Biomedical subjects

Ronald S Harwerth

Publications and source records attributed to Ronald S Harwerth.

17 recordsLinked to original sources

PubMed2006

Visual field defects and retinal ganglion cell losses in patients with glaucoma.

OBJECTIVE: To determine whether the structure-function relationships for glaucoma in humans and experimental glaucoma in monkeys are similar. METHODS: The study was based on retinal ganglion cell density and visual thresholds in patients with documented glaucoma. Data were analyzed with a model that predicted ganglion cell density from standard clinical perimetry, which was then compared with histologic cell counts. RESULTS: The model, without free parameters, produced accurate and relatively precise quantification of ganglion cell density associated with visual field defects. For 437 sets of data, the unity correlation for predicted vs measured cell density had a coefficient of determination of 0.39. The mean absolute deviation of the predicted vs measured values was 2.59 decibels (dB), and the mean +/- SD of the distribution of residual errors of prediction was -0.26 +/- 3.22 dB. CONCLUSIONS: Visual field defects based on standard clinical perimetry are proportional to neural losses caused by glaucoma. CLINICAL RELEVANCE: The evidence for quantitative structure-function relationships provides a scientific basis for interpreting glaucomatous neuropathy from visual thresholds and supports the application of standard perimetry to establish the stage of the disease.

Aged↗

PubMed2006

Brief daily periods of unrestricted vision can prevent form-deprivation amblyopia.

PURPOSE: To characterize how the mechanisms that produce unilateral form-deprivation amblyopia integrate the effects of normal and abnormal vision over time, the effects of brief daily periods of unrestricted vision on the spatial vision losses produced by monocular form deprivation were investigated in infant monkeys. METHODS: Beginning at 3 weeks of age, unilateral form deprivation was initiated in 18 infant monkeys by securing a diffuser spectacle lens in front of one eye and a clear plano lens in front of the fellow eye. During the treatment period (18 weeks), three infants wore the diffusers continuously. For the other experimental infants, the diffusers were removed daily and replaced with clear, zero-powered lenses for 1 (n=5), 2 (n=6), or 4 (n=4) hours. Four infants reared with binocular zero-powered lenses and four normally reared monkeys provided control data. RESULTS: The degree of amblyopia varied significantly with the daily duration of unrestricted vision. Continuous form deprivation caused severe amblyopia. However, 1 hour of unrestricted vision reduced the degree of amblyopia by 65%, 2 hours reduced the deficits by 90%, and 4 hours preserved near-normal spatial contrast sensitivity. CONCLUSIONS: The severely amblyogenic effects of form deprivation in infant primates are substantially reduced by relatively short daily periods of unrestricted vision. The manner in which the mechanisms responsible for amblyopia integrate the effects of normal and abnormal vision over time promotes normal visual development and has important implications for the management of human infants with conditions that potentially cause amblyopia.

Amblyopia↗

PubMed2006

Effect of experimental glaucoma in primates on oscillatory potentials of the slow-sequence mfERG.

PURPOSE: To determine the effect of experimental glaucoma in macaque monkeys on oscillatory potentials (OPs) in the slow-sequence multifocal electroretinogram (mfERG). METHODS: Photopic slow-sequence mfERGs were recorded from anesthetized adult macaque monkeys and normal human subjects. The stimulus consisted of 103 equal-sized hexagons within 17 degrees of the fovea. The m-sequence was slowed, with 14 blank frames, approximately 200 ms, interleaved between flashes for monkeys and 7 blank frames, approximately 100 ms, for humans, to produce waveforms similar to the photopic full-field flash ERG. Recordings were made under control conditions (24 monkey eyes, 7 human) and after laser-induced experimental glaucoma in monkeys (n = 8). A Fourier fast transform [FFT] was used to determine the frequency ranges of the major OPs. OP amplitudes were quantified by using root mean square (RMS) for two-frequency bands in five horizontal and four vertical locations. Visual field defects were assessed using behavioral static perimetry. Full-field photopic flash ERGs also were recorded. RESULTS: OPs in two distinct frequency bands were discriminated in the monkey mfERG: fast OPs, with a peak frequency of 143 +/- 20 Hz, and slow OPs, with a peak at 77 +/- 8 Hz. There were similar findings in humans and with the flash ERG in monkeys. The fast OP RMS in monkey control eyes was significantly larger in temporal than nasal retina (P < 0.01) and in superior versus inferior retina (P < 0.05) as reported previously. The slow OP RMS was largest in the foveal region. Experimental glaucoma reduced fast OP RMS in all locations studied, even when visual field defects were moderate (MD = -5 to -10 dB; P < 0.05), whereas the slow OP RMS was reduced significantly primarily in the foveal region when field defects were severe (MD < -10 dB; P < 0.05). The fast OP RMS showed a moderate correlation with local visual field sensitivity and with local ganglion cell density (calculated from visual field sensitivity). For the slow OPs the correlation was much poorer. Consistent with previous studies, the photopic negative response (PhNR) amplitude was significantly reduced when the visual sensitivity was minimally affected. CONCLUSIONS: OPs in the ERG of primates fall in two frequency bands: fast OPs with a peak frequency around 143 Hz and slow OPs, with a peak frequency around 77 Hz. The fast OPs, which rely more on the integrity of retinal ganglion cells and their axons than do the slow OPs, have potential utility for monitoring the progression of glaucoma and the effects of treatment.

Animals↗

PubMed2005

Scaling the structure--function relationship for clinical perimetry.

PURPOSE: The full ranges of glaucomatous visual field defects and retinal ganglion cell losses extend over several orders of magnitude and therefore an interpretation of the structure-function relationship for clinical perimetry requires scaling of both variables. However, the most appropriate scale has not been determined. The present study was undertaken to compare linear and logarithmic transformations, which have been proposed for correlating the perimetric defects and neural losses of glaucoma. METHODS: Perimetry, by behavioural testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma. Ganglion cell densities were measured in histologic sections of retina that corresponded to specific perimetry test locations for the treated and control eyes. The linear (percentage) and logarithmic (decibel) relationships for sensitivity loss as a function of ganglion cell loss were analysed. RESULTS: With decibel scaling, visual sensitivity losses and ganglion cell densities were linearly correlated with high coefficients of determination (r(2)), although the parameters of the functions varied with eccentricity. The structure-function relationships expressed as linear percentage-loss functions were less systematic in two respects. Firstly, the relationship exhibited considerable scatter in the data for small losses in visual sensitivity and, secondly, visual sensitivity losses became saturated with larger losses in ganglion cell density. The parameters of the percentage-loss functions also varied with eccentricity, but the variation was less than for the decibel-loss functions. CONCLUSIONS: Linear scaling of perimetric defects and ganglion cell losses might potentially improve the structure-function relationship for visual defects associated with small amounts of cell loss, but the usefulness of the relationship is limited because of the high variability in that range. With log--log co-ordinates, the structure--function relationship for clinical perimetry is relatively more accurate and precise for cell losses greater than about 3 dB. The comparatively greater accuracy and precision of decibel loss functions are a likely consequence of the logarithmic scale of stimulus intensities for perimetry measurements and because the relationship between visual sensitivity and the number of neural detectors is a form of probability summation.

Animals↗

PubMed2005

Directional bias of neurons in V1 and V2 of strabismic monkeys: temporal-to-nasal asymmetry?

PURPOSE: Strabismus that develops shortly after birth is known to cause temporal-to-nasal eye movement asymmetries under monocular viewing. The neural mechanisms underlying this deficit are not well understood. In the current study, the hypothesis that this eye movement anomaly reflects a similar asymmetry in the directional response properties of neurons in the early stages of cortical processing was examined. METHODS: Strabismus was simulated with optical methods in infant monkeys between 4 and 14 weeks of age. When the monkeys were mature, microelectrode recording experiments were conducted in the primary visual cortex (V1) and visual area 2 (V2). After the spatial frequency of sine wave-grating stimuli for each neuron was optimized, each neuron's responsiveness to 24 directions of stimulus movement was measured. The preferred direction and the strength of directional bias were determined by a vector summation method: RESULTS: There was not an overabundance of neurons in V1 or V2 of strabismic monkeys preferring the temporal-to-nasal direction of stimulus movement. However, the average directional bias was significantly reduced in these strabismic monkeys. Interocular suppression was highly prevalent, and this suppression was stronger and more common in neurons dominated by the ipsilateral eye. CONCLUSIONS: The results suggest that the eye movement asymmetries in strabismic subjects do not result from similar asymmetries in the directional properties of V1 or V2 neurons, but rather reflect impoverished cortical signals to the brain stem nuclei that control eye movements.

Animals↗

PubMed2004

Stereoscopic depth magnitude estimation: effects of stimulus spatial frequency and eccentricity.

To determine the effects of stimulus spatial frequency and retinal eccentricity on the perception of depth magnitude derived from disparity cues alone, subjects were asked to estimate the magnitude of depth of a stereoscopically viewed Gabor patch presented to the central or peripheral field with either crossed or uncrossed absolute disparity. Disparity vergence responses to the same Gabor stimuli were separately estimated subjectively by determining the offset required for dichoptic nonius alignment following presentation of the stimulus. The normalized stereoscopic magnitude estimation data generally showed that crossed disparities were perceived with greater depth than uncrossed disparities of the same magnitude, whether presented to the central or peripheral field. Asymmetries in magnitude of depth perception ranged from mild differences between depth directions to complete lack of depth perception for one direction. Disparity vergence response functions varied from (1) appropriate initiation of vergence to both directions of disparity, (2) initiation of vergence to only one direction of disparity, or (3) an attenuated initiation of vergence response to either direction of disparity. Within subjects, their asymmetries in magnitude of depth perception did not correlate with their asymmetries in vergence initiation. The similarity of the asymmetric depth magnitude estimation for a given individual at both stimulus locations tested suggests that common neural mechanisms are responsible for central and peripheral depth magnitude estimation. The lack of correlation between the perceptual and motor responses to the same stimuli suggests that the neural pathways for these responses diverge shortly after the detection of disparity in primary visual cortex.

Adult↗

PubMed2004

Glutathione content is altered in Müller cells of monkey eyes with experimental glaucoma.

Extracellular levels of glutamate are thought to be increased in glaucoma and thus contribute to retinal damage. An increase in glutamate concentration or duration in the extracellular retinal space is expected to impact glutathione content in Müller cells since glutamate is the rate-limiting constituent in glutathione synthesis. We have investigated whether glutathione content is changed in retinal Müller cells of monkeys with experimental glaucoma using immunocytochemistry and image analysis. Müller cells in glaucomatous retinas showed significantly greater immunoreactivity (27-57%) for glutathione than those in fellow control retinas, increasing with the duration of elevated intraocular pressure (IOP). This pattern of labeling was prominent in all four monkeys studied. The presence of more glutathione in Müller cells of glaucomatous retinas is consistent with an increase in extracellular glutamate and an increase in transport and metabolism of glutamate.

Animals↗

PubMed2004

Ocular dominance column width and contrast sensitivity in monkeys reared with strabismus or anisometropia.

PURPOSE: To study the relationship between the width of ocular dominance columns in primary visual cortex and spatial contrast sensitivity functions in monkeys with strabismus or anisometropia during infancy. METHODS: Adult monkeys having had monocular visual abnormalities induced in infancy were tested behaviorally for spatial contrast sensitivity and then subjected to functional enucleation of one eye to reveal the ocular dominance columns (ODCs) of the primary visual cortex by cytochrome oxidase (CO) staining. The relative widths of the left and right eyes' ODCs were measured and related to the contrast sensitivity functions. RESULTS: The relative widths of the ODCs having input from eyes with strabismic or anisometropic amblyopia were reduced in proportion to the age of onset and the duration of the early visual abnormality. The relative losses in contrast sensitivity were in ordinal agreement with the losses in relative width of the ODCs. CONCLUSIONS: Amblyopia induced by the early monocular abnormalities of strabismus or anisometropia is proportional to the loss in cortical afference as reflected in the reduction in width of the respective ODCs in the primary visual cortex.

Amblyopia↗

PubMed2004

Neural losses correlated with visual losses in clinical perimetry.

