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Measurement of the Magnitude and Axis of Corneal Polarization With Scanning Laser Polarimetry
Robert N. Weinreb, MD;
Christopher Bowd, PhD;
David S. Greenfield, MD;
Linda M. Zangwill, PhD
Arch Ophthalmol. 2002;120:901-906.
ABSTRACT
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Background Scanning laser polarimetry uses a polarization compensator to isolate
corneal birefringence from the birefringence of the retinal nerve fiber layer.
This compensator assumes a fixed corneal polarization magnitude (CPM) of 60
nm and a fixed corneal polarization axis (CPA) of 15° in all subjects.
Objectives To measure the CPM and CPA with a scanning laser polarimeter and to
determine if the assumed compensation values are representative of those observed
in healthy and glaucomatous eyes.
Methods The CPM and CPA were measured in 51 healthy eyes and 55 glaucomatous
eyes using a modified scanning laser polarimeter (GDx Nerve Fiber Analyzer;
Laser Diagnostic Technologies Inc, San Diego, Calif) with an experimental
variable CPM and CPA compensator. The CPM and CPA distributions in healthy
and glaucomatous eyes were compared, and the CPM and CPA relationships with
age, corneal thickness, and corneal curvature were also investigated. Nasally
upward CPA values (in degrees) were recorded as negative; nasally downward
CPA values were recorded as positive.
Results The CPM and CPA measurements were normally distributed with many eyes
having values different from those assumed by the GDx corneal compensator.
For healthy and glaucomatous eyes combined, CPM measurements ranged from 7
nm to 91 nm (mean ± SD, 40.0 ± 15.7 nm). The CPA measurements
ranged from -13° to 73° (mean ± SD, 24.5° ±
17.4°). A significant effect of age on CPA was observed when all eyes
were combined (R2 = 0.10; P<.001). There were no differences in CPM or CPA between healthy
and glaucomatous eyes after adjusting for age. No effects of corneal thickness
on CPM (R2 = 0.04; P = .05) or CPA (R2 = 0.01; P = .24) or of corneal curvature on CPM (R2 = 0.002; P = .67) or CPA (R2 = 0.009; P = .34)
were observed.
Conclusions The range of CPM and CPA values observed in glaucomatous and healthy
eyes suggests that the narrow-band corneal compensator used by the GDx scanning
laser polarimeter is inappropriately compensating for anterior segment birefringence
in many eyes.
INTRODUCTION
RETINAL SCANNING laser polarimetry evaluates the thickness of the retinal
nerve fiber layer (RNFL) by assessing the change in polarization of an illuminating
laser beam that is reflected from the retina.1-2
This technique is based on the substantial birefringent (birefractive) properties
of the RNFL. Light refracted from the RNFL (an anisotropic structure) is polarized,
resulting in 2 refracted rays. One of the rays (the ordinary ray) travels
with the same velocity as the illuminating beam along the optical axis of
the tissue (fast axis) while the other ray (the extraordinary ray) travels
with a velocity that is dependent on the propagation direction within the
tissue (slow axis). The distance of separation (retardance) between the 2
rays increases with greater tissue thickness. However, the RNFL is not the
only birefringent structure of the eye; the Henle fiber layer in the macula
is also birefringent. This layer, consisting of elongated photoreceptor fibers
extending radially from the fovea, is structurally similar to the RNFL and
exhibits significant birefringence. The cornea and, to a much lesser extent,
the lens exhibit birefringence as well.
