Histochem J 1,323-360[Medline][Order article via Infotrieve]
  14. Hopwood, D. (1990) Fixation and fixatives Bancroft, JD Stevens, A eds. . Theory and Practice of Histological Techniques 3rd ed. ,21-142 Churchill Livingstone London.
  15. Blidner, RA, Downs, JC, Hart, RT, Burgoyne, CF (2001) Peripapillary scleral thickness in the perfusion-fixed normal monkey eye [ARVO Abstract] Invest Ophthalmol Vis Sci 42(4),S329-360Abstract nr 1774



This article has been cited by other articles:


Home page
 Arch OphthalmolHome page
M. T. Nicolela, A. S. Soares, M. M. Carrillo, B. C. Chauhan, R. P. LeBlanc, and P. H. Artes
Effect of moderate intraocular pressure changes on topographic measurements with confocal scanning laser tomography in patients with glaucoma.
Arch Ophthalmol, May 1, 2006; 124(5): 633 - 640.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
I. A. Sigal, J. G. Flanagan, and C. R. Ethier
Factors Influencing Optic Nerve Head Biomechanics
Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4189 - 4199.
[Abstract] [Full Text] [PDF]

Home page
 Br. J. Ophthalmol.Home page
B C Chauhan, D M Hutchison, R P LeBlanc, P H Artes, and M T Nicolela
Central corneal thickness and progression of the visual field and optic disc in glaucoma
Br. J. Ophthalmol., August 1, 2005; 89(8): 1008 - 1012.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
J. C. Downs, J-K. F. Suh, K. A. Thomas, A. J. Bellezza, R. T. Hart, and C. F. Burgoyne
Viscoelastic Material Properties of the Peripapillary Sclera in Normal and Early-Glaucoma Monkey Eyes
Invest. Ophthalmol. Vis. Sci., February 1, 2005; 46(2): 540 - 546.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
C. F. Burgoyne, J. C. Downs, A. J. Bellezza, and R. T. Hart
Three-Dimensional Reconstruction of Normal and Early Glaucoma Monkey Optic Nerve Head Connective Tissues
Invest. Ophthalmol. Vis. Sci., December 1, 2004; 45(12): 4388 - 4399.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
J. B. Jonas, E. Berenshtein, and L. Holbach
Lamina Cribrosa Thickness and Spatial Relationships between Intraocular Space and Cerebrospinal Fluid Space in Highly Myopic Eyes
Invest. Ophthalmol. Vis. Sci., August 1, 2004; 45(8): 2660 - 2665.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
B. C. Chauhan, J. Pan, M. L. Archibald, T. L. LeVatte, M. E. M. Kelly, and F. Tremblay
Effect of Intraocular Pressure on Optic Disc Topography, Electroretinography, and Axonal Loss in a Chronic Pressure-Induced Rat Model of Optic Nerve Damage
Invest. Ophthalmol. Vis. Sci., September 1, 2002; 43(9): 2969 - 2976.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
J. C. Downs, R. A. Blidner, A. J. Bellezza, H. W. Thompson, R. T. Hart, and C. F. Burgoyne
Peripapillary Scleral Thickness in Perfusion-Fixed Normal Monkey Eyes
Invest. Ophthalmol. Vis. Sci., July 1, 2002; 43(7): 2229 - 2235.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Downs, J. C.
Right arrow Articles by Burgoyne, C. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Downs, J. C.
Right arrow Articles by Burgoyne, C. F.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS