August 2004
Volume 45, Issue 8
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Visual Psychophysics and Physiological Optics  |   August 2004
Red-Green Chromatic Mechanisms in Normal Aging and Glaucomatous Observers
Author Affiliations
  • Peter Karwatsky
    From the Visual Psychophysics and Perception Laboratory, École d’Optométrie, Université de Montréal, Montréal, Québec, Canada; and the
  • Olga Overbury
    Sir Mortimer B. Davis Jewish General Hospital, Ste. Catherine, Montréal, Québec, Canada.
  • Jocelyn Faubert
    From the Visual Psychophysics and Perception Laboratory, École d’Optométrie, Université de Montréal, Montréal, Québec, Canada; and the
Investigative Ophthalmology & Visual Science August 2004, Vol.45, 2861-2866. doi:10.1167/iovs.03-1256
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      Peter Karwatsky, Olga Overbury, Jocelyn Faubert; Red-Green Chromatic Mechanisms in Normal Aging and Glaucomatous Observers. Invest. Ophthalmol. Vis. Sci. 2004;45(8):2861-2866. doi: 10.1167/iovs.03-1256.

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

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Abstract

purpose. This study was designed to determine whether normal aging and glaucoma are associated with red-green (R/G) chromatic processing abnormalities, a function that is primarily performed by the parvocellular visual pathway.

methods. Chromatic processing mechanisms were examined in 98 glaucomatous observers (between the ages of 49 and 93 years; mean age, 70.8 ± 9.4 [SD]) and 67 normal observers (between the ages of 49 and 88; mean age, 70.6 ± 10.6 years) with the use of the minimum-motion and motion-nulling paradigms. Phakic glaucomatous (n = 60; mean age, 68.7 ± 8.9 years) and normal (n = 32; mean age, 69.8 ± 10.6 years) and pseudophakic glaucomatous (n = 38; mean age, 74 ± 9.4 years) and normal (n = 35; mean age, 71.4 ± 10.6 years) subjects were tested to evaluate the effects of lenticular aging on color perception.

results. Phakic observers (normal or glaucomatous) displayed significantly different minimum-motion values than did both their younger counterparts and all the pseudophakic subjects. These results suggest that normal aging with the presence of a natural lens is accompanied by a significant decrease in green-light sensitivity, an effect that is not exacerbated by glaucoma and is primarily related to optical factors. The data also revealed no differences in color motion perception between groups, indicating that the higher cortical mechanisms of the parvocellular pathway implicated in the analysis of information about the middle and long wavelengths of the visible spectrum are not selectively affected by the disease process and normal aging.

conclusions. Normal aging and glaucoma do not produce significant R/G chromatic processing deficits at retinal and postretinal levels when optical factors are excluded. The authors propose the hypothesis that glaucoma-related effects on motion perception and blue-on-yellow perimetry should be viewed as evidence of loss of ganglion cells that necessitates integration of information over larger retinal areas and more receptor cells than in the R/G chromatic system. Ganglion cells with large receptive fields involve more neural connections and are less numerous than those that respond to R/G information. The functional consequence of this could be that the loss of a single ganglion cell with a larger receptive field would have a greater impact on visual function than the loss of a ganglion cell with a smaller receptive field, such as the ones that process R/G information. The authors believe that glaucoma-induced functional loss is best viewed as related to receptive field structure and function rather than to anatomic cell-type damage.

Glaucoma is not a single entity. It is a combination of signs and symptoms, generally involving increased intraocular pressure, increased optic nerve cupping and visual field defects. 1 The latter are presumed to originate from the destruction of a portion of the ganglion cells in the retina. These neural elements can be divided into two main systems, the parvo (P)- and magno (M)-cellular pathways, which comprise P- and M-ganglion cells, respectively. P cells constitute approximately 80% to 90% of the retinal ganglion cell population. 2 3 The P system is preferentially activated by high spatial and low temporal frequencies, is involved in 90% of color processing, and typically has smaller receptive fields. 3 The pathway can be subdivided into type-I and -II P cells, the latter of the two being the more color responsive. In contrast, the magnocellular system represents approximately 10% of the ganglion cells, uniformly concentrated throughout the retina. 3 M cells respond preferentially to high temporal and low spatial frequencies in addition to having large receptive fields and conducting impulses at a quick rate. 2 4 Recent anatomic evidence suggests that another pathway, known as the koniocellular pathway (K cells), may play a role in color processing. This pathway may constitute 8% to 10% of the cell population and is believed to be involved in processing information from the short-wavelength–sensitive cones (S cones). 5 6  
There is significant evidence to show that the M pathway is affected early in the glaucomatous process. 7 8 For example, an attenuation of both the pattern electroretinogram, 9 (using stimuli that preferentially isolate high temporal frequencies), and low-contrast visual-evoked potentials, 10 has been identified in the disorder and attributed to M-cell loss. A decrease in low spatial frequency contrast sensitivity, 11 an increase of peripheral displacement thresholds, 12 diffuse flicker sensitivity, 13 and temporal modulation of visual field losses 14 15 in glaucomatous eyes are further indicators of M-pathway degeneration. 
Recent evidence has demonstrated that glaucoma-related loss may not be specific to the M-cell system, 16 17 18 and we should therefore also observe some color deficits. It is generally accepted that color processing is also affected by glaucoma. Support for this notion is provided by studies showing that color-processing mechanisms are impaired in glaucomatous eyes, particularly in the blue, blue-yellow and blue-green parts of the visible spectrum. 19 A decrease in blue-light (short-wavelength) sensitivity has been detected in many individuals with the disease. 20 Losses in high-pass resolution perimetry 21 and a decline in blue-on-yellow perimetry 22 23 further suggest the degeneration of type-I P cells, type-II P cells, and K cells. 
The minimum-motion and motion-nulling paradigms, 24 requiring a judgment of isoluminance and chromatic motion, respectively, have been used successfully in several studies to evaluate color processing in normal observers. It has, for example, allowed investigators to assess the impact of red/green (R/G) chromatic gratings on motion perception in healthy individuals 25 26 and in normal aging. 27 These techniques have the potential of determining the anatomic location of the chromatic deficits brought on by the disorder. More specifically, a change in the judgment in minimum motion (isoluminance) would indicate that impaired color vision stems from an ocular (optical or cellular) deficiency, whereas an alteration in motion nulling (chromatic motion perception) would demonstrate that a given disease process affects the postretinal constituents of the visual system. 27 Given the recent suggestion that there may be postretinal damage in glaucoma, 28 29 it is important to assess such functions in patients with glaucoma. 
Optical density of the intraocular lens increases in a linear fashion throughout life. 30 31 This inevitably results in reduced retinal illuminance at short wavelengths and, to a lesser extent, at longer wavelengths. Several reports have shown reduced color processing as a function of age. 32 33 34 In a recent study of color processing with the minimum-motion and motion-nulling paradigms, we have demonstrated that most of the age-related color processing changes are attributable to lens factors. 27 In that study, older pseudophakic observers had similar minimum-motion responses to younger subjects and a lens opacity model of the data successfully predicted the age-related changes in performance in the phakic observers. 
The main objectives of the present study were to verify whether minimum-motion and motion-nulling processes are altered by aging and glaucoma and to determine whether the deficits possibly identified in color vision are due to ocular and/or postretinal factors. To that effect, we evaluated chromatic processing mechanisms using the minimum-motion and motion-nulling paradigms in both normal individuals and glaucomatous observers of various ages. Both groups included phakic and pseudophakic subjects to account for the influence of lenticular aging on light absorption. 
Materials and Methods
Subjects
A total of 98 individuals with glaucoma (between the ages of 49 and 93 years; mean age, 70.8 ± 9.4 [SD]) and 67 normal observers (between the ages of 49 and 88 years; mean age, 70.6 ± 10.6) were tested. Of these, 60 glaucomatous (mean age, 68.7 ± 8.9) and 32 normal (mean age, 69.8 ± 10.6) observers were phakic, whereas 38 subjects with glaucoma (mean age, 74 ± 9.4 years) and 35 normal (mean age, 71.4 ± 10.6) subjects were pseudophakic. In each subject, the best corrected visual acuity was 20/40 or better in the eye that was to be tested. Control participants were free of ocular disease. Individuals with congenital color defects were excluded from the study through preexperimental color screening using Farnsworth D-15 saturated color plates. No ocular diseases other than glaucoma were present in participants with the disorder. An individual was considered to have glaucoma when he or she displayed increased intraocular pressure and visual field defects and was undergoing the prescribed treatment. The diagnosis was made by the examining ophthalmologist at the time of the patient’s most recent visit. Each subject had undergone a recent, complete ophthalmic examination before being tested. Individuals with various degrees of glaucoma were included. Patients with moderate to severe visual field defects were also enrolled in the study, provided that they met the minimal visual acuity requirement for testing (20/40 or better in the test eye). To determine whether subjects in the more advanced stages of glaucoma perform differently from those with milder disease, some severely affected individuals were also included in the test group. The cutoff point used for the inclusion of these subjects was a pattern standard deviation (PSD) of ≥7.00 in their most recent visual field examination (Humphrey perimeter; Carl Zeiss Meditec, Dublin, CA). All pseudophakes had the same lens implanted (model LX10BD; Alcon, Fort Worth, TX). 
Apparatus
A standard 19-in. monitor (PT 813; ViewSonic Corp., Walnut, CA) interfaced with a computer (Power Macintosh 7300/200; Apple Computer, Cupertino, CA) was used to present the visual stimuli. The general calibration procedures that were used have been described. 35 The spectral characteristics of the phosphors (light-emitting substances) of the computer screen have been specified by Faubert. 36 37 Luminance and chromaticity measurements were obtained with a chromometer (CS-100; Minolta, Osaka, Japan). 
Stimuli
The stimuli used for the red-green (R/G) minimum-motion (isoluminance task) described later consisted of a light-red/dark-green sinusoidal grating superimposed on a dark-red/light-green grating of a similar type. 24 38 These R/G gratings were counterphased, differing by 90° in their spatial and temporal characteristics 25 26 (0.5 cyc/deg and 2 Hz, respectively). They were presented through a circular aperture, subtending a visual angle 4° in diameter. A black/white random-dot pattern with a mean luminance of 19 cd/m2 served as the stimulus background. A black target was further used for central fixation and to facilitate fixation. The maximum luminance levels available for the R and G stimulus components were 19.0 and 57.5 cd/m2, respectively. The guns of the monitor had CIE u′v′ coordinates of 0.413 and 0.524 for the red gun and 0.124 and 0.556 for the green. 
The luminance modulation of the R/G stimulus can thus be represented as  
\[R(x,t)\ {=}\ 0.5\ {\cdot}\ L_{\mathrm{R}}\ {\cdot}\ \left\{{[}1\ {+}\ m\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x)\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{T}}t){]}\ {+}\ {[}1\ {+}\ \mathrm{cos}(2{\pi}f_{\mathrm{S}}x)\ {\cdot}\ \mathrm{cos}(2{\pi}f_{\mathrm{T}}t){]}\right\},\]
 
\[G(x,t)\ {=}\ 0.5\ {\cdot}\ L_{\mathrm{G}}\ {\cdot}\ \left\{{[}1\ {+}\ m\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x)\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{T}}t){]}\ {+}\ {[}1\ {-}\ \mathrm{cos}(2{\pi}f_{\mathrm{S}}x)\ {\cdot}\ \mathrm{cos}(2{\pi}f_{\mathrm{T}}t){]}\right\},\]
 
where R(x,t) and G(x,t) are the luminances of the monitor’s red and green phosphors as a function of horizontal position (x) and time (t), L R and L G are the mean luminances of the red and green phosphor respectively, f S and f T are the spatial and the temporal frequencies of the gratings respectively, and m is the Michelson contrast of an achromatic grating. The luminance contrast of the achromatic grating was 10% Michelson contrast. 
A subjective impression of motion was achieved when viewing the superimposed R/G gratings. If the R luminance was greater than the G, the subjects had an impression that the bars composing the gratings were moving in a rightward direction. If the G luminance was higher than the R, leftward motion was perceived. When the luminance components of the color gratings were equal, a flicker was seen (no movement was perceived). The luminance of the R component was kept constant, while the experimenter adjusted that of the G component until the subject saw flicker. 
The stimuli used for the motion-nulling task (color motion) described later consisted of a slight variation of the aforementioned R/G gratings. These remained spatially counterphased but were temporally in phase. The chromatic contrast of the R and G was preset at 60% of the screen phosphors’ maximum value. The isoluminant R/G grating drifting toward the right was presented, superimposed on a bright-yellow/dark-yellow achromatic grating drifting in the opposite direction. The isoluminance used was adjusted for each observer, as determined from the previous minimum-motion measures. Both gratings had a spatial frequency of 0.5 cyc/deg and drifted at a velocity of 4° per second (temporal frequency of 2 Hz). The contrast of the isoluminant R/G grating remained constant, while the luminance contrast of the achromatic grating was adjusted. 
The luminance modulation of the red and green phosphors for this task can be represented as  
\[R(x,t)\ {=}\ R_{\mathrm{max}}\ {\cdot}\ \left\{1\ {+}\ \left[\frac{m\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x\ {-}\ 2{\pi}f_{\mathrm{T}}t)\ {+}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x\ {-}\ 2{\pi}f_{\mathrm{T}}t)}{1\ {+}\ m}\right]\right\},\]
 
