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1 From the Glaucoma Service and Dana Center for Preventive Ophthalmology, Wilmer Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
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Abstract |
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METHODS. Seventeen eyes of 13 persons with well-documented glaucoma histories and Humphrey threshold visual field tests (San Leandro, CA) were obtained from eye banks. RGC number was estimated by histologic counts of retinal sections and by counts of remaining axons in the optic nerves. The locations of the retinal samples corresponded to specific test points in the visual field. The data for glaucoma patients were compared with 17 eyes of 17 persons who were group matched for age, had no ocular history, and had normal eyes by histologic examination.
RESULTS. The mean RGC loss for the entire retina averaged 10.2%, indicating that many eyes had early glaucoma damage. RGC body loss averaged 35.7% in eyes with corrected pattern SD probability less than 0.5%. When upper to lower retina RGC counts were compared with their corresponding visual field data within each eye, a 5-dB loss in sensitivity was associated with 25% RGC loss. For individual points that were abnormal at a probability less than 0.5%, the mean RGC loss was 29%. In control eyes, the loss of RGCs with age was estimated as 7205 cells per year in persons between 55 and 95 years of age. In optic nerves from glaucoma subjects, smaller axons were significantly more likely to be present than larger axons (R2 = 0.78, P < 0.001).
CONCLUSIONS. At least 25% to 35% RGC loss is associated with statistical abnormalities in automated visual field testing. In addition, these data corroborate previous findings that RGCs with larger diameter axons preferentially die in glaucoma.
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Introduction |
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Four previous reports have compared the number of remaining RGCs to the visual field findings in the same eyes by manual, static, and kinetic testing on the Goldmann perimeter.1 2 3 4 In most persons in whom defects were detectable, there was considerable RGC loss. Among 10 eyes of seven persons with suspected glaucoma with normal field test results on the Goldmann perimeter, 7 were more than 2 SD below the normal mean RGC axon number for the whole optic nerve, and 3 were 1 SD below the normal RGC axon number. Eyes with normal manual field tests results varied from 12% to 53% RGC loss. It is not possible to estimate the degree to which these eyes are representative of all eyes with ocular hypertension. Another report detected no histologic RGC loss in five persons with normal visual fields (two of these were tested by automated perimetry).5 Many eyes with ocular hypertension would be expected to have no RGC damage; however, that some with suspected glaucoma have statistically significant injury suggests that damage can occur before detection.
Visual field testing is now conducted with automated perimeters and standard thresholding algorithms. In histologic RGC counts from three eyes that had undergone Octopus (two eyes; Interzeag, Haag-Streit Services, Mason, OH) or Humphrey (one eye; San Leandro, CA) automated tests, a considerable number of RGC bodies were dead at a given retinal location before detectable abnormality in a visual field test.4 Furthermore, these and other data from similar material in human and monkey eyes with experimental glaucoma indicated that RGC loss in early glaucoma was selectively greater among larger ganglion cells,1 3 4 6 7 8 9 10 11 12 although all RGC sizes were affected.13 14
There are at least two explanations for RGC death before detectable field loss. First, there is considerable redundancy in the visual system. A stimulus projected onto a particular retinal location affects many RGCs, whose responses would depend on the normal density of their functional areas and the type of stimulus.15 Even when some RGCs are dead, others subserving the same area could signal the presence of the target. Second, there is considerable variability in psychophysical testing, as well as substantial variation in the responses of normal persons. These variations generate broad limits within which abnormal responses from a subject with glaucoma would be masked until they significantly exceeded the normal range.
This study provided extensive correlations between the degree of RGC loss and the automated visual field tests in eyes of individuals with glaucoma. In addition, the proportion of RGCs of various axonal diameters was compared with the extent of loss to re-examine the hypothesis that larger cells are more susceptible to injury.
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Methods |
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Approximately 50 control human eye bank eyes were obtained through similar sources from donors with no ocular history. After gross inspection of the retina and anterior segment at the dissecting microscope to eliminate those eyes with visible disease, light microscopic evaluation of the retina and optic nerve was conducted to rule out detectable ocular disorders that would affect RGC number. In addition, we required excellent preservation of control and glaucoma tissues, judged by light microscopic examinations before acceptance of each eye for the study.