Because all birefringent structures cause a change in the polarization
of an illuminating beam, the total retardance of a beam illuminating the parapapillary
retina consists largely of contributions from the RNFL and cornea. The accuracy
of RNFL measurements with scanning laser polarimetry depends on its ability
to extract the RNFL retardance from the measured total retardance. To minimize
corneal birefringence, the commercial scanning laser polarimeter (GDx Nerve
Fiber Analyzer; Laser Diagnostic Technologies Inc, San Diego, Calif) has an
integrated component that compensates for the corneal contribution. This fixed
compensator assumes that all individuals have a slow axis of corneal birefringence
of 15° nasally downward and a magnitude of 60 nm. The measured total retardation
has been suggested as largely reflecting the retardance of the RNFL. For several
years, however, this suggestion has been questioned.2
Recently, new data indicate that this assumption is not valid for many individuals.3-4
Using a specially designed corneal polarimeter in which the measurement
of the corneal polarization axis (CPA) is based on the observer's threshold
for detecting the fourth Purkinje image (image formed by the reflection of
illuminating light from the posterior surface of the crystalline lens), Greenfield
et al3 established the distribution of the
CPA in 112 healthy eyes and reported a range between 90° nasally downward
and 54° nasally upward, in contrast to the 15° nasally downward assumed
by the GDx fixed compensator (although the mode of distribution was between
10° and 20° nasally downward). Similarly, Knighton and Huang4 used a modified version of the corneal polarimeter
used by Greenfield and colleagues to measure the central anterior segment
birefringence of 146 healthy eyes and demonstrated that corneal polarization
magnitude (CPM) ranged from 0 nm to 250 nm when double passing the cornea,
in contrast to the 60 nm (120-nm double pass) assumed by the GDx fixed compensator.
Because the wide range of these measurements deviates significantly from the
assumed values of the fixed compensator, this could be a significant source
of error in RNFL assessment with the current GDx.
Greenfield et al3, 5 recently
demonstrated the important effect of the CPA on the discriminating power of
scanning laser polarimetry in mild to moderate glaucoma. To exclude the contribution
of corneal birefringence, however, the compensator must account for the variation
not only in the birefringence axis but also in the magnitude. The purpose
of this study was to use a GDx scanning laser polarimeter with a variable
corneal compensator to describe the variation in both CPM and CPA birefringence
in healthy subjects and patients with glaucoma.
SUBJECTS AND METHODS
SUBJECTS
Patients with glaucoma and healthy subjects meeting entry criteria were
enrolled in this prospective study. A total of 106 individuals were evaluated
at the University of California, San Diego, Glaucoma Center, including 55
patients with glaucoma and 51 healthy subjects. Of these individuals, 47 were
men and 59 were women; 81 subjects were white, 9 were Asian American, 6 were
African American, 6 were Hispanic, and 3 were Indo-European. One eye per subject
was included by random selection.
Prior to imaging, all subjects underwent a complete ophthalmologic examination
including refraction and best-corrected visual acuity, slitlamp biomicroscopy,
intraocular pressure measurement, a dilated stereoscopic fundus examination,
stereoscopic photography of the optic disc, and Swedish Interactive Threshold
Algorithm (SITA) or standard (achromatic) full-threshold visual field testing
with program 24-2 (Humphrey Field Analyzer; Humphrey Instruments, Dublin,
Calif). Only eyes with a visual acuity of 20/40 or better were included. The
range of refractive error in the subject population was –9.0 diopters
(D) to 2.88 D (mean ± SD, -0.92 ± -1.91 D). Eyes
with coexisting retinal disease, uveitis, or nonglaucomatous optic neuropathy
were excluded from this investigation. Informed consent was obtained from
all participants. All methods were approved by the University of California,
San Diego, Human Subjects Committee and adhered to the Declaration of Helsinki
for research involving human subjects.
Healthy subjects had no history of ocular disease or increased intraocular
pressure and normal ophthalmologic examination results, including an intraocular
pressure of 22 mm Hg or less (Goldmann applanation tonometry), a healthy appearance
of the optic disc and RNFL (no diffuse or focal rim thinning, cupping, or
RNFL defects indicative of glaucoma or other ocular abnormalities), and a
normal finding on SITA or standard full-threshold Humphrey 24-2 visual field
tests. Normal visual field indexes were defined as a mean defect (MD) and
corrected pattern standard deviation within 95% confidence limits and a glaucoma
hemifield test result within normal limits. The mean ± SD age of the
healthy subjects was 46.8 ± 16.3 years (range, 21.4-82.8 years).
Patients with glaucoma had evidence of a repeatable visual field defect
on SITA or standard full-threshold 24-2 tests, defined as a corrected pattern
standard deviation outside of the 95% normal limits or a glaucoma hemifield
test result outside of the 99% normal limits. Two consecutive abnormal visual
fields were required. The mean MD ± SD on the test nearest the imaging
date was –6.49 ± 4.94 dB (range, -20.92 to 0.26 dB). Intraocular
pressure was not used to classify this group. The mean ± SD age of
the patients with glaucoma was 69.4 ± 9.5 years (range, 50.7-89.8 years).