\[G(x,t)\ {=}\ G_{\mathrm{max}}\ {\cdot}\ \left\{1\ {+}\ \left[\frac{m\ {\cdot}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x\ {-}\ 2{\pi}f_{\mathrm{T}}t)\ {-}\ \mathrm{sin}(2{\pi}f_{\mathrm{S}}x\ {+}\ 2{\pi}f_{\mathrm{T}}t)}{1\ {+}\ m}\right]\right\},\]
 
where R MAX is the maximum luminance of the red phosphor and G MAX is the maximum luminance of the green phosphor. Similar to the minimum-motion technique, depending on the contrast of the achromatic grating, observers perceive motion in the direction of the color grating, the achromatic grating, or counterphase flicker (see Refs. 27 , 39 for greater detail). 
Experimental Procedure
The general procedures used in the present investigation have been described elsewhere. 26 27 Observers were tested in accordance with the Declaration of Helsinki for research involving human subjects. Briefly, the observer was positioned 57 cm from the display monitor with the subject’s correction for that distance in place. Testing was monocular. 
For the R/G minimum-motion task, the observer verbally expressed the direction of the grating with a “left,” “right,” or “no-direction” response, and the experimenter adjusted accordingly (method of adjustment). Having the experimenter perform the adjustments instead of the observer has the added benefit of ensuring the validity of measurements from these inexperienced psychophysical observers, who could have been responding to perceived flicker resulting from nonisoluminant stimuli (for an explanation, see Ref. 40 ). The experimenter did not see the monitor that observers viewed during testing. The color luminance contrast of the chromatic grating (C) was recorded at the end of each trial, when observers indicated that they saw no net direction of motion. This value was obtained by  
\[C\ {=}\ (R_{\mathrm{MOD}}\ {-}\ G_{\mathrm{MOD}})/(L_{\mathrm{R}}\ {+}\ L_{\mathrm{G}}),\]
 