Characteristics of Visual Field Data
In 15 fields (12 persons), we obtained the Statpac 1 (Humphrey)
analysis, including the sensitivity in decibels, difference from
age-normal value, probability of the sensitivity’s falling within the
normal range (total deviation), and global indices. Only three of the
eyes had had a Statpac 2 analysis, including the Humphrey Glaucoma
Hemifield Test. We were unable to obtain from the manufacturer the
normative data with which to calculate this parameter on the other
eyes. All fields satisfied the Statpac level of reliability for
false-positive errors, and all had fewer than 33% fixation losses.
Because the levels of false-negative errors exceeding Humphrey limits
can be seen in reliable subjects with substantial glaucoma injury, no
limit was placed on false-negative errors. In each case, the field test
used was the final test before death, unless the final test did not
meet the criteria for reliability.
Preparation of Ocular Tissues
Each of the eyes had been fixed within 24 hours of death (most
within 12 hours) in aldehyde fixative (Tables 1
2
and 3)
, and the time from death to fixation did not differ
significantly between normal and glaucoma-affected eyes. The normal and
glaucomatous eyes were group-matched for age, race, and gender. The
retina was separated at the ora serrata and optic nerve, and relaxing
incisions were made to produce a flat preparation. The position of the
optic disc, fovea, and retinal blood vessels were used for orientation.
Measurements were made with a caliper to approximate the positions on
the retina that corresponded to the locations for 28 selected test
points in the Humphrey 24-2 program (Fig. 1)
. Because there is a high correlation among adjacent test points, the
selected locations were spaced throughout the field and included at
least two test points from each Humphrey cluster in the Glaucoma
Hemifield Test.
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Quantitative Analysis of Specimens
The number of RGCs was estimated from at least four retinal
sections from each retinal position that corresponded to a field test
point. Among cells in the ganglion cell layer, those that satisfied the
following characteristics were included as presumed
RGCs15
: round or oval cell outline, round or oval nucleus,
and cell diameter greater than 7 µm. Section length was measured, and
the data were expressed as cells per millimeter retinal length
(density). The four sections were averaged to give a mean density for
each location. The density of glaucomatous eyes was divided by the mean
density of normal eyes to give a percentage of normal value for points,
clusters, hemifield, and whole retina. Sections were unsatisfactory for
counting in 13 locations from seven eyes, representing missing data
from 2.7% of the 476 possible locations in glaucoma-affected eyes.
Most retinal counting was performed by one observer, but some data were collected by a second observer. We performed comparisons of counting by these two persons, with masked, repeated counting of 10 sections from 10 eyes. The average difference for both intra- and interobserver counting was less than 2%, and analysis of variance found no significant difference either between or within persons (P > 0.5 for both).
Some of the neuron-like cells that we included in our counting may have been amacrine cells. Our methodology required the higher resolution of resin embedding and 1-µm sectioning, thus precluding the labeling of RGC bodies by immunohistologic techniques that are possible only in frozen or paraffin-embedded sections. In a previous investigation,4 we determined the diameter of RGC bodies in wholemounts of human retina. This was not possible in enough of the present material, because of variation in tissue preservation.
In addition to counting RGC bodies, RGC axons in the optic nerve of both control and glaucomatous eyes were studied. The optic nerve was removed from each eye after razor slices were made for orientation, one slice at the superior nerve pole, and two slices nasally. A sample of each nerve 1-mm thick was embedded in epoxy resin, sectioned at 1 µm and stained with toluidine blue. The number and size distribution of myelinated axons was determined using an image analysis system (Vidas; Carl Zeiss, Thornwood, NY).3 Axon diameter was measured inside the myelin sheath. A trained observer edited each sampled area to remove capillaries, glial tissue, and degenerated axons that may have otherwise been included as intact nerve fibers. Optic nerve data were obtained on 16 eyes from 16 control persons, and from 13 eyes of 11 glaucoma patients.
There was a reasonable correlation between the number of RGCs estimated from counts in the retina compared with RGC axon number estimated from each eye (data for glaucomatous eyes: linear regression, R2 = 0.35, P = 0.022, n = 13 eyes of 11 persons; for one eye per person: R2 = 0.35, P = 0.05, n = 11). There may be differences between retinal and optic nerve counts, because the areas sampled in the retina represented locations only within the central 24°, whereas the optic nerve data were a 5% random sample of RGC axons from the entire retina. The number of RGC bodies counted was 1.4% of the estimated total number of RGCs in glaucomatous eyes and 1.0% in control eyes.