Patients with glaucoma were significantly older than healthy subjects (t test; P<.001).
MEASUREMENTS
The experimental setup was a commercial GDx system, modified so that
the original fixed corneal compensator was replaced with a variable corneal
compensator, as described by Zhou and Weinreb.6
In brief, the GDx variable corneal compensator comprises a set of 4 linear
retarders in the path of the measurement beam. The first 2 retarders are optical
lenses that have equal retardance and form a variable cornea and lens compensator.
The third retarder is composed of the cornea and lens, and the fourth retarder
is the retinal birefringent structure (RNFL or macular Henle fibers).
The CPM and CPA were determined by aligning the fast axis of the first
retarder with the slow axis of the second, identical retarder (essentially
setting the compensating retarders to 0 nm) and imaging the macula. The resulting
retardation profile represents the additive effects of cornea, lens, and macular
Henle fiber birefringence. The compensating retarders were then adjusted to
minimize the effects of anterior segment birefringence, resulting in a flat
macular retardation profile. The CPM and CPA values that resulted in adequate
compensation were then recorded. Nasally upward CPA values (in degrees) were
recorded as negative; nasally downward CPA values were recorded as positive.
For each subject, 3 sets of CPM and CPA measurements were acquired,
and a mean value was used for the analyses. We determined the within-subject
variability for CPM and CPA for each individual by calculating the SD of the
3 measurements from which these means were obtained. Ultrasound pachymetry
was used to measure corneal thickness (Pachette GDH 500; DGH Technology Inc,
Philadelphia, Pa), and keratometry was used to measure corneal curvature (Keratometer
12990; Reichert Ophthalmic Instruments, Depew, NY).
We also determined the percentage of variance in the change of CPM and
CPA measurements across time that was attributable to interpatient and intervisit
factors; we used a cohort of 13 healthy eyes that were imaged 3 times during
the course of 3 months or less using the criteria, instrument, and procedures
described previously. The mean ± SD age of these subjects was 46.3
± 12.8 years (range, 24.6-73.2 years) on their first imaging date.
Seven subjects were men, and 6 were women. Nine subjects were white, 3 were
African American, and 1 was Hispanic.
ANALYSIS
We compared CPM and CPA measurements between healthy and glaucomatous
eyes using 2-tailed t tests. We also reported and
compared the SDs of the CPM and CPA as indexes of measurement variability.
The relationships of corneal thickness, corneal curvature, and subject age
with CPM and CPA were assessed using linear regression. To determine sources
of variability across time in CPM and CPA measurements, we employed a random-effects
analysis of variance model using restricted maximum likelihood. The components
of this model were subject (between-subject variability), visit (between-visit
variability), and residuals.
RESULTS
The mean ± SD CPM in all eyes combined was 40.0 ± 15.7
nm (range, 7-91 nm). The distribution of CPM measurements was normal (Shapiro-Wilk W test), with a mode between 40 nm and 50 nm (29 eyes;
27%) and a median of 40.0 nm (Figure 1).
The mean ± SD CPA in all eyes combined was 24.5° ± 17.4°
(range, -13° to 73°). The distribution of CPA measurements was
normal (Shapiro-Wilk W test), with the largest percentage
of eyes between 10° and 20° (20%) and between 30° and 40°
(18%). The median CPA was 21.8° (Figure
2). Table 1 indicates
the CPM, CPA, corneal thickness, corneal curvature, and refraction results
for all eyes. The CPM and CPA were not linearly related (R2 = 0.4; P = .54) (Figure 3).
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Figure 1. The distribution of corneal polarization
magnitude in all subjects (n = 106). The data are normally distributed (Shapiro-Wilk W test; P = .40) with a mean
± SD of 40.0 ± 15.7 nm.
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Figure 2. The distribution of corneal polarization
axis (CPA) in all subjects (n = 106). The data are normally distributed (Shapiro-Wilk W test; P = .33) with a mean
± SD of 24.5° ± 17.4°. Nasally upward CPA values were
recorded as negative; nasally downward CPA values were recorded as positive.