where R MOD is the amplitude of luminance modulation of the red phosphor and G MOD, of the green phosphor. Five measurements were taken for each testing condition. 
Immediately after the minimum-motion task was completed, motion nulling was performed in an attempt to evaluate the L-M postretinal chromatic mechanisms. The experimenter adjusted the luminance contrast of an achromatic grating depending on the observer’s perceived direction of motion. The Michelson contrast of the achromatic grating was recorded at the end of each trial. The Michelson contrast of a luminance grating which nulls the motion of a chromatic grating is considered to be the chromatic grating’s equivalent luminance contrast. As in the minimum-motion procedure, five measurements were taken. If selective losses to postretinal chromatic mechanisms occur, then the luminance contrast necessary to null the motion of an isoluminant chromatic grating should decrease as a function of age or disease. This would indicate a selective loss in contrast sensitivity to chromatic stimuli relative to achromatic stimuli. 
Statistical Analysis
Analyses of variance (ANOVAs) were performed to compare group mean values for the different study parameters. An initial two (glaucoma versus normal) by two (phakic versus pseudophakic) by four (age category) ANOVA was performed. The age range and descriptive statistics of the main groups (glaucoma versus normal and phakic versus pseudophakic) are given in the subject section. The four age categories used for the ANOVAs were (1) 49 to 59, (2) 60 to 69, (3) 70 to 79, and (4) 80+ years and the breakdown for the four age categories for the normal observers was phakic normal: (1) range, 49 to 59 years; n = 6; mean age, 55.2 ± 3.9; (2) range, 61 to 69 years; n = 10; mean age, 64.3 ± 3.9; (3) range, 70 to 78 years; n = 8; mean age, 73.6 ± 2.9; and (4) range, 80 to 88 years; n = 8; mean age, 83.6 ± 3.0; and pseudophakic normal: (1) range, 49 to 58 years; n = 5; mean age, 54.2 ± 4.0; (2) range, 60 to 68 years; n = 10; mean age, 64.2 ± 4.1; (3) range, 71 to 77 years; n = 10; mean age, 75.2 ± 2.0, and (4) range, 80 to 88 years; n = 10; mean age, 83.4 ± 3.3. 
For the glaucomatous observers the breakdown was phakic glaucomatous: (1) range, 49 to 59 years; n = 11; mean age, 54.4 ± 3.4; (2) range, 60 to 69 years; n = 16; mean age, 65.1 ± 3.0; (3) range, 70 to 79 years; n = 27; mean age, 73.9 ± 2.7; (4) range, 80 to 84; n = 6; mean age, 81.7 ± 1.4; and pseudophakic glaucomatous: (1) range, 50 to 58 years; n = 3; mean age, 54.3 ± 4.0; (2) range, 63 to 68 years; n = 8; mean age, 65.1 ± 1.7; (3) range, 70 to 79 years; n = 17; mean age, 75.6 ± 3.3; and (4) range, 80 to 93 years; n = 10; mean age, 84.4 ± 4.1. 
Results
R/G Minimum Motion
The ANOVA on minimum motion shows a significant main effect of lens (phakic versus pseudophakic) (F(1,149) = 27.398, P = 0.017). The simple main effects of group (F(1,149) = 4.721, P = 0.487) and age (F(3,149) = 2.864, P = 0.272) categories were not significant. Furthermore, the age by group (F(3,149) = 0.202, P = 0.889) age by lens (F(3,149) = 4.663, P = 0.119) group by lens (F(1,149) = 1.807, P = 0.240) and age by group by lens (F(3,149) = 0.335, P = 0.800) interactions were not significant. 
Average values of R/G minimum motion were plotted as a function of age for the glaucoma and normal groups in Figures 1A and 1B , for phakic and pseudophakic individuals, respectively. As can be seen in Figure 1A , independent of the disorder, phakic observers demonstrated a loss of sensitivity to green light during the aging process. To test this effect, a separate 2 (group) by 4 (age) ANOVA was performed only on the phakic observers. The results of this ANOVA show a significant main effect of group (F(1,84) = 8.270, P = 0.045) and age (F(3,84) = 15.107, P = 0.026) but no significant group by age interaction (F(3,84) = 0.315, P = 0.815). Figures 2A and 2B show the individual data as a function of age for the phakic and pseudophakic observers, respectively. Several regression models were assessed, and the best fit of the individual data points was represented by a linear function. The best-fit regression line is plotted for the phakic observers, and one can observe the slight but steady change of the slope as a function of age for both normal and glaucomatous observers. In other words, with increasing age, both subjects with normal eyes and those with glaucoma must have more green to achieve perceptual R/G isoluminance. 
Motion Nulling
The ANOVA on motion nulling shows no significant effects with any condition. In fact, all the F values were below 1 except for the simple main effect of age (F(3,149) = 2.327, P = 0.532) and the age by lens interaction term (F(3,149) = 1.785, P = 0.323). This lack of effect can be seen in Figures 3A and 3B where motion-nulling values are plotted as a function of age category for normal and glaucomatous observers. Figures 4A and 4B show the individual data and indicate that the lack of effect is not an artifact of averaging the data as a function of category. 
The performance of glaucomatous observers in the visual tasks used in this study did not vary according to disease severity. More precisely, the average measurements of minimum motion and motion nulling obtained in subjects in the more advanced stages of the illness were well within the group mean values. 
Discussion