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Results |
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The mean number of axons in the optic nerves of the control eyes was 534,396 ± 113,373. The average age for these persons without glaucoma was 76.4 years (Table 1) . When total axon number was compared with age (Fig. 2) , a significant decline in fibers was detected, with a slope indicating loss of 7205 fibers per year (linear regression: R2 = 0.50, P = 0.002). This slope was used to calculate an age-normal relationship to estimate the percentage of normal axons present in each glaucomatous optic nerve. The variance of data at each individual data point for RGC counting was substantial, and meaningful regressions for age were not obtainable. Therefore, loss of RGC bodies was calculated by comparison to the average of all control eyes at the relevant location.
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Cluster and Point-by-Point Comparison of RGC and Field Data
Our method included two or three points from each of the five
clusters in the Glaucoma Hemifield Test of the Humphrey perimeter. As
with the upper–lower retina comparison, the data comparing cluster 1
(Fig. 6
; nearest the fovea) found a highly significant relation between
the difference in two upper points and two lower points in percentage
of normal RGCs compared with the difference in their threshold loss in
the corresponding test points (Fig. 7
; R2 = 0.34, P =
0.014, n = 17; for one eye per person:
R2 = 0.28, P =
0.07, n = 13). The other clusters had insignificant
relationships between histologic and functional findings. Cluster 1 has
the highest density of RGCs in the retina, whereas the other clusters
have substantially lower density. These low densities provide few RGCs
and wide variability in attempting to make these correlations at
clusters other than cluster 1.
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Discussion |
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The density of RGC bodies was 10 times higher in the perifoveal retina than for retinal locations corresponding to points at the outer measurement zone of the field test (20–30o from fixation). If we assume that some of the cells we counted in the ganglion cell layer were actually amacrine cells and not RGCs, our estimates of percentage of loss would actually be understated. For example, if 50% of identified neurons were amacrines (a very unlikely result in the central retina), then our estimate of 50% loss would have had to involve loss of 100% of the original RGCs, with the 50% non-RGCs remaining. In addition, if amacrines are included in our counts and if they atrophy in proportion to the loss of RGCs, then our estimates would be unaffected.
Some measures of field test results could not be closely correlated with the RGC numbers. There is substantial variation in the total number of RGCs from one eye to another, placing relatively broad confidence limits on any estimate of histologic damage. Furthermore, there is very significant variability in field test results both among persons and for the same subject within and between tests. The reproducibility of our histologic counting methods is excellent and adds only minimally to the variability in correlations. Finally, some field measures would not be expected to correlate with glaucoma damage very closely, because they are measures of general sensitivity loss that can be influenced by other disorders, age, and test conditions. For example, the MD index was less specifically linked to glaucoma damage than CPSD.17
The validity of our RGC counting was supported by the correlation of the retinal data with the optic nerve fiber counting in the same eyes. The number of fibers in the normal optic nerve has varied from 600,000 to 1.2 million in various reports.18 19 20 21 22 23 24 Many investigators have either suggested or statistically demonstrated that RGC numbers decline with age. Age-related loss estimates have varied from as few as 2,000 to as many as 12,000 RGCs dying per year. The normal number of RGCs in this report was lower, and our estimated loss with age was higher than our own previous estimates. This probably resulted from the substantially older age of our control subjects (compared with past reports), who were selected to match the age of the glaucoma patients. Inspection of data from other investigators reveals that the loss of RGCs with age may accelerate after middle age.24 The control subjects of this study were nearly 20 years older than those in our previous reports,3 23 in which only a modest loss of RGCs was estimated with aging. If we assume that the loss of RGCs increases with advancing age, subjects with glaucoma who have loss of the majority of RGCs could undergo progressive impairment with an age-related loss of 7000 fibers per year, despite any effort to treat the disease.