PURPOSE: The validity of clinical perimetry for evaluation of the pathology of glaucoma is based on correlated losses in retinal ganglion cells and visual sensitivity, but procedures to quantify neural losses from visual field defects have not been developed. The purpose of the present study was to investigate the neural and sensitivity losses from experimental glaucoma to establish the framework for a quantitative model for the structure-function relationships of standard clinical perimetry. METHODS: Perimetry, by behavioral testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma. Ganglion cell densities were obtained from sections of retina that corresponded to 16 perimetry test locations. Perimetry sensitivity as a function of ganglion cell density at corresponding retina/visual field locations was analyzed. RESULTS: The structure-function relationships were linear on log-log coordinates, with parameters that varied systematically with eccentricity. The slope value varied from 1.25 dB/dB at 4.2 degrees from fixation to a value of 2.32 dB/dB at 24 degrees from fixation, whereas the intercept value varied from -25.2 dB to -55.7 dB over the same range of eccentricities. The structure-function relationships produced a model to predict the ganglion cell density underlying a given level of visual sensitivity and location in the visual field. The model, with no free parameters, produced an accurate and relatively precise quantification of retinal ganglion cell losses caused by experimental glaucoma in monkeys. However, because the early detection of glaucoma is limited by intersubject variability, ganglion cell losses of 40% to 50% were necessary before visual sensitivity losses exceeded the normal 95% confidence limits. CONCLUSIONS: With retinal eccentricity as a factor, the neural losses from glaucoma are predictable from visual sensitivity measurements by clinical perimetry. The relationships derived from experimental glaucoma in monkeys also accurately predict the rate of age-related losses of retinal ganglion cells in humans, based on the normative perimetry data for age-related reductions in visual sensitivity. The success of the model in this study suggested that it is potentially applicable to the clinical interpretation of the state of glaucomatous optic neuropathy.

Animals↗

PubMed2003

Stereopsis is perturbed by vergence error.

Fixation disparity or vergence noise produce instantaneous vergence errors. These errors are analogous to the imposition of a pedestal disparity, which is known to elevate stereothresholds. In this study, stereothresholds were measured as a function of induced vergence errors in subjects with normal binocular vision. Stereo half-images were viewed in the dark through a custom mirror haploscope. Vergence constant error and vergence variability were induced by introducing horizontal disconjugate position offsets in a pair of moveable mirrors within the haploscope, resulting in forced vergence demands of 6(Delta) base-in to 12(Delta) base-out. In addition, vergence variability was simulated by producing oscillatory disconjugate retinal image motion via motion of the moveable mirrors. The motion of the mirrors was either sinusoidal (frequency=2-6 Hz) or random, with peak-to-peak amplitudes of 0 degrees -0.5 degrees per eye. Stereopsis worsened systematically with induced or simulated VV that exceeded approximately 1.5' disparity. The results were similar regardless of whether the vergence error was induced by forced vergence or was simulated by periodic or random disconjugate retinal image motion. Stereothresholds were invariant with the frequency of disconjugate oscillation, within the range of frequencies and amplitudes tested. Hence, the simulated vergence velocity is not the essential factor that limits stereopsis within Panum's fusional area. The results indicate that the stereothreshold is elevated if the vergence error exceeds a critical value.

Adult↗

PubMed2003

Stereothresholds with simulated vergence variability and constant error.

Stereothresholds are elevated by vergence constant error (fixation disparity), vergence noise, or both. This study investigated the separate and combined effects of simulated vergence constant error and variability on stereothresholds in four normal observers. Targets were 30 arc min bright vertical lines presented separately to the two eyes for 150 ms in darkness. Vergence constant error, simulated as a pedestal disparity, was induced by altering the screen positions of the stereo half-images relative to a previously visible binocular fixation point. Vergence variability was simulated simultaneously by disconjugate motion (amplitude=0-0.5 deg per eye; frequency=2 or 4 Hz) of a pair of scanning mirrors in a Wheatstone stereoscope that was used to present the images to each eye. Various combinations of pedestal disparity and simulated vergence variability produce equivalent stereothresholds whenever the calculated mean deviation (sigma/instantaneous vergence errors//N) of the stimulus from the fixation plane is the same. In particular, stereothresholds are optimal for mean deviations up to approximately 1.4 arc min and then increase according to a power function with an exponent of 0.61. The results imply that vergence constant errors and vergence variability impair stereothresholds because of the resulting mean deviation from the horopter.

Adult↗

PubMed2003

Temporal integration for stereoscopic vision.