Our findings indicate that both healthy and glaucomatous subjects who were phakic and of advanced age showed different motion-nulling values than their younger counterparts, requiring a greater level of green light to perceive the gratings flickering in counterphase. These results suggest that the normal aging process is accompanied by a decline in green-light sensitivity. Although the glaucomatous observers displayed this particular chromatic change with increasing years, the disease itself did not appear to contribute to the loss of sensitivity to middle- and long-wavelength stimuli with advancing age. Evidence for this notion is provided by the current findings, which demonstrated that the isoluminances of phakic individuals with glaucoma did not differ significantly from those of healthy control subjects. 
Studies have implicated optical factors (i.e., crystalline lens opacity) in several age-induced changes in chromatic vision. 27 30 41 If an increase in the optical density of the lens is the main candidate responsible for age-dependent alterations of color perception, the differences in the R/G isoluminances in subjects of various ages should disappear when one controls for this factor (see Nguyen-Tri et al. 27 for a model on the impact of lenticular senescence on this task). This was, in fact, the case in the present study. Specifically, the phakic elderly (glaucomatous and healthy) observers evaluated herein displayed a decrease in green-light sensitivity relative to younger phakic subjects, but the elderly individuals with artificial lenses did not. The latter participants responded instead in a manner similar to that of younger pseudophakes. It appears therefore that lenticular aging can account for the age-related anomaly detected in phakic observers on the minimum-motion task. In other words, the observed diminution in green-light absorption is related to the yellowing of the crystalline lens that occurs during the course of normal aging. On the basis of these findings, we can argue that the actual processing of R/G information within the eye remains relatively intact with age and in glaucoma. That is, the photoreceptors and P-ganglion cells of the retina that respond to the middle wavelengths of the spectrum appear to be resistant to the effects of both age and the disease process. 
The data obtained in the present study further show that normal and glaucomatous subjects of different ages displayed a similar ability to null motion in the motion-nulling task. There seems therefore to be no significant detriment in chromatic motion perception during the aging process, independent of glaucoma. This finding held true regardless of whether individuals were phakic or pseudophakic, indicating that media opacity in the form of aging lens changes has no effect on motion nulling, when it is controlled by isoluminance. These results suggest that the cortical elements that respond to chromatic motion stimuli are resistant to age- and glaucoma-induced damage. 
It is important to note that first-order stimuli (defined by luminance or color) were used in the present study. Simple processing mechanisms are believed to underlie the perception of such visual stimuli. By contrast, the cortical analysis of complex or second-order stimuli is thought to involve a greater number of processing steps and neuronal interactions. 42 Some investigators 43 have shown a greater loss in second-order motion compared with first-order stimuli in a normal aging population. This implies possible damage to higher cortical areas thought to process more complex stimuli. In glaucoma, we assume that the damage is primarily at the level of the retinal ganglion cells. However, recent evidence demonstrates that neurons both at the lateral geniculate nucleus and cortical V1 levels can be affected by glaucoma. 18 29 The fact that we found no evidence of selective R/G chromatic motion processing relative to luminance processing in normal aging and glaucomatous individuals is further evidence that first-order mechanisms are relatively spared by aging. 42  
Although the data obtained in the present investigation show that long- and middle-wavelength–sensitive P cells are resistant to degenerative changes, it would be false to assume that the P system is entirely immune to the ravaging effects of glaucoma or aging. A decline in high-pass resolution perimetry 21 has been noted in afflicted patients. These clinical abnormalities are indicative of P-cell degeneration. Disease-induced alterations in the processing of blue, blue-yellow, and blue-green wavelength stimuli have also been documented. 19 Consistent with this view, previous reports have demonstrated a selective decline in the sensitivity to short- as opposed to longer-wavelength stimuli in patients with glaucoma 20 as well as during the course of normal aging 44 which would be indicative of K-cell loss. The selective effects of aging and glaucoma on short-wavelength information, however, may be the result of a lack of redundancy in the cells that process this type of information. It may be that both the large M cells responsible to high temporal information and the ganglion cells responsible for processing information from the S cones carry relatively greater weight for visual processing, as they are far fewer in number than cells that process R/G information. As a consequence, they would be more susceptible to disease processes. Another possibility has to do with the anatomic structure of these cell types. Both M cells and S-cone–sensitive ganglion cells have much larger receptive fields and therefore must integrate input from receptor cells over a larger retinal area. It is possible that the mechanisms responsible for integrating neural information from larger retinal areas are more susceptible to early aging and glaucomatous damage. Similar arguments have been used to explain the possible underlying age-related cortical changes that affect visual perception. 42  
 
