May 2003
Volume 44, Issue 5
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Glaucoma  |   May 2003
Scanning Laser Polarimetry with Variable Corneal Compensation: Identification and Correction for Corneal Birefringence in Eyes with Macular Disease
Author Affiliations
  • Harmohina Bagga
    From the Department of Ophthalmology, University of Miami School of Medicine, Bascom Palmer Eye Institute, Miami, Florida.
  • David S. Greenfield
    From the Department of Ophthalmology, University of Miami School of Medicine, Bascom Palmer Eye Institute, Miami, Florida.
  • Robert W. Knighton
    From the Department of Ophthalmology, University of Miami School of Medicine, Bascom Palmer Eye Institute, Miami, Florida.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1969-1976. doi:10.1167/iovs.02-0923
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      Harmohina Bagga, David S. Greenfield, Robert W. Knighton; Scanning Laser Polarimetry with Variable Corneal Compensation: Identification and Correction for Corneal Birefringence in Eyes with Macular Disease. Invest. Ophthalmol. Vis. Sci. 2003;44(5):1969-1976. doi: 10.1167/iovs.02-0923.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

purpose. In scanning laser polarimetry with variable corneal compensation (SLP-VCC), the macula is used as an intraocular polarimeter to calculate and neutralize corneal birefringence based on an intact Henle’s layer. The purpose of this investigation was to validate this strategy in eyes with macular structural disease.

methods. A nerve fiber analyzer was modified to enable the measurement of corneal polarization axis and magnitude so that compensation for corneal birefringence was eye specific. Normal subjects and patients with a variety of pathologic macular conditions underwent complete ocular examination, SLP-VCC, and direct measurement of the corneal polarization axis (CPA), with a slit-lamp–mounted corneal polarimeter. Macular birefringence patterns were classified as well defined, weak, or indeterminate bow ties. A new “screen” method is described that determines the anterior segment birefringence without relying on the presence of macular bow-tie patterns.

results. Forty-seven eyes (20 normal, 27 with maculopathy) of 47 patients (mean age, 59.0 ± 19.0 years; range, 24–88) were enrolled. The correlation between CPA measured with corneal polarimetry (CPA by PIV [fourth Purkinje image]) and SLP-VCC was less in eyes with macular disease (R 2 = 0.22, P = 0.024) compared with normal eyes (R 2 = 0.72, P < 0.0001). Eyes with macular disease had significantly (P = 0.007) more indeterminate macular bow ties (8/27; 29%) than did normal eyes (0/20). The magnitude of difference between CPA by PIV and CPA by SLP-VCC was significantly (P = 0.0007) greater in eyes with indeterminate bow-tie patterns than in weak and well-defined patterns. Although no relationship was observed between CPA and 12 retardation parameters obtained with SLP-VCC in normal eyes (P > 0.05), eyes with macular disease showed a significant association between CPA and average thickness (R 2 = 0.27, P = 0.005), ellipse average (R 2 = 0.24, P = 0.0085), superior average (R 2 = 0.24, P = 0.009), inferior average (R 2 = 0.28, P = 0.004), and superior integral (R 2 = 0.37, P = 0.0008), suggesting incomplete corneal compensation. Greater correlation between CPA by PIV and CPA derived by SLP-VCC was found by using the screen method (R 2 = 0.83, P < 0.0001) compared with the bow-tie method (R 2 = 0.22, P = 0.024) in eyes with maculopathy.

conclusions. Macular strategies for neutralization of corneal birefringence using SLP-VCC can fail if Henle’s layer is disrupted by macular disease. The screen method provides a more robust measure of the anterior segment birefringence in some eyes with macular disease.