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Table 1. Corneal Polarization Magnitude, Corneal Polarization Axis,
Corneal Thickness, Corneal Curvature, and Refraction Measurements From Glaucomatous
Eyes, Healthy Eyes, and All Eyes Combined*
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Figure 3. The linear regression relationship
between corneal polarization magnitude and corneal polarization axis (CPA)
for all eyes combined (n = 106). Nasally upward CPA values were recorded as
negative; nasally downward CPA values were recorded as positive.
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EFFECTS OF AGE
There was a negative, although likely not statistically significant,
relationship (slope, -0.26) between age and CPM in healthy eyes (R2 = 0.09; P<.04)
but not in glaucomatous eyes (R2<0.001; P = .90). For multiple comparisons,  = .005 based
on regression analyses between CPM and age, corneal thickness, corneal curvature,
and refraction in glaucomatous eyes, healthy eyes, and all eyes combined.
There was also a negative relationship (slope, -0.34) between age and
CPA in healthy eyes (R2 = 0.13; P = .008) but not in glaucomatous eyes (R2 = 0.004; P = .65) ( =
.005 as mentioned previously). However, the age of healthy subjects ranged
from 21 to 82 years (61-year range), whereas that of patients with glaucoma
ranged from 51 to 90 years (39-year range). Therefore, we evaluated whether
the larger age range of healthy subjects was a possible reason for the difference
in the age/CPM/CPA relationships between the diagnostic groups by completing
additional univariate and multivariate analyses. When we included only healthy
subjects older than 50 years (n = 17) in the linear regression of age with
CPM and CPA, the relationships were no longer statistically significant (R2 = 0.001 and P =
.64, and R2 = 0.007 and P = .29, respectively). For CPM, when both age and diagnosis were included
in a linear regression model using all subjects, the effect of age was not
significant (P = .12). When age and diagnosis were
included in a linear regression model with CPA, the effect of age remained
(P = .02). Table
2 and Table 3 indicate
the relationships of CPM and CPA with age (as well as corneal thickness, corneal
curvature, and refraction). Figure 4
and Figure 5 show the relationships
between age and CPM and CPA, respectively.
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Table 2. Linear Regression Relationships Between Corneal Polarization
Magnitude and Age, Corneal Thickness, Corneal Curvature, Refraction, Race,
and Sex*
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Table 3. Linear Regression Relationships Between Corneal Polarization
Axis and Age, Corneal Thickness, Corneal Curvature, and Refraction*
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Figure 4. The linear regression relationship
between age and corneal polarization magnitude for all eyes combined (n =
106).
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Figure 5. The linear regression relationship
between age and corneal polarization magnitude (CPA) for all eyes combined
(n = 106). Nasally upward CPA values were recorded as negative; nasally downward
CPA values were recorded as positive.
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EFFECTS OF DIAGNOSIS
The mean ± SD CPM was similar in individuals with glaucoma (39.0
± 16.5 nm; range, 7-91 nm) and healthy subjects (41.1 ± 14.3
nm; range, 11-75 nm) (P = .48). In univariate analysis,
the mean ± SD CPA was marginally lower in patients with glaucoma (20.5°
± 18.3°; range, -13° to 73°) compared with healthy
subjects (28.8° ± 15.4°; range, -6° to 57° (P = .01; = .01 for multiple comparisons) (Table 1). On further investigation, however,
the effect of diagnosis on CPA was influenced by the significant age difference
between diagnostic groups (t test; P<.001). Multivariate linear regression indicated that after adjusting
for age, the difference between healthy and glaucomatous eyes was no longer
statistically significant (P = .66). Furthermore,
when the healthy group was truncated to include only patients the same age
as or older than the youngest patient with glaucoma (n = 17), the mean ±
SD CPA in the healthy group (19.3° ± 15.9°; range, -5.7°
to 48.7°) was similar to that in the glaucoma group (20.5° ±
18.3°) (P = .82).
