Abstract
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.
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
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).
Early Experimental Glaucoma
In both eyes of four monkeys, ONH surface compliance
testing
4 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.
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) .
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
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 ).
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
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 (133μ
m), 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
Yanoff
7 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 Yanoff
7 ).
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. Nemeth
2 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
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@lsuhsc.edu
| Monkey | | Weight (kg) | Estimated Age (y) | Eye | Normal Axial Length (mm) | | Normal Mean IOP (mm Hg) | Max. Postlaser IOP* (mm Hg) | Duration of Elevated IOP* (w) | Preperfusion Axial Length (mm) | | State of Eye at Perfusion | | Duration of Acute IOP, † Elevation (min) |
| No. | ID | | | | IOP 10 | IOP 30 | | | | IOP 10 | IOP 30 | Chronic Condition | Acute IOP, † (mm Hg) | |
| Normal monkeys | | | | | | | | | | | | | | |
| 1 | 1T | 7.5 | 6 | R | 21.3 | 21.7 | 8 | — | — | 21.3 | 21.7 | Normal | 45 | 60–80 |
| | | | L | 21.4 | 21.5 | 8 | — | — | 21.4 | 21.6 | Normal | 10 | |
| 2 | 1S | 6.0 | 6 | R | 21.1 | 21.2 | 9 | — | — | 21.1 | 21.1 | Normal | 45 | 15 |
| | | | L | 20.9 | 21.0 | 10 | — | — | 20.9 | 21.0 | Normal | 10 | |
| 3 | 1Z | 7.5 | 6 | R | 21.8 | 21.9 | 11 | — | — | 21.9 | 21.9 | Normal | 30 | 15 |
| | | | L | 21.6 | 21.8 | 10 | — | — | 21.5 | 21.7 | Normal | 10 | |
| 4 | 2D | 8.3 | 5 | R | 21.6 | 21.6 | 10 | — | — | 21.5 | 21.5 | Normal | 30 | 15 |
| | | | L | 21.5 | 21.5 | 8 | — | — | 21.5 | 21.6 | Normal | 10 | |
| Early–glaucoma monkeys | | | | | | | | | | | | | | |
| 5 | 1W | 5.7 | 6 | R | 20.5 | 20.6 | 6 | — | — | 20.2 | 20.5 | Normal | 10 | 15 |
| | | | L | 20.5 | 20.5 | 6 | 19 | 3 | 20.6 | 20.9 | Early glaucoma | 30 | |
| 6 | 2A | 5.8 | 11 | R | 20.6 | 20.8 | 9 | 18 | 4 | 21.0 | 21.1 | Early glaucoma | 30 | 15 |
| | | | L | 20.5 | 20.7 | 11 | — | — | 20.7 | 20.5 | Normal | 10 | |
| 7 | 1U | 6.8 | 7 | R | 20.4 | 20.5 | 8 | 25 | 3 | 20.6 | 20.8 | Early glaucoma | 45 | 60–80 |
| | | | L | 20.3 | 20.3 | 9 | — | — | 20.4 | 20.5 | Normal | 10 | |
| 8 | 1V | 6.8 | 7 | R | 20.8 | 21.0 | 9 | 47 | 7 | 22.3 | 22.4 | Early glaucoma | 30 | 15 |
| | | | L | 20.8 | 20.9 | 8 | — | — | 21.0 | 21.0 | Normal | 10 | |
Table 2. Reproducibility Study: Posterior Scleral Thickness at Four Measurement
Points in Both Eyes of Two Monkeys
Table 2. Reproducibility Study: Posterior Scleral Thickness at Four Measurement
Points in Both Eyes of Two Monkeys
| Measurement Point | Monkey 8 | | | | | | Monkey 1 | | | | | |
| High IOP–Early Glaucoma Eye (R) | | | Low IOP–Normal Eye (L) | | | High IOP–Normal Eye (R) | | | Low IOP–Normal Eye (L) | | |
| Day | | | Day | | | Day | | | Day | | |
| 1 | 2 | 3 | 1 | 2 | 3 | 1 | 2 | 3 | 1 | 2 | 3 |
| Foveal (S) | 243 | 243 | 242 | 289 | 292 | 293 | 334 | 339 | 340 | 305 | 310 | 298 |
| Midposterior (S) | 142 | 146 | 129 | 162 | 162 | 159 | 171 | 169 | 166 | 233 | 226 | 197 |
| Posterior-equatorial (S) | 65 | 68 | 70 | 84 | 84 | 87 | 188 | 189 | 179 | 132 | 125 | 127 |
| Equatorial (IN) | 84 | 81 | 86 | 120 | 121 | 114 | 211 | 194 | 204 | 224 | 216 | 214 |
Table 3. Scleral Thickness Overall and by Region and Treatment and Calculated
Increase in Scleral Wall Stress Due to Scleral Thinning
Table 3. Scleral Thickness Overall and by Region and Treatment and Calculated
Increase in Scleral Wall Stress Due to Scleral Thinning
| Region | Low IOP–Normal (n = 8 eyes)* | High IOP–Normal (n = 4 eyes)* | Increase in Tangential Scleral Stress (%) | High IOP–Early Glaucoma (n = 4 eyes)* | Increase in Tangential Scleral Stress (%) |
| Foveal | 307 ± 9 | 265 ± 12, † | 14 | 273 ± 12, † | 11 |
| Midposterior | 199 ± 7 | 189 ± 10 | NS | 168 ± 10†‡ | 16 |
| Posterior-equatorial | 133 ± 7 | 122 ± 10 | NS | 116 ± 10, † | 13 |
| Equatorial | 179 ± 7 | 168 ± 12 | NS | 169 ± 10 | NS |
| Overall | 204 ± 3 | 186 ± 4, † | 9 | 182 ± 4, † | 11 |
The authors thank Stephanie Hager, Bud Hirons, Juan Reynaud, and
Lindell Skinner for technical assistance.
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