With normal binocular vision, maximal stereoacuity requires an extended viewing duration, but the relationship between the critical viewing duration for stereopsis and other variables affecting stereoacuity is unknown. The purposes of the study were to investigate the properties of normal temporal integration for stereoscopic vision with respect to the effects of contrast and spatial frequency of the stimuli and to determine whether the temporal summation of disparity is affected in deficient stereopsis caused by abnormal binocular vision during infancy. Psychophysical methods were used to measure stereothresholds in human and monkey subjects with either normal binocular vision or abnormal binocular vision. The results showed that the critical viewing duration for stereoscopic depth discrimination was independent of variations in basic stimulus parameters and/or the subject's stereoacuity. A critical duration of approximately 100 ms was found for both local (narrowband Gabor and broadband line targets) and global (dynamic random dots) stimuli. Although stereothresholds increased with decreasing stimulus contrast, the properties of temporal integration did not. Stereothresholds were substantially elevated for monkeys and humans with abnormal binocular vision, but the critical durations for these subjects were not significantly different from those of subjects with normal binocular vision. Overall, the results demonstrate that the general properties of temporal integration for stereopsis are similar to other detection and discrimination tasks that do not require binocular processing. In addition, increased integration time does not account for the elevated stereothresholds of subjects with abnormal binocular vision.

Animals↗

PubMed2003

Binocular deficits associated with early alternating monocular defocus. II. Neurophysiological observations.

Experiencing binocularly conflicting signals early in life dramatically alters the binocular responses of cortical neurons. Because visual cortex is highly plastic during a critical period of development, cortical deficits resulting from early abnormal visual experience often mirror the nature of interocular decorrelation of neural signals from the two eyes. In the preceding paper, we demonstrated that monkeys that experienced early alternating monocular defocus (-1.5, -3.0, or -6.0 D) show deficits in stereopsis that generally reflected the magnitude of imposed monocular defocus. Because these results indicated that alternating monocular defocus affected the higher spatial frequency components of visual scenes more severely, we employed microelectrode recording methods to investigate whether V1 neurons in these lens-reared monkeys exhibited spatial-frequency-dependent alterations in their binocular response properties. We found that a neuron's sensitivity to interocular spatial phase disparity was reduced in the treated monkeys and that this reduction was generally more severe for units tuned to higher spatial frequencies. In the majority of the affected units, the disparity-sensitivity loss was associated with interocular differences in monocular receptive field properties. The present results suggest that the behavioral deficits in stereopsis produced by abnormal visual experience reflect at least in part the constraints imposed by alterations at the earliest stages of binocular cortical processing and support the hypothesis that the local disparity processing mechanisms in primates are spatially tuned and can be independently compromised by early abnormal visual experience.

Amblyopia↗

PubMed2003

Binocular deficits associated with early alternating monocular defocus. I. Behavioral observations.

To study the binocular vision deficits associated with anisometropia, monkeys were reared with alternating monocular defocus, which allowed monocular mechanisms to develop normally while binocular mechanisms were selectively compromised. A defocusing contact lens of -1.5 D, -3 D, or -6 D was worn on alternate eyes on successive days (n = 3 per lens power) from 3 wk to 9 mo of age. The control subjects were two normally reared monkeys and two human observers. Functional binocular vision was assessed through behavioral measurements of stereoscopic depth discrimination thresholds as a function of spatial frequency. To characterize the extent of the deficits in disparity processing at a given spatial frequency, the contrast required to support stereopsis was determined for a range of disparities that exceeded the subjects' measured stereoacuity. The lens-reared monkeys showed spatial-frequency-selective deficits in stereopsis that depended on the magnitude of the simulated anisometropia experienced during the rearing period. For a given spatial frequency, the treated monkeys generally required higher than normal contrasts to support stereopsis even for large disparities. Moreover, a given increase in contrast produced smaller than normal improvements in stereo discrimination in our treated subjects, which suggests that in addition to deficits in contrast sensitivity, disparity-sensitive mechanisms exhibited low contrast gains. The spatial-frequency selective nature of the binocular deficits produced by the imposed anisometropia indicate that disparity processing mechanisms are normally spatial-frequency selective and that mechanisms tuned to different spatial frequencies can be differentially affected by abnormal binocular visual experience.

Amblyopia↗

PubMed2003

Binocular vision with primary microstrabismus.