Assessment of retinal ganglion cell loss is critical for the early detection and monitoring of glaucomatous damage. Studies have shown that retinal nerve fiber layer (RNFL) damage can precede visual field defects by as much as 6 years. 1 2 3 Several techniques to evaluate the RNFL, such as red-free ophthalmoscopy, RNFL photography, photogrammetry, and densitometry of RNFL reflectance, have been described. 4 5 6 7 8  
In scanning laser polarimetry (SLP), a confocal scanning laser ophthalmoscope with an integrated polarimeter is used for quantitative evaluation of the thickness of the retinal nerve fiber layer (RNFL). 9 10 11 12 13 14 Differences in RNFL thickness assessed by SLP have been described between normal and glaucomatous eyes 11 15 16 and normal eyes and those with ocular hypertension. 14 Among glaucomatous eyes, good correlation between structural damage to the RNFL and visual field loss has been reported. 17 18 19  
The parallel arrangement of the microtubules within the retinal ganglion cell axons causes the RNFL to behave like a form birefringent medium. SLP estimates RNFL thickness based on the retardation of the laser beam caused by the birefringence of the RNFL. 11 20 Because the cornea is also birefringent 21 the instrument has a proprietary anterior segment compensator device that assumes all individuals to have a fixed slow corneal axis of 15° nasally downward and retardance of 60 nm. However, recent studies have reported a wide range in the distribution of corneal polarization axis and magnitude. 22 23 24 25 Thus, deviation from the fixed compensator settings in either the axis or magnitude of corneal birefringence causes incomplete neutralization of corneal birefringence and erroneous RNFL thickness assessment. To maximize the diagnostic precision of RNFL thickness measurements, it is imperative to eliminate the corneal contribution of birefringence by performing eye-specific measurements of corneal polarization axis and magnitude. 22 24 26 27  
The concept of using the macula as an intraocular polarimeter has been described. 23 27 28 (Knighton RW, Huang X-R, ARVO Abstract 482, 2000). Henle’s layer of the macula is radially birefringent, 29 30 (Delori FC, Webb RH, Parker JS, ARVO Abstract 13, 1979) owing to the uniform arrangement of the photoreceptor axons. Macular polarimetry images obtained without compensating the corneal birefringence demonstrate a distinct bow-tie or double-humped pattern. Based on the assumption that the corneal birefringence interacts with an intact Henle’s layer to produce the bow-tie patterns, the macular bow-tie patterns can provide a strategy to determine corneal birefringence. The bright arms of the bow tie are formed where the slow axis of the cornea is parallel with the slow axis of Henle’s layer, resulting in summation of retardation. The dark arms are formed where the slow axis of the cornea is perpendicular to the slow axis of Henle’s layer, and retardation cancels. Thus, the slow axis of the anterior segment birefringence can be read out directly from the orientation of the bright arms of the bow tie. The shape of the retardation profile on a circle around the macula reflects the combined magnitude of the anterior segment birefringence and that of the Henle’s layer, from which it is possible to extract the magnitude of the anterior segment birefringence. 27 We hypothesized, therefore, that disruption of the intact Henle’s layer by alterations in the normal macular histology may limit the usefulness of this strategy. The purpose of our investigation was to determine the robustness of this strategy in eyes with macular disease. 
Methods
Normal eyes and eyes with macular disease meeting the eligibility criteria were enrolled in this investigation. One eye per subject was enrolled. If both eyes of a patient were eligible for the study, the right eye was selected. All patients were aged between 19 and 90 years and had refractive error not exceeding 5.00 D sphere and/or 2.00 D cylinder. All patients underwent complete ophthalmic examination, including slit lamp biomicroscopy, applanation tonometry, dilated funduscopic examination, corneal polarization axis measurements, and scanning laser polarimetry. Informed consent was obtained from all the subjects by means of a consent form approved by the Institutional Review Board for Human Research of the University of Miami School of Medicine, and all procedures adhered to the tenets of the Declaration of Helsinki. 
Patients with various types of macular disease were enrolled in this investigation. Normal subjects had no history of ocular disease. All had intraocular pressure less than or equal to 21 mm Hg by Goldmann applanation tonometry, visual acuity of 20/40 or better, normal optic disc and fundus appearance by stereoscopic examination, no previous intraocular surgery, no family history of glaucoma, and normal visual fields. A normal optic nerve was defined as vertical cup–disc asymmetry less than 0.2, cup-to-disc ratio less than 0.6, and intact neuroretinal rim without peripapillary hemorrhages, notches, localized pallor, or RNFL defect. Achromatic automated perimetry was performed with a visual field analyzer (Humphrey Field Analyzer; Humphrey-Zeiss Systems, Inc., Dublin, CA, programs 24-2 or 30-2). Visual field reliability criteria included less than 25% fixation losses and false-positive and false-negative rates. Perimetry was performed within 3 months of clinical examination and RNFL thickness determination. Normal visual field indices were defined as a mean defect and corrected standard deviation within 95% confidence limits and a glaucoma hemifield test result within normal limits. 
The slow axis of corneal polarization (CPA) was determined independently of SLP, by a specially constructed, noninvasive, slit lamp–mounted corneal polarimeter based on an apparatus originally described by Bone. 31 The details of the instrument are described elsewhere. 22 25 Briefly, it involves the observation of the fourth Purkinje image (PIV) of a light-emitting diode (LED) through rotating, crossed, linear polarizers. The crossed polarizers cancel any reflections that have not experienced a change in polarization state. PIV, which represents the LED reflection from the posterior surface of the lens, disappears when the axes of the linear polarizers are aligned with the axes of corneal birefringence. The slow axis (henceforth referred to as CPA by PIV) is then identified by inserting an auxiliary retarder with known axis in front of the cornea and observing the change in intensity of the PIV image. 
Bow-Tie Method for Corneal Compensation