Figure 1.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, SEM.
Figure 1.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, SEM.
Figure 2.
 
(A) Individual minimum-motion values plotted as a function of age in both normal and glaucomatous phakic observers. (B) Individual minimum-motion values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 2.
 
(A) Individual minimum-motion values plotted as a function of age in both normal and glaucomatous phakic observers. (B) Individual minimum-motion values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 3.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, 1 SEM.
Figure 3.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, 1 SEM.
Figure 4.
 
(A) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous phakic observers. (B) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 4.
 
(A) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous phakic observers. (B) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Lewis TL, Fingeret M. Primary Care of the Glaucomas. 1993; Appleton & Lange Norwalk, CT.
Merigan WH, Katz LM, Maunsell JH. The effects of parvocellular lateral geniculate lesions on the acuity and contrast sensitivity of macaque monkeys. J Neurosci. 1991;11:994–1001. [PubMed]
Livingstone M, Hubel D. Segregation of form, color, movement, and depth: anatomy, physiology, and perception. Science. 1988;240:740–749. [CrossRef] [PubMed]
Merigan WH. P and M pathway specialization in the macaque. Valberg A Lee BB eds. Pigments to Perception. 1991;117–125. Plenum Press New York.
Dacey DM, Petersen MR. Dendritic field size and morphology of midget and parasol ganglion cells of the human retina. Proc Natl Acad Sci USA. 1992;89:9666–9670. [CrossRef] [PubMed]
Dacey DM. Morphology of a small-field bistratified ganglion cell type in the macaque and human retina. Vis Neurosci. 1993;10:1081–1098. [CrossRef] [PubMed]
Quigley HA, Green WR. The histology of human glaucoma cupping and optic nerve damage: clinicopathologic correlation in 21 eyes. Ophthalmology. 1979;86:1803–1830. [CrossRef] [PubMed]
Quigley HA, Dunkelberger GR, Green WR. Retinal ganglion cell atrophy correlated with automated perimetry in human eyes with glaucoma. Am J Ophthalmol. 1989;107:453–464. [CrossRef] [PubMed]
Bielik M, Zwas F, Shin DH, Tsai CS. PERG and spectral sensitivity in ocular hypertensive and chronic open-angle glaucoma patients. Graefes Arch Clin Exp Ophthalmol. 1991;229:401–405. [CrossRef] [PubMed]
Klistorner AI, Graham SL. Early magnocellular loss in glaucoma demonstrated using the pseudorandomly stimulated flash visual evoked potential. J Glaucoma. 1999;8:140–148. [PubMed]
Velten IM, Korth M, Horn FK, Budde WM. Temporal contrast sensitivity with peripheral and central stimulation in glaucoma diagnosis. Br J Ophthalmol. 1999;83:199–205. [CrossRef] [PubMed]
Westcott MC, Fitzke FW, Crabb DP, Hitchings RA. Characteristics of frequency-of-seeing curves for a motion stimulus in glaucoma eyes, glaucoma suspect eyes, and normal eyes. Vision Res. 1999;39:631–639. [CrossRef] [PubMed]
Tyler CW. Specific deficits of flicker sensitivity in glaucoma and ocular hypertension. Invest Ophthalmol Vis Sci. 1981;20:204–212. [PubMed]
Faubert J, Balazsi GA, Brussell EM, Overbury O. Multi-flash campimetry and other psychophysical tests in glaucoma. Doc Ophthalmol. 1987;49:425–432.
Casson EJ, Johnson CA, Nelson-Quigg JM. Temporal modulation perimetry: the effects of aging and eccentricity on sensitivity in normals. Invest Ophthalmol Vis Sci. 1993;34:3096–3102. [PubMed]
Morgan JE, Uchida H, Caprioli J. Retinal ganglion cell death in experimental glaucoma. Br J Ophthalmol. 2000;84:303–310. [CrossRef] [PubMed]
Morgan JE. Retinal ganglion cell shrinkage in glaucoma. J Glaucoma. 2002;11:365–370. [CrossRef] [PubMed]
Yucel YH, Zhang Q, Gupta N, Kaufman PL, Weinreb RN. Loss of neurons in magnocellular and parvocellular layers of the lateral geniculate nucleus in glaucoma. Arch Ophthalmol. 2000;118:378–384. [CrossRef] [PubMed]
Adams AJ, Heron G, Husted R. Clinical measures of central vision function in glaucoma and ocular hypertension. Arch Ophthalmol. 1987;105:782–787. [CrossRef] [PubMed]
Glovinsky Y, Quigley HA, Dunkelberger GR. Retinal ganglion cell loss is size dependent in experimental glaucoma. Invest Ophthalmol Vis Sci. 1991;32:484–491. [PubMed]
Chauhan BC, House PH, McCormick TA, LeBlanc RP. Comparison of conventional and high-pass resolution perimetry in a prospective study of patients with glaucoma and healthy controls. Arch Ophthalmol. 1999;117:24–33. [CrossRef] [PubMed]
Johnson CA, Adams AJ, Casson EJ, Brandt JD. Blue-on-yellow perimetry can predict the development of glaucomatous visual field loss. Arch Ophthalmol. 1993;111:645–650. [CrossRef] [PubMed]