PURPOSE: Patients with primary microstrabismus have a high degree of binocularity, which suggests that their ocular misalignment may have a sensory rather than an oculomotor origin, as in large-angle strabismus. The purpose of these experiments was to determine whether microstrabismic subjects have sensory abnormalities that could give rise to a small angle of strabismus. METHODS: The binocular disparity response functions for sensory and motor processes were compared in seven orthotropic subjects and six strabismic subjects (four with primary microstrabismus and two with infantile esotropia). Binocularity was assessed by disparity vergence (central and peripheral stimuli) and depth discrimination (relative and absolute disparities) measures. Motor and sensory disparity response functions were both determined by psychophysical methods: vergence responses by dichoptic nonius alignment and sensory responses by forced-choice depth discrimination. RESULTS: All the strabismic subjects demonstrated normal retinal correspondence with peripheral binocular stimuli and anomalous retinal correspondence with central fusion stimuli. The microstrabismic subjects' disparity vergence responses with peripheral fusion stimuli were centered on disparities relative to their angle of strabismus. However, with central fusion stimuli, the disparity vergence responses were relative to the subjective angle of strabismus. The microstrabismic subjects' stereoacuities were substantially reduced, but their discrimination responses did not show an asymmetry indicative of an unrepresented population of disparity-selective mechanisms. CONCLUSIONS: The data do not support a sensory abnormality as the primary cause of microstrabismus. The results are not compatible with an oculomotor adaptation to an inherent anomalous correspondence or with a strabismus caused by an absence of a class of disparity-selective mechanisms. Thus, just as in large-angle strabismus, the anomalous retinal correspondence and defective stereopsis of microstrabismus appear to be consequences of abnormal visual experience caused by an interocular deviation.

Child↗

PubMed2002

Visual field defects and neural losses from experimental glaucoma.

Glaucoma is a relatively common disease in which the death of retinal ganglion cells causes a progressive loss of sight, often leading to blindness. Typically, the degree of a patient's visual dysfunction is assessed by clinical perimetry, involving subjective measurements of light-sense thresholds across the visual field, but the relationship between visual and neural losses is inexact. Therefore, to better understand of the effects of glaucoma on the visual system, a series of investigations involving psychophysics, electrophysiology, anatomy, and histochemistry were conducted on experimental glaucoma in monkeys. The principal results of the studies showed that, (1) the depth of visual defects with standard clinical perimetry are predicted by a loss of probability summation among retinal detection mechanisms, (2) glaucomatous optic atrophy causes a non-selective reduction of metabolism of neurons in the afferent visual pathway, and (3) objective electrophysiological methods can be as sensitive as standard clinical perimetry in assessing the neural losses from glaucoma. These experimental findings from glaucoma in monkeys provide fundamental data that should be applicable to improving methods for assessing glaucomatous optic neuropathy in patients.

Animals↗

PubMed2002

Vitreal glutamate concentration in monkeys with experimental glaucoma.

PURPOSE: To investigate the hypothesis that the pathophysiology for the death of retinal ganglion cells in glaucoma involves excitotoxic effects from elevated concentrations of vitreal glutamate. METHODS: Experimental glaucoma was induced in the right eyes of 18 rhesus monkeys by argon laser treatments to the trabecular meshwork. After significant visual field defects and/or typical clinical glaucomatous changes had developed (1.5-13 months), the eyes were removed, and a sample (0.1-0.2 mL) of posterior vitreous was collected. Similar vitreous samples also were collected from eight untreated monkeys. The vitreous samples were analyzed in a masked fashion by high-pressure liquid chromatography in two independent laboratories. Mean levels of vitreal glutamate were determined for the treated and control eyes and differences between groups of eyes were evaluated by Student's t-test. RESULTS: The mean level (+/- SD) of vitreal glutamate in the eight untreated monkeys was 5.0 +/- 2.0 microM. A similar level of 5.7 +/- 1.8 microM was measured in the untreated eyes of monkeys with experimental glaucoma. In the glaucomatous eyes, the mean concentration of vitreal glutamate was 5.7 +/- 2.6 microM, which was not significantly different from the concentrations in the control eyes. CONCLUSIONS: Vitreal glutamate concentrations were not elevated in eyes with anatomic and functional damage from experimental glaucoma. This finding is in contradiction to previous reports that vitreal glutamate increases to toxic levels and probably contributes to glaucomatous damage of retinal ganglion cells.

Amino Acids↗