We have shown that larger RGCs are preferentially susceptible to death from glaucoma in human eyes,3 4 6 8 9 11 12 and this was corroborated in studies of the retina,5 the optic nerve,7 or the lateral geniculate body10 of persons with glaucoma and in experimental monkeys.6 12 Selectivity is not always demonstrable in the monkey model,13 14 27 especially when very rapid damage is caused by short-term, high intraocular pressure. If RGC axons were to decrease their diameter before death, an apparently selective loss of larger axons might be simulated. We have previously demonstrated that our data are not compatible with this hypothesis.8 The present glaucoma axon data show no shift of axon diameter to smaller sizes. Axon diameter and cell body size are correlated with functional RGC behavior, and psychophysical tests that exploit the loss of the functions subserved by larger RGCs including scotopic,28 motion,29 and frequency-doubling paradigms30 show promise in glaucoma diagnosis. The translation of anatomic selectivity into useful psychophysical tests depends on the sensitivity with which loss of particular RGCs can be detected by functional testing.15 31
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Footnotes |
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Submitted for publication February 23, 1999; revised July 26, 1999; accepted October 26, 1999.
Commercial relationships policy: N.
Corresponding author: Harry A. Quigley, Wilmer 120, 600 N. Wolfe Street, Johns Hopkins Hospital, Baltimore, MD 21287. hquigley{at}jhmi.edu
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W. A. Hare, E. WoldeMussie, R. N. Weinreb, H. Ton, G. Ruiz, M. Wijono, B. Feldmann, L. Zangwill, and L. Wheeler Efficacy and Safety of Memantine Treatment for Reduction of Changes Associated with Experimental Glaucoma in Monkey, II: Structural Measures Invest. Ophthalmol. Vis. Sci., August 1, 2004; 45(8): 2640 - 2651. [Abstract] [Full Text] [PDF]
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R. H. Farkas, I. Chowers, A. S. Hackam, M. Kageyama, R. W. Nickells, D. C. Otteson, E. J. Duh, C. Wang, D. F. Valenta, T. L. Gunatilaka, et al. Increased Expression of Iron-Regulating Genes in Monkey and Human Glaucoma Invest. Ophthalmol. Vis. Sci., May 1, 2004; 45(5): 1410 - 1417. [Abstract] [Full Text] [PDF]
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N. J. Reus and H. G. Lemij The Relationship between Standard Automated Perimetry and GDx VCC Measurements Invest. Ophthalmol. Vis. Sci., March 1, 2004; 45(3): 840 - 845. [Abstract] [Full Text] [PDF]
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W. H. Swanson, J. Felius, and F. Pan Perimetric Defects and Ganglion Cell Damage: Interpreting Linear Relations Using a Two-Stage Neural Model Invest. Ophthalmol. Vis. Sci., February 1, 2004; 45(2): 466 - 472. [Abstract] [Full Text] [PDF]
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D. C. Hood, P. Thienprasiddhi, V. C. Greenstein, B. J. Winn, N. Ohri, J. M. Liebmann, and R. Ritch Detecting Early to Mild Glaucomatous Damage: A Comparison of the Multifocal VEP and Automated Perimetry Invest. Ophthalmol. Vis. Sci., February 1, 2004; 45(2): 492 - 498. [Abstract] [Full Text] [PDF]
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K. R. G. Martin, H. A. Quigley, D. J. Zack, H. Levkovitch-Verbin, J. Kielczewski, D. Valenta, L. Baumrind, M. E. Pease, R. L. Klein, and W. W. Hauswirth Gene Therapy with Brain-Derived Neurotrophic Factor As a Protection: Retinal Ganglion Cells in a Rat Glaucoma Model Invest. Ophthalmol. Vis. Sci., October 1, 2003; 44(10): 4357 - 4365. [Abstract] [Full Text] [PDF]
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 J. H. Kang, L. R. Pasquale, W. Willett, B. Rosner, K. M. Egan, N. Faberowski, and S. E. Hankinson Antioxidant Intake and Primary Open-Angle Glaucoma: A Prospective Study Am. J. Epidemiol., August 15, 2003; 158(4): 337 - 346. [Abstract] [Full Text] [PDF]