SLP imaging was performed by one experienced operator (HB) with an experimental instrument—SLP with variable corneal compensation (SLP-VCC)—consisting of a commercial nerve fiber analyzer (GDx system; Laser Diagnostic Technology, San Diego, CA) modified so that the original corneal compensator was replaced with a VCC. The magnitude of the variable compensator was set by a dial from 0 to 120 nm, and the axis was set by another dial from −90° to +90°. Nasally upward CPAs (in degrees) were recorded as negative; nasally downward CPAs were recorded as positive. Macular polarimetry images with the variable compensator set at 0 nm retardance were acquired to determine the axis and magnitude of the anterior segment birefringence. The magnitude and axis of corneal birefringence was determined from the measured macular retardation profile. Details of the experimental setup and method for individually measuring the axis and magnitude are described elsewhere. 27 For each subject, corneal polarization magnitude (CPM) and CPA measurements were acquired three times, and a the mean of these was used in the analyses. 
Among the cohort of normal eyes and eyes with maculopathy, we classified patterns of uncompensated macular bow-tie images into three categories: well defined, weak, or indeterminate. A well-defined macular bow tie was defined as having two complete bright arms oriented 180° apart. As illustrated in Figure 1 , the bright and dark arms of the bow tie are perpendicular to each other and meet in the center of the fovea. With corneal compensation, the retardation in the macula became much weaker and more uniform. A weak macular bow tie (Fig. 2) was defined as absence of both bright arms of the macular bow tie and calculated macular retardance of less than 28 nm. An indeterminate bow-tie pattern (Fig. 3) was defined as partial or complete disruption of at least one of the bright arms of the bow tie. 
Screen Method for Corneal Compensation
Although the macular bow-tie method for determining anterior segment birefringence is robust in eyes with normal maculas, we found that it failed to provide good compensation in some eyes with maculopathy (see the Results section). Patients with glaucoma often have coexisting macular disease, and we therefore thought it desirable to develop another method for measuring the anterior segment birefringence that did not depend on an intact Henle’s fiber layer. Because the new method used the imaged fundus as a single, large screen, we called it the “screen” method. Analytical details of the screen method are presented elsewhere 32 ; a brief description follows. 
A basic assumption of SLP is that the fundus of the eye acts as a polarization-preserving reflector—that is, the polarization state of the detected beam results from the cumulative effect of all the birefringent structures through which it passes. 23 We made the additional assumption that, in polarization images of the posterior pole, anterior segment birefringence has an equal effect on all pixels. We therefore returned to the image series initially captured by the instrument (images from crossed and parallel polarization channels obtained with 20 different azimuths of incident linear polarization) 32 33 and averaged a large portion of each image (Fig. 4) . This produced a series of values from which average birefringence was calculated. 32 33 The gray area in Figures 4C and 4D may be thought of as a single detector measuring the average behavior of the posterior pole. The contribution of macular birefringence to this average was expected to be small, because, in most eyes, macular birefringence is much less than anterior segment birefringence, is circularly symmetric, and covers only a portion of the image. The average birefringence was ascribed entirely to a double pass of the measuring beam through the anterior segment. Unlike in the macular bow-tie method, in which the slow axis of the anterior segment was aligned with the bright arms of the bow tie, the axis calculated by the screen method could not be identified as fast or slow and, therefore, had a 90° ambiguity (Figs. 4C 4D) . The correct axis was chosen based on the knowledge that the slow axis of most corneas is oriented nasally downward. 22 34 This selection method worked well for all the subjects tested, but in principle could occasionally fail. The choice of axis was tested by obtaining another macular image with the selected axis. The wrong axis would result in a higher rather than lower overall retardance in the image. A 90° rotation of the compensator would then select the correct axis. 
We compared the macular bow-tie and screen methods on the uncompensated SLP images obtained from the 20 normal subjects (Fig. 5) . The anterior segment birefringence determined by the two methods agreed closely. 
Statistical Analysis
Statistical analyses were performed on computer (SPSS ver. 10.0; SPSS Science, Inc., Chicago, IL). Analysis of variance (ANOVA) was used to compare different measures among the groups. Statistical correlations were evaluated by Pearson correlation coefficient. P ≤ 0.05 was considered statistically significant. 
Results
Forty-seven 47 patients (20 normal, 27 with macular disease) with a mean age of 59.0 ± 19.0 years (range, 24–88) were enrolled; one eye of each was examined. Macular disease consisted of 12 eyes with age-related macular degeneration (AMD), 7 eyes with epiretinal membrane (ERM), 4 eyes with cystoid macular edema (CME), 2 eyes with central serous retinopathy (CSR), and 2 eyes with pattern dystrophy. Five eyes with maculopathy had coexisting glaucomatous optic neuropathy (average visual field mean defect −4.2 ± 1.9 dB). The demographics of the patients are listed in Table 1
Among normal eyes, macular bow-tie patterns were classified as well defined in 19 (95%) of 20 eyes, weak in 1 (5%) of 20 eyes, and indeterminate in none of the eyes. Among eyes with maculopathy (Table 2) , macular bow-tie patterns were characterized as well defined in 15 (55%) of 27 eyes, weak in 4 (15%) of 27 eyes, and indeterminate in 8 (30%) of 27 eyes. Normal eyes had significantly (P = 0.003) more well-defined macular bow ties than eyes with maculopathy; eyes with maculopathy had significantly (P = 0.007) more indeterminate bow ties (Fig. 6) . We evaluated the variance of CPA measurements (Table 2) derived by corneal polarimetry (PIV) and SLP-VCC. Mean variance (SD2) of CPA by PIV measurements was similar (P = 0.84) in normal eyes (1.9 ± 2.8; range, 0–11.5) and eyes with maculopathy (1.8 ± 2.4; range 0–11.5). Mean variance of CPA measurements derived using SLP-VCC was similar (P = 0.39) in normal eyes (2.9 ± 2.4; range, 0–9) and eyes with maculopathy (4.7 ± 8.9; range, 0–47). 