OTHER EFFECTS
No significant correlations were found between corneal thickness, corneal
curvature, or refraction and CPM or CPA in healthy or glaucomatous eyes (for
all comparisons, P .05). There were no differences
in CPM or CPA in either the healthy or glaucoma group between white subjects
and those of other races (possibly because 81 [77%] of 105 subjects were white,
resulting in little power to detect a difference) or between men and women
(for all comparisons, P>.10).
VARIABILITY OF CPM AND CPA MEASUREMENTS
For CPM and CPA, the mean standard deviation of the 3 measurements used
to create the single average measurement analyzed for each subject was 8%
and 13.5% of the mean CPM and CPA values (coefficient of variation), respectively,
indicating minimal interimage variability. The mean ± SD variability
(the SD of 3 images that comprised the mean image used for analysis) was 3.2
± 2.8 nm and 3.3° ± 2.8° for CPM and CPA, respectively.
In the 13 healthy subjects with 3 sets of CPM and CPA measurements within
3 months, the variability of these measurements across time was overwhelmingly
attributable to differences among subjects (93% of the variance for both CPM
and CPA). Intervisit variability accounted for 0% and 1% of the variability
in CPM and CPA, respectively.
COMMENT
In our study, the intersubject variability of both the measured CPM
and CPA was large. The CPM in our subject population ranged from 7 nm to 91
nm in glaucomatous eyes and from 11 nm to 75 nm in healthy eyes. The CPA ranged
from –13° to 74° in glaucomatous eyes and from -6°
to 57° in healthy eyes. The mean CPM and CPA were different from the values
assumed by the GDx. The mean CPM of 40 nm in our study is in contrast to the
assumed CPM of 60 nm with the fixed GDx corneal compensator. Similarly, the
mean CPA of 24.5° in our study is in contrast to the assumed CPA of 15°
with the fixed compensator. These findings, coupled with large intersubject
variability in the measurements, suggest that inaccurate GDx RNFL measurements
exist in a subset of patients. The inaccuracies may increase with a greater
disparity between actual values and compensated values, although this hypothesis
was not tested. These results illustrate the need for a variable or wide-band
compensator if RNFL birefringence is to be effectively isolated from anterior
segment contributions.
Our reported results (healthy and glaucomatous eyes combined) for CPA
(mean ± SD, 24.5° ± 17.4°) are similar to those of Greenfield
and colleagues (healthy eyes only),3, 7
who reported a mean ± SD CPA of 24.8° ± 21.4° using
a different device. Our mean ± SD CPA for healthy eyes was also similar
to their results (28.8° ± 15.4°). The mode of CPA distribution
reported in the study by Greenfield et al3
was between 11° and 22° (34% of eyes), similar to that assumed by
the GDx corneal compensator. In our study, the distribution for all eyes combined
was normal, with 20% of eyes having a CPA between 10° and 20° and
18% of eyes with a CPA between 30° and 40°.
Our reported results (healthy and glaucomatous eyes combined) for CPM
are also similar to those reported previously by Knighton and Huang.4 They reported a CPM ranging from 0 nm to 250 nm (double
pass). The observed range in our population was slightly less broad (single
pass: 7-91 nm; double pass: 14-182 nm). These authors reported a moderate
relationship between CPM and CPA (Pearson r = approximately
0.50), whereas this relationship was not observed in our study (R2 = 0.004; P = .54).
Along with the results of Greenfield et al3
and Knighton and Huang,4 our results provide
insight into the relatively poor performance of the GDx scanning laser polarimeter
for discriminating between glaucomatous and healthy eyes that has been reported
in some studies (although other studies have reported good discrimination,8-11 sometimes
using parameters with no equivalent in the commercially available GDx). Studies
from our laboratory12-13 reported
significantly lower sensitivities at fixed specificities for various GDx parameters
compared with those obtained using other imaging and visual function techniques;
however, receiver operating characteristic curve areas for the best parameter
using each technique were similar. In some cases, GDx parameters performed
no better than chance at discriminating between healthy and glaucomatous eyes.
This finding might be due to an overall increase in the RNFL thickness profile
in some glaucomatous eyes, caused by improperly compensated CPM or CPA,3 that results in their classification as normal.