Johnson CA, Adams AJ, Casson EJ, Brandt JD. Progression of early glaucomatous visual field loss as detected by blue-on-yellow and standard white-on-white automated perimetry. Arch Ophthalmol. 1993;111:651–656. [CrossRef] [PubMed]
Anstis SM, Cavanagh P. A minimum motion technique for judging equiluminance. Mollon JD Sharpe LT eds. Color Vision: Physiology and Psychophysics. 1983;155–166. Academic Press London.
Bilodeau L, Faubert J. Isoluminance and chromatic motion perception throughout the visual field. Vision Res. 1997;37:2073–2081. [CrossRef] [PubMed]
Bilodeau L, Faubert J. The oblique effect with colour defined motion throughout the visual field. Vision Res. 1999;39:757–763. [CrossRef] [PubMed]
Nguyen-Tri D, Overbury O, Faubert J. The role of lenticular senescence in age-related color vision changes. Invest Ophthalmol Vis Sci. 2003;44:3698–3704. [CrossRef] [PubMed]
Gupta N, Yucel YH. Brain changes in glaucoma. Eur J Ophthalmol. 2003;13:S32–S35. [PubMed]
Yucel YH, Zhang Q, Weinreb RN, Kaufman PL, Gupta N. Effects of retinal ganglion cell loss on magno-, parvo-, koniocellular pathways in the lateral geniculate nucleus and visual cortex in glaucoma. Prog Retin Eye Res. 2003;22:465–481. [CrossRef] [PubMed]
Weale RA. Age and the transmittance of the human crystalline lens. J Physiol. 1988;395:577–587. [CrossRef] [PubMed]
Werner JS. Development of scotopic sensitivity and the absorption spectrum of the human ocular media. J Opt Soc Am. 1982;72:247–258. [CrossRef] [PubMed]
Mantyjarvi M. Normal test scores in the Farnsworth-Munsell 100 hue test. Doc Ophthalmol. 2001;102:73–80. [CrossRef] [PubMed]
Shinomori K, Schefrin BE, Werner JS. Age-related changes in wavelength discrimination. J Opt Soc Am A Opt Image Sci Vis. 2001;18:310–318. [CrossRef] [PubMed]
Swanson WH, Fish GE. Age-related changes in the color-match-area effect. Vision Res. 1996;36:2079–2085. [CrossRef] [PubMed]
Faubert J. Effect of target size, temporal frequency and luminance on temporal modulation visual fields. Mills RP Heijl A eds. Perimetry Update 1990/91. 1991;381–390. Kugler New York.
Faubert J. Seeing depth in colour: more than just what meets the eyes. Vision Res. 1994;34:1165–1186. [CrossRef] [PubMed]
Faubert J. Colour induced stereopsis in images with achromatic information and only one other colour. Vision Res. 1995;35:3161–167. [CrossRef] [PubMed]
Cavanagh P. Contribution of color to motion. Valberg A Lee BB eds. From Pigments to Perception: Advances in Understanding Visual Processes. 1991;151–164. Plenum Press New York.
Cavanagh P, Anstis S. The contribution of color to motion in normal and color-deficient observers. Vision Res. 1991;31:2109–2148. [CrossRef] [PubMed]
Cavanagh P, MacLeod DI, Anstis SM. Equiluminance: spatial and temporal factors and the contribution of blue-sensitive cones. J Opt Soc Am A. 1987;4:1428–1438. [CrossRef] [PubMed]
Weale RA. The lenticular nucleus, light, and the retina. Exp Eye Res. 1991;53:213–218. [CrossRef] [PubMed]
Faubert J. Visual perception and aging. Can J Exp Psychol. 2002;56:164–176. [CrossRef] [PubMed]
Habak C, Faubert J. Larger effect of aging on the perception of higher-order stimuli. Vision Res. 2000;40:943–950. [CrossRef] [PubMed]
Johnson CA, Adams AJ, Twelker JD, Quigg JM. Age-related changes in the central visual field for short-wavelength-sensitive pathways. J Opt Soc Am A. 1988;5:2131–2139. [CrossRef] [PubMed]
Figure 1.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, SEM.
Figure 1.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, SEM.
Figure 2.
 
(A) Individual minimum-motion values plotted as a function of age in both normal and glaucomatous phakic observers. (B) Individual minimum-motion values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 2.
 
(A) Individual minimum-motion values plotted as a function of age in both normal and glaucomatous phakic observers. (B) Individual minimum-motion values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 3.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, 1 SEM.
Figure 3.
 
(A) Minimum-motion values plotted as a function of age category (50–59 years, n = 17; 60–69 years, n = 26; 70–79 years, n = 35; 80+ years, n = 14) for both normal and glaucomatous phakic observers. (B) Minimum-motion values plotted as a function of age category (50–59 years, n = 8; 60–69 years, n = 18; 70–79 years, n = 27; 80+ years, n = 20) for both normal and glaucomatous pseudophakic observers. Error bars, 1 SEM.
Figure 4.
 
(A) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous phakic observers. (B) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
Figure 4.
 
(A) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous phakic observers. (B) Individual motion-nulling values plotted as a function of age for both normal and glaucomatous pseudophakic observers.
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