Among normal eyes, there was no difference (P = 0.97, paired t-test) between mean CPA by PIV (27° ± 14°, range 0–59°) compared with mean CPA derived by SLP-VCC (mean, 23 ± 14°; range, 5–45°). Among eyes with maculopathy, there was a difference that did not achieve statistical significance (P = 0.08, paired t-test) between mean PIV (19° ± 18°; range, 20–61°) and mean CPA derived by SLP-VCC (25° ± 22°; range, −15–86°). Figure 7 shows scatterplots comparing the CPA by PIV with CPA derived by SLP-VCC (bow-tie method) and comparing CPA by PIV with CPA derived by SLP-VCC (screen method) in normal eyes and eyes with maculopathy. With the bow-tie method, eyes with maculopathy had a weaker correlation (R 2 = 0.22, P = 0.024) than normal eyes (R 2 = 0.72, P < 0.0001). With the screen method, eyes with maculopathy demonstrated similar correlation (R 2 = 0.83, P < 0.0001) as normal eyes (R 2 = 0.73, P < 0.0001). The magnitude of difference between the CPA by PIV and CPA by SLP-VCC was significantly greater (P = 0.0007) in eyes with indeterminate bow-tie patterns (mean, 26° ± 25°) than in eyes with weak (mean, 14.0° ± 14°) and well-defined (mean, 7.0° ± 4.6°) bow-tie patterns. There was no association between the magnitude of difference in CPA derived by both methods and the subtype of maculopathy (P = 0.22). 
To determine whether complete neutralization of corneal birefringence was accomplished by using SLP-VCC in normal eyes and eyes with maculopathy, we evaluated the statistical associations between 12 SLP retardation parameters and the CPA derived with SLP-VCC. No relationship was observed in normal eyes (P > 0.05 for all parameters). Eyes with macular disease showed a significant association between CPA and average thickness (R 2 = 0.27, P = 0.005), ellipse average (R 2 = 0.24, P = 0.008), superior average (R 2 = 0.24, P = 0.009), inferior average (R 2 = 0.28, P = 0.004), and superior integral (R 2 = 0.37, P = 0.0008), suggesting incomplete corneal compensation (Table 3)
A subgroup of five eyes with macular disease comprising two cases of exudative AMD, two cases of ERM, and one case of CSR were also imaged with the corneal compensator axis set to the CPA by PIV measurements rather than the CPA derived by SLP-VCC, and the correlation with the 12 SLP retardation parameters was recalculated. Using the CPA derived by SLP-VCC, we noted a significant association between CPA and symmetry (R 2 = 0.8, P = 0.027), average thickness (R 2 = 0.9, P = 0.017), and ellipse average (R 2 = 0.9, P = 0.021). After substitution of the CPA by PIV axis, there was no significant association between CPA and any retardation parameters (P > 0.05 for all parameters), suggesting complete neutralization of corneal birefringence (Table 4) . Figure 8 illustrates a macular polarimetry image obtained with SLP-VCC in an eye with exudative macular degeneration and an indeterminate macular bow-tie pattern. After corneal compensation, persistence of the macular bow tie suggested incomplete corneal compensation. After substitution of the CPA derived by SLP-VCC (54° nasally downward) with the CPA by PIV (4° nasally downward), a uniform pattern of retardation appeared, suggesting complete corneal compensation. 
Discussion
SLP-VCC determines eye-specific corneal birefringence measurements based on the characteristics of macular birefringence. Macular polarimetry images without corneal compensation usually display a distinct bow-tie or double-humped pattern. Based on the assumption that the corneal birefringence interacts with an intact Henle’s layer to produce the bow-tie patterns, the macular bow-tie patterns can provide a potential means of determination and quantification of corneal birefringence. 27 It therefore follows that disruption of the bow-tie images by macular disease could limit the use of this strategy. This study was performed to explore this limitation. 
The adequacy of corneal compensation was assessed by a number of measures. CPA was measured independently in all eyes with a PIV-based corneal polarimeter. The agreement between the CPA by PIV – and SLP-VCC–generated CPA measurements was greater in eyes with well-defined macular bow ties than in eyes with indeterminate bow ties. Adequate compensation was also defined as the absence of a correlation between retardance parameters and CPA. In the normal group, none of the retardation parameters showed a significant association with SLP-VCC–derived CPA. Conversely, in eyes with macular disease, a significant association was observed between summary retardation parameters (average thickness, ellipse average, superior average, inferior average, and superior integral) and CPA derived from SLP-VCC by the macular bow-tie method (Table 3) . Ideally, no significant association should exist between the CPA and any of these parameters obtained after corneal compensation. The presence of such an association suggests residual uncompensated corneal birefringence. In a previous study involving SLP with fixed corneal compensation, Greenfield et al. 22 found a strong correlation between SLP summary parameters and CPA by PIV. In the present study, the absence of a correlation after substitution of the CPA derived by SLP-VCC with the CPA by PIV (Table 4) further emphasized inadequate corneal compensation. Finally, inspection of the macular retardation image provides a means for assessment of corneal compensation. A fully compensated macular image shows a uniform pattern of retardation with magnitude of less than 28 nm. As illustrated in Figure 8 , a persistent macular bow tie after compensation was suggestive of residual corneal birefringence artifact that dissipated after CPA substitution with the CPA by PIV
Indeterminate macular bow-tie patterns were associated with residual uncompensated corneal birefringence artifact and were observed in 30% of eyes with various forms of macular comorbidity, including atrophic and exudative AMD, ERM, and CME. We hypothesize that macular disease that disrupts the integrity of Henle’s layer produces indeterminate bow-tie patterns and results in failure of the bow-tie algorithm for corneal compensation. Alternative strategies for determining the parameters of corneal compensation are warranted in such eyes. 
This investigation provides validation of a new screen method for corneal compensation. It is based on the observation that the ocular fundus acts as a polarization-preserving screen that displays anterior segment birefringence. Extraction of anterior segment birefringence information both within and outside the potential zone of macular artifact provides a more useful means of complete corneal compensation. Our data suggest that this strategy works well in normal eyes (Fig. 5) and eyes with maculopathy (Fig. 7)
In conclusion, eye-specific correction of CPA and CPM is obtainable by macular-based strategies for neutralization of corneal birefringence by using SLP-VCC. Such strategies may fail if Henle’s layer is anatomically disrupted by macular disease. Some eyes with macular disease and indeterminate macular bow-tie patterns may exhibit residual corneal birefringence after corneal compensation, rendering erroneous RNFL thickness assessments. The screen method may provide a more robust measure of the anterior segment birefringence in such eyes. 
 