Another likely effect of inappropriate CPM and/or CPA compensation is
the inclusion of inaccurate normal data in the GDx normative database.14 Such inclusion would increase the reported variability
in the measurement of RNFL birefringence, resulting in a range of normative
values for GDx parameters that would provide artificially high specificity
or artificially low sensitivity.
In our study, we reported a significant relationship between CPA and
age (R2 = 0.10; for all eyes, P<.001). Knighton and Huang found no such relationship in a larger
number of eyes (n = 146; R<0.2; P<.09) spanning a similar age range (21-71 years). The difference
between their results and ours might be due to variations in the tested populations.
They did not report the distribution of ages for their subjects. Another possibility
is that these results are due to methodological differences.4
The significant relationship observed in our study suggests that the CPA may
change with time, although longitudinal studies are necessary for this conclusion.
Greenfield and Knighton7 have shown a mean
change in CPA of 4° in healthy eyes during the course of 1 year; however,
the magnitude of this change was likely within the limits of measurement variability.
Because the reported effect of age on CPA in healthy eyes was relatively small
for the full range of ages examined (21-82 years), it is unlikely that this
effect would meaningfully influence the longitudinal monitoring of GDx-measured
RNFL thickness in patients with glaucoma during a 20- to 30-year course of
the disease. This idea is reinforced by the lack of an age effect on CPA in
our glaucoma group (age range, 51-90 years).
We also investigated the relationships between corneal thickness, corneal
curvature, and refraction on CPM and CPA. Modest or weak relationships were
observed between corneal thickness and CPM in glaucomatous eyes and all eyes
combined (R2 = 0.07 and P = .08, and R2 = 0.04 and P = .05, respectively), but not in healthy eyes. No significant
effects of these variables on CPA were observed. Although small, the effects
of corneal thickness on CPM may have some relevance to GDx imaging prior to
and after laser-assisted in situ keratomileusis (LASIK). The effect of LASIK
on GDx measurements has been investigated,15-17
but its direct effects on CPM and CPA have not been reported. A weak cross-sectional
relationship between corneal thickness and CPM and CPA does not imply that
CPM and/or CPA will remain stable after a LASIK-induced change in corneal
thickness.
We used macular imaging to determine the CPM and CPA. One limitation
of this technique is that some macular abnormalities that disrupt the Henle
layer and/or macular birefringence may affect the ability of this method to
measure CPM and CPA. Because both glaucoma and macular degeneration are age-associated
diseases, some patients may not provide stable macular images for correct
CPM and CPA determination cross-sectionally and across time. This issue requires
additional study.
In summary, our results indicate that the CPA and CPM vary widely in
healthy and glaucomatous eyes. Although a substantial percentage of eyes show
CPM and CPA values that are within the range compensated for by the commercially
available GDx scanning laser polarimeter, the evaluation of many other patients
results in data that are very different from these values. Furthermore, there
is a small cross-sectional effect of age on CPA, indicating the possibility
of change with time. For scanning laser polarimetry to best detect and monitor
glaucoma, these findings must be addressed.
AUTHOR INFORMATION
Submitted for publication February 26, 2002; final revision received
March 25, 2002; accepted March 27, 2002.
Supported in part by the Joseph Drown Foundation, Los Angeles, Calif
(Dr Weinreb); grants EY11008 (Dr Zangwill) and EY08684 (Dr Greenfield) from
the National Eye Institute, Bethesda, Md; and an unrestricted grant from Research
to Prevent Blindness (New York, NY) to the University of California, San Diego.
Corresponding author and reprints: Robert N. Weinreb, MD, Glaucoma
Center, University of California, San Diego, 9500 Gilman Dr, La Jolla, CA
92093-0946.
From the Glaucoma Center and Diagnostic Imaging Laboratory, Department
of Ophthalmology, University of California, San Diego (Drs Weinreb, Bowd,
and Zangwill), and the Department of Ophthalmology and Bascom Palmer Eye Institute,
University of Miami School of Medicine, Miami, Fla (Dr Greenfield). Dr Weinreb
is a consultant who has received research support from Laser Diagnostic Technologies,
San Diego. Dr Greenfield is a member of the clinical advisory board, Laser
Diagnostic Technologies.
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