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D. Raz, I. Perlman, C. L. Percicot, G. N. Lambrou, and R. Ofri Functional Damage to Inner and Outer Retinal Cells in Experimental Glaucoma Invest. Ophthalmol. Vis. Sci., August 1, 2003; 44(8): 3675 - 3684. [Abstract] [Full Text] [PDF]
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A. Stroux, M. Korth, A. Junemann, J. B. Jonas, F. Horn, A. Ziegler, and P. Martus A Statistical Model for the Evaluation of Sensory Tests in Glaucoma, Depending on Optic Disc Damage Invest. Ophthalmol. Vis. Sci., July 1, 2003; 44(7): 2879 - 2884. [Abstract] [Full Text] [PDF]
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P. H. Artes, D. B. Henson, R. Harper, and D. McLeod Multisampling Suprathreshold Perimetry: A Comparison with Conventional Suprathreshold and Full-Threshold Strategies by Computer Simulation Invest. Ophthalmol. Vis. Sci., June 1, 2003; 44(6): 2582 - 2587. [Abstract] [Full Text] [PDF]
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D. C. Hood, V. C. Greenstein, J. G. Odel, X. Zhang, R. Ritch, J. M. Liebmann, J. E. Hong, C. S. Chen, and P. Thienprasiddhi Visual Field Defects and Multifocal Visual Evoked Potentials: Evidence of a Linear Relationship Arch Ophthalmol, December 1, 2002; 120(12): 1672 - 1681. [Abstract] [Full Text] [PDF]
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M. A. Kass, D. K. Heuer, E. J. Higginbotham, C. A. Johnson, J. L. Keltner, J. P. Miller, R. K. Parrish II, M. R. Wilson, M. O. Gordon, and for the Ocular Hypertension Treatment Study Group The Ocular Hypertension Treatment Study: A Randomized Trial Determines That Topical Ocular Hypotensive Medication Delays or Prevents the Onset of Primary Open-Angle Glaucoma Arch Ophthalmol, June 1, 2002; 120(6): 701 - 713. [Abstract] [Full Text] [PDF]
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D. F. Garway-Heath, M. J. Greaney, and J. Caprioli Correction for the Erroneous Compensation of Anterior Segment Birefringence with the Scanning Laser Polarimeter for Glaucoma Diagnosis Invest. Ophthalmol. Vis. Sci., May 1, 2002; 43(5): 1465 - 1474. [Abstract] [Full Text] [PDF]
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S. J. McKinnon, D. M. Lehman, L. A. Kerrigan-Baumrind, C. A. Merges, M. E. Pease, D. F. Kerrigan, N. L. Ransom, N. G. Tahzib, H. A. Reitsamer, H. Levkovitch-Verbin, et al. Caspase Activation and Amyloid Precursor Protein Cleavage in Rat Ocular Hypertension Invest. Ophthalmol. Vis. Sci., April 1, 2002; 43(4): 1077 - 1087. [Abstract] [Full Text] [PDF]
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K. Kashiwagi, Y. Iizuka, M. Araie, Y. Suzuki, and S. Tsukahara Effects of Retinal Glial Cells on Isolated Rat Retinal Ganglion Cells Invest. Ophthalmol. Vis. Sci., October 1, 2001; 42(11): 2686 - 2694. [Abstract] [Full Text] [PDF]
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J. B. Kerrison, K. Buchanan, M. L. Rosenberg, R. Clark, K. Andreason, D. V. Alfaro, H. E. Grossniklaus, L. A. Kerrigan-Baumrind, D. F. Kerrigan, N. R. Miller, et al. Quantification of Optic Nerve Axon Loss Associated With a Relative Afferent Pupillary Defect in the Monkey Arch Ophthalmol, September 1, 2001; 119(9): 1333 - 1341. [Abstract] [Full Text] [PDF]
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C. Bowd, L. M. Zangwill, C. C. Berry, E. Z. Blumenthal, C. Vasile, C. Sanchez-Galeana, C. F. Bosworth, P. A. Sample, and R. N. Weinreb Detecting Early Glaucoma by Assessment of Retinal Nerve Fiber Layer Thickness and Visual Function Invest. Ophthalmol. Vis. Sci., August 1, 2001; 42(9): 1993 - 2003. [Abstract] [Full Text] [PDF]
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H. Levkovitch–Verbin, H. A. Quigley, L. A. Kerrigan–Baumrind, S. A. D’Anna, D. Kerrigan, and M. E. Pease Optic Nerve Transection in Monkeys May Result in Secondary Degeneration of Retinal Ganglion Cells Invest. Ophthalmol. Vis. Sci., April 1, 2001; 42(5): 975 - 982. [Abstract] [Full Text]
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