Figure 1.
 
Well-defined bow tie in an eye with atrophic AMD. Left: fundus image; middle: retardation image of the macula obtained without corneal compensation illustrates a well-defined bow tie. The bright and dark arms of the bow tie were perpendicular to each other and met in the center of the fovea. Right: after corneal compensation, retardation in the macula was much weaker and more uniform. The CPA derived from SLP-VCC was 29° nasally downward and was in close agreement with the CPA by PIV of 25° nasally downward.
Figure 1.
 
Well-defined bow tie in an eye with atrophic AMD. Left: fundus image; middle: retardation image of the macula obtained without corneal compensation illustrates a well-defined bow tie. The bright and dark arms of the bow tie were perpendicular to each other and met in the center of the fovea. Right: after corneal compensation, retardation in the macula was much weaker and more uniform. The CPA derived from SLP-VCC was 29° nasally downward and was in close agreement with the CPA by PIV of 25° nasally downward.
Figure 2.
 
Weak bow tie in an eye with an ERM, nonproliferative diabetic retinopathy, and previous laser treatment. Left: fundus image; middle: uncompensated macular image illustrates a weak bow tie. Both bright arms of the macular bow tie were relatively indistinct, although there was a suggestion of dark arms oriented 180° apart. Right: corneal compensation caused little change in the appearance of the macular image.
Figure 2.
 
Weak bow tie in an eye with an ERM, nonproliferative diabetic retinopathy, and previous laser treatment. Left: fundus image; middle: uncompensated macular image illustrates a weak bow tie. Both bright arms of the macular bow tie were relatively indistinct, although there was a suggestion of dark arms oriented 180° apart. Right: corneal compensation caused little change in the appearance of the macular image.
Figure 3.
 
Indeterminate bow tie in an eye with atrophic AMD. Left: fundus image from the nerve fiber analyzer’s brightness channel; middle: uncompensated macular image illustrates an indeterminate bow tie characterized by partial or complete loss of at least one of the arms of the bow tie. Right: after corneal compensation, the bow-tie pattern persisted, indicative of residual uncompensated corneal birefringence. Considerable disparity was identified between the CPA derived by SLP-VCC (3° nasally downward) and CPA by PIV (24° nasally downward).
Figure 3.
 
Indeterminate bow tie in an eye with atrophic AMD. Left: fundus image from the nerve fiber analyzer’s brightness channel; middle: uncompensated macular image illustrates an indeterminate bow tie characterized by partial or complete loss of at least one of the arms of the bow tie. Right: after corneal compensation, the bow-tie pattern persisted, indicative of residual uncompensated corneal birefringence. Considerable disparity was identified between the CPA derived by SLP-VCC (3° nasally downward) and CPA by PIV (24° nasally downward).
Figure 4.
 
Screen method for determining corneal birefringence. SLP images were obtained with no corneal compensation. (A) Retardance image of a normal macula shows the bow tie pattern caused by the interaction of the corneal birefringence with the radially oriented macular birefringence. (B) Retardance image with no apparent bow tie due to maculopathy (CME with ERM). (C) The uniform gray square shows the 213 × 213-pixel area averaged for the eye in (A). Scattered saturated pixels and a central 31 × 31-pixel square that contained an instrumental artifact were excluded from the average. The cross shows the perpendicular axes determined by the birefringence calculation. The arms of the cross are aligned with the bow tie, as they should be if the screen method and bow tie method agree. (D) Same as (C), but for the eye in (B).
Figure 4.
 
Screen method for determining corneal birefringence. SLP images were obtained with no corneal compensation. (A) Retardance image of a normal macula shows the bow tie pattern caused by the interaction of the corneal birefringence with the radially oriented macular birefringence. (B) Retardance image with no apparent bow tie due to maculopathy (CME with ERM). (C) The uniform gray square shows the 213 × 213-pixel area averaged for the eye in (A). Scattered saturated pixels and a central 31 × 31-pixel square that contained an instrumental artifact were excluded from the average. The cross shows the perpendicular axes determined by the birefringence calculation. The arms of the cross are aligned with the bow tie, as they should be if the screen method and bow tie method agree. (D) Same as (C), but for the eye in (B).
Figure 5.
 
Comparison in 20 normal subjects of two methods for determining anterior segment birefringence. The birefringence determined by the screen method agreed well with that determined by the macular bow-tie method, both for the magnitude (left; R 2 = 0.96, P < 0.0001) and the direction (right; R 2 = 0.95, P < 0.0001) of anterior segment birefringence. Solid line: line of equality.
Figure 5.
 
Comparison in 20 normal subjects of two methods for determining anterior segment birefringence. The birefringence determined by the screen method agreed well with that determined by the macular bow-tie method, both for the magnitude (left; R 2 = 0.96, P < 0.0001) and the direction (right; R 2 = 0.95, P < 0.0001) of anterior segment birefringence. Solid line: line of equality.
Table 1.
 
Patient Demographics
Table 1.
 
Patient Demographics
Normal (n = 20) Maculopathy (n = 27) P
Age (y)* 40.2 ± 10.8 (24–59) 73.9 ± 8.2 (56–88) <0.0001, †
Gender (n)
 M 3 14 0.009, ‡
 F 17 13
Race (n)
 White 15 27
 Black 2 0 0.05, ‡
 Hispanic 2 0
 Other 1 0
Table 2.
 
CPA Value and Variability and Macular Bow-Tie Birefringence Pattern among Eyes with Macular Disease
Table 2.
 
CPA Value and Variability and Macular Bow-Tie Birefringence Pattern among Eyes with Macular Disease
No. Macular Disease Bow-Tie Pattern CPA Value CPA SD2
PIV SLP-VCC PIV SLP-VCC
1 AMD (atrophic) Indeterminate 24 3 2.7 1.5
2 Indeterminate 56 57 2.7 1.5
3 Well defined 23 15 0.9 13.5
4 Well defined 47 41 3.5 6.0
5 Well defined 29 25 0.9 6.0
6 Well defined 23 27 0.9 0.2
7 Well defined 24 22 2.7 2.9
8 Weak 32 27 0.9 1.5
9 AMD (exudative) Indeterminate 4 54 6.2 2.0
10 Indeterminate 19 37 0.9 13.5
11 Indeterminate 2 18 0.9 2.9
12 Well defined 30 44 0.9 2.7
13 ERM Indeterminate 11 86 0.9 8.0
15 Indeterminate 5 −15 0.9 0.7
18 Indeterminate 6 2 11.5 0.7
17 Well defined 0 5 0 0.9
14 Weak −20 17 2.7 6.0
16 Weak 10 −8 2.7 46.9
19 Weak 61 57 0.9 6.2
20 CME Well defined 5 20 0.9 3.5
21 Well defined 16 13 0 0.9
22 Well defined 42 44 0 2.9
23 Well defined 21 23 0.9 0.9
24 CSR Well defined −4 11 0 4.7
25 Well defined 3 13 0.9 0.7
26 Pattern dystrophy Well defined 12 1 0.9 0.2
27 Well defined 29 27 0.9 0.7
Figure 6.
 
Histogram showing the distribution of the bow-tie patterns in normal eyes and eyes with macular disease. Eyes with macular disease had significantly more indeterminate bow ties.
Figure 6.
 
Histogram showing the distribution of the bow-tie patterns in normal eyes and eyes with macular disease. Eyes with macular disease had significantly more indeterminate bow ties.
Figure 7.
 
Correlation between CPA by PIV and CPA derived by SLP-VCC (left; bow-tie method) in normal eyes (top; R 2 = 0.72, P < 0.0001) and eyes with maculopathy (bottom; R 2 = 0.22, P = 0.024) and the correlation between CPA by PIV and CPA derived by SLP-VCC (right; screen method) in normal eyes (R 2 = 0.73, P < 0.0001) and eyes with maculopathy (R 2 = 0.83, P < 0.0001).
Figure 7.
 
Correlation between CPA by PIV and CPA derived by SLP-VCC (left; bow-tie method) in normal eyes (top; R 2 = 0.72, P < 0.0001) and eyes with maculopathy (bottom; R 2 = 0.22, P = 0.024) and the correlation between CPA by PIV and CPA derived by SLP-VCC (right; screen method) in normal eyes (R 2 = 0.73, P < 0.0001) and eyes with maculopathy (R 2 = 0.83, P < 0.0001).
Table 3.
 
Correlation between CPA Derived with the Macular Bow-Tie Method and 12 Peripapillary Retardation Parameters in Normal Eyes and Eyes with Macular Disease
Table 3.
 
Correlation between CPA Derived with the Macular Bow-Tie Method and 12 Peripapillary Retardation Parameters in Normal Eyes and Eyes with Macular Disease
SLP-VCC Parameter Normal Maculopathy
R 2 P R 2 P
Symmetry 0.001 0.87 0.01 0.65
Superior ratio 0.03 0.48 0.01 0.58
Inferior ratio 0.03 0.50 0.02 0.52
Superior/nasal 0.01 0.62 0.04 0.28
Maximum Modulation 0.04 0.41 0.03 0.34
Ellipse modulation 0.01 0.74 0.001 0.88
Number 0.004 0.40 0.11 0.08
Average thickness 0.01 0.60 0.27 0.01
Ellipse average 0.004 0.77 0.24 0.01
Superior average 0.01 0.69 0.24 0.01
Inferior average 0.01 0.69 0.28 0.004
Superior integral 0.001 0.92 0.37 0.001
Table 4.
 
Association between CPA and Peripapillary Retardation Parameters with and without Substitution with PIV
Table 4.
 
Association between CPA and Peripapillary Retardation Parameters with and without Substitution with PIV
SLP-VCC Parameter Before Substitution After Substitution
R 2 P R 2 P
Symmetry 0.84 0.03 0.12 0.56
Superior ratio 0.02 0.80 0.42 0.23
Inferior ratio 0.07 0.66 0.22 0.42
Superior/nasal 0.05 0.70 0.36 0.28
Maximum modulation 0.10 0.60 0.39 0.26
Ellipse modulation 0.09 0.61 0.37 0.27
Number 0.04 0.73 0.11 0.57
Average thickness 0.88 0.01 0.01 0.83
Ellipse average 0.86 0.02 0.02 0.79
Superior average 0.63 0.11 0.12 0.56
Inferior average 0.14 0.52 0.07 0.67
Superior integral 0.50 0.18 0.09 0.60
Figure 8.
 
Macular polarimetry image obtained with SLP-VCC in an eye with exudative macular degeneration (fundus image, top left) illustrates an indeterminate macular bow-tie pattern (top right). The macular bow tie persisted after corneal compensation with parameters provided by the bow-tie method (bottom left), suggesting incomplete corneal compensation. After substitution of the CPA derived by SLP-VCC (54° nasally downward) with the CPA by PIV (4° nasally downward), a uniform weak pattern of retardation suggested complete corneal compensation (bottom right).
Figure 8.
 
Macular polarimetry image obtained with SLP-VCC in an eye with exudative macular degeneration (fundus image, top left) illustrates an indeterminate macular bow-tie pattern (top right). The macular bow tie persisted after corneal compensation with parameters provided by the bow-tie method (bottom left), suggesting incomplete corneal compensation. After substitution of the CPA derived by SLP-VCC (54° nasally downward) with the CPA by PIV (4° nasally downward), a uniform weak pattern of retardation suggested complete corneal compensation (bottom right).
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Figure 1.
 
Well-defined bow tie in an eye with atrophic AMD. Left: fundus image; middle: retardation image of the macula obtained without corneal compensation illustrates a well-defined bow tie. The bright and dark arms of the bow tie were perpendicular to each other and met in the center of the fovea. Right: after corneal compensation, retardation in the macula was much weaker and more uniform. The CPA derived from SLP-VCC was 29° nasally downward and was in close agreement with the CPA by PIV of 25° nasally downward.
Figure 1.
 
Well-defined bow tie in an eye with atrophic AMD. Left: fundus image; middle: retardation image of the macula obtained without corneal compensation illustrates a well-defined bow tie. The bright and dark arms of the bow tie were perpendicular to each other and met in the center of the fovea. Right: after corneal compensation, retardation in the macula was much weaker and more uniform. The CPA derived from SLP-VCC was 29° nasally downward and was in close agreement with the CPA by PIV of 25° nasally downward.
Figure 2.
 
Weak bow tie in an eye with an ERM, nonproliferative diabetic retinopathy, and previous laser treatment. Left: fundus image; middle: uncompensated macular image illustrates a weak bow tie. Both bright arms of the macular bow tie were relatively indistinct, although there was a suggestion of dark arms oriented 180° apart. Right: corneal compensation caused little change in the appearance of the macular image.
Figure 2.
 
Weak bow tie in an eye with an ERM, nonproliferative diabetic retinopathy, and previous laser treatment. Left: fundus image; middle: uncompensated macular image illustrates a weak bow tie. Both bright arms of the macular bow tie were relatively indistinct, although there was a suggestion of dark arms oriented 180° apart. Right: corneal compensation caused little change in the appearance of the macular image.
Figure 3.
 
Indeterminate bow tie in an eye with atrophic AMD. Left: fundus image from the nerve fiber analyzer’s brightness channel; middle: uncompensated macular image illustrates an indeterminate bow tie characterized by partial or complete loss of at least one of the arms of the bow tie. Right: after corneal compensation, the bow-tie pattern persisted, indicative of residual uncompensated corneal birefringence. Considerable disparity was identified between the CPA derived by SLP-VCC (3° nasally downward) and CPA by PIV (24° nasally downward).
Figure 3.
 
Indeterminate bow tie in an eye with atrophic AMD. Left: fundus image from the nerve fiber analyzer’s brightness channel; middle: uncompensated macular image illustrates an indeterminate bow tie characterized by partial or complete loss of at least one of the arms of the bow tie. Right: after corneal compensation, the bow-tie pattern persisted, indicative of residual uncompensated corneal birefringence. Considerable disparity was identified between the CPA derived by SLP-VCC (3° nasally downward) and CPA by PIV (24° nasally downward).
Figure 4.
 
Screen method for determining corneal birefringence. SLP images were obtained with no corneal compensation. (A) Retardance image of a normal macula shows the bow tie pattern caused by the interaction of the corneal birefringence with the radially oriented macular birefringence. (B) Retardance image with no apparent bow tie due to maculopathy (CME with ERM). (C) The uniform gray square shows the 213 × 213-pixel area averaged for the eye in (A). Scattered saturated pixels and a central 31 × 31-pixel square that contained an instrumental artifact were excluded from the average. The cross shows the perpendicular axes determined by the birefringence calculation. The arms of the cross are aligned with the bow tie, as they should be if the screen method and bow tie method agree. (D) Same as (C), but for the eye in (B).
Figure 4.
 
Screen method for determining corneal birefringence. SLP images were obtained with no corneal compensation. (A) Retardance image of a normal macula shows the bow tie pattern caused by the interaction of the corneal birefringence with the radially oriented macular birefringence. (B) Retardance image with no apparent bow tie due to maculopathy (CME with ERM). (C) The uniform gray square shows the 213 × 213-pixel area averaged for the eye in (A). Scattered saturated pixels and a central 31 × 31-pixel square that contained an instrumental artifact were excluded from the average. The cross shows the perpendicular axes determined by the birefringence calculation. The arms of the cross are aligned with the bow tie, as they should be if the screen method and bow tie method agree. (D) Same as (C), but for the eye in (B).
Figure 5.
 
Comparison in 20 normal subjects of two methods for determining anterior segment birefringence. The birefringence determined by the screen method agreed well with that determined by the macular bow-tie method, both for the magnitude (left; R 2 = 0.96, P < 0.0001) and the direction (right; R 2 = 0.95, P < 0.0001) of anterior segment birefringence. Solid line: line of equality.
Figure 5.
 
Comparison in 20 normal subjects of two methods for determining anterior segment birefringence. The birefringence determined by the screen method agreed well with that determined by the macular bow-tie method, both for the magnitude (left; R 2 = 0.96, P < 0.0001) and the direction (right; R 2 = 0.95, P < 0.0001) of anterior segment birefringence. Solid line: line of equality.
Figure 6.
 
Histogram showing the distribution of the bow-tie patterns in normal eyes and eyes with macular disease. Eyes with macular disease had significantly more indeterminate bow ties.
Figure 6.
 
Histogram showing the distribution of the bow-tie patterns in normal eyes and eyes with macular disease. Eyes with macular disease had significantly more indeterminate bow ties.
Figure 7.
 
Correlation between CPA by PIV and CPA derived by SLP-VCC (left; bow-tie method) in normal eyes (top; R 2 = 0.72, P < 0.0001) and eyes with maculopathy (bottom; R 2 = 0.22, P = 0.024) and the correlation between CPA by PIV and CPA derived by SLP-VCC (right; screen method) in normal eyes (R 2 = 0.73, P < 0.0001) and eyes with maculopathy (R 2 = 0.83, P < 0.0001).
Figure 7.
 
Correlation between CPA by PIV and CPA derived by SLP-VCC (left; bow-tie method) in normal eyes (top; R 2 = 0.72, P < 0.0001) and eyes with maculopathy (bottom; R 2 = 0.22, P = 0.024) and the correlation between CPA by PIV and CPA derived by SLP-VCC (right; screen method) in normal eyes (R 2 = 0.73, P < 0.0001) and eyes with maculopathy (R 2 = 0.83, P < 0.0001).
Figure 8.
 
Macular polarimetry image obtained with SLP-VCC in an eye with exudative macular degeneration (fundus image, top left) illustrates an indeterminate macular bow-tie pattern (top right). The macular bow tie persisted after corneal compensation with parameters provided by the bow-tie method (bottom left), suggesting incomplete corneal compensation. After substitution of the CPA derived by SLP-VCC (54° nasally downward) with the CPA by PIV (4° nasally downward), a uniform weak pattern of retardation suggested complete corneal compensation (bottom right).
Figure 8.
 
Macular polarimetry image obtained with SLP-VCC in an eye with exudative macular degeneration (fundus image, top left) illustrates an indeterminate macular bow-tie pattern (top right). The macular bow tie persisted after corneal compensation with parameters provided by the bow-tie method (bottom left), suggesting incomplete corneal compensation. After substitution of the CPA derived by SLP-VCC (54° nasally downward) with the CPA by PIV (4° nasally downward), a uniform weak pattern of retardation suggested complete corneal compensation (bottom right).
Table 1.
 
Patient Demographics
Table 1.
 
Patient Demographics
Normal (n = 20) Maculopathy (n = 27) P
Age (y)* 40.2 ± 10.8 (24–59) 73.9 ± 8.2 (56–88) <0.0001, †
Gender (n)
 M 3 14 0.009, ‡
 F 17 13
Race (n)
 White 15 27
 Black 2 0 0.05, ‡
 Hispanic 2 0
 Other 1 0
Table 2.
 
CPA Value and Variability and Macular Bow-Tie Birefringence Pattern among Eyes with Macular Disease
Table 2.
 
CPA Value and Variability and Macular Bow-Tie Birefringence Pattern among Eyes with Macular Disease
No. Macular Disease Bow-Tie Pattern CPA Value CPA SD2
PIV SLP-VCC PIV SLP-VCC
1 AMD (atrophic) Indeterminate 24 3 2.7 1.5
2 Indeterminate 56 57 2.7 1.5
3 Well defined 23 15 0.9 13.5
4 Well defined 47 41 3.5 6.0
5 Well defined 29 25 0.9 6.0
6 Well defined 23 27 0.9 0.2
7 Well defined 24 22 2.7 2.9
8 Weak 32 27 0.9 1.5
9 AMD (exudative) Indeterminate 4 54 6.2 2.0
10 Indeterminate 19 37 0.9 13.5
11 Indeterminate 2 18 0.9 2.9
12 Well defined 30 44 0.9 2.7
13 ERM Indeterminate 11 86 0.9 8.0
15 Indeterminate 5 −15 0.9 0.7
18 Indeterminate 6 2 11.5 0.7
17 Well defined 0 5 0 0.9
14 Weak −20 17 2.7 6.0
16 Weak 10 −8 2.7 46.9
19 Weak 61 57 0.9 6.2
20 CME Well defined 5 20 0.9 3.5
21 Well defined 16 13 0 0.9
22 Well defined 42 44 0 2.9
23 Well defined 21 23 0.9 0.9
24 CSR Well defined −4 11 0 4.7
25 Well defined 3 13 0.9 0.7
26 Pattern dystrophy Well defined 12 1 0.9 0.2
27 Well defined 29 27 0.9 0.7
Table 3.
 
Correlation between CPA Derived with the Macular Bow-Tie Method and 12 Peripapillary Retardation Parameters in Normal Eyes and Eyes with Macular Disease
Table 3.
 
Correlation between CPA Derived with the Macular Bow-Tie Method and 12 Peripapillary Retardation Parameters in Normal Eyes and Eyes with Macular Disease
SLP-VCC Parameter Normal Maculopathy
R 2 P R 2 P
Symmetry 0.001 0.87 0.01 0.65
Superior ratio 0.03 0.48 0.01 0.58
Inferior ratio 0.03 0.50 0.02 0.52
Superior/nasal 0.01 0.62 0.04 0.28
Maximum Modulation 0.04 0.41 0.03 0.34
Ellipse modulation 0.01 0.74 0.001 0.88
Number 0.004 0.40 0.11 0.08
Average thickness 0.01 0.60 0.27 0.01
Ellipse average 0.004 0.77 0.24 0.01
Superior average 0.01 0.69 0.24 0.01
Inferior average 0.01 0.69 0.28 0.004
Superior integral 0.001 0.92 0.37 0.001
Table 4.
 
Association between CPA and Peripapillary Retardation Parameters with and without Substitution with PIV
Table 4.
 
Association between CPA and Peripapillary Retardation Parameters with and without Substitution with PIV
SLP-VCC Parameter Before Substitution After Substitution
R 2 P R 2 P
Symmetry 0.84 0.03 0.12 0.56
Superior ratio 0.02 0.80 0.42 0.23
Inferior ratio 0.07 0.66 0.22 0.42
Superior/nasal 0.05 0.70 0.36 0.28
Maximum modulation 0.10 0.60 0.39 0.26
Ellipse modulation 0.09 0.61 0.37 0.27
Number 0.04 0.73 0.11 0.57
Average thickness 0.88 0.01 0.01 0.83
Ellipse average 0.86 0.02 0.02 0.79
Superior average 0.63 0.11 0.12 0.56
Inferior average 0.14 0.52 0.07 0.67
Superior integral 0.50 0.18 0.09 0.60
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