Astigmatism in infant monkeys reared with cylindrical lenses.
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To determine whether developing primate eyes are capable of growing in a manner that eliminates astigmatism, we reared infant monkeys with cylindrical spectacle lenses in front of one or both eyes that optically simulated with-the-rule, against-the-rule, or oblique astigmatism (+1.50-3.00x90, x180, x45 or x135). Refractive development was assessed by retinoscopy, keratometry and A-scan ultrasonography. In contrast to control monkeys, the cylinder-lens-reared monkeys developed significant amounts of astigmatism. The astigmatism was corneal in nature, bilaterally mirror symmetric and oblique in axis, and reversible. The ocular astigmatism appeared to be due to a reduction in the rate of corneal flattening along the steeper meridian while the other principal meridian appeared to flatten at a more normal rate. However, regardless of the orientation of the optically imposed astigmatism, the axis of the ocular astigmatism was not appropriate to compensate for the astigmatic error imposed by the treatment lenses. Our results indicate that visual experience can alter corneal shape, but there was no evidence that primates have an active, visually regulated "sphericalization" mechanism. (+info)
Refraction changes in children developing convergent or divergent strabismus.
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Strabismus and amblyopia were studied in a cohort of children born in 1979 or 1980 in the area of Vasteras, Sweden. Forty percent of the children had participated in a voluntary eye examination at 1 year of age. All children diagnosed as strabismic and/or amblyopic between 1979 and 1988 at any of the three eye clinics in the area were included in this study. Strabismic cases were mostly detected by the parents while microstrabismus and straight eye amblyopia were found at the general 4 years of age screening at children's health centres. In 57 cases with (n = 31) and without amblyopia (n = 41) it was possible to obtain several refraction values between 1 and 6 years of age. In this study we concentrated on manifest esotropia and exotropia. The aim of the study was to describe changes of refraction before and after onset of strabismus and to establish risk indicators that identified populations at risk of developing strabismus. We found that patients with esotropia show a more pronounced hypermetropia than exotropic cases at the time of detection of strabismus. This difference becomes more definite over time, since hypermetropia increased in the deviating eye in the esotropic cases while refractive errors remained stationary in most of the exotropic eyes. It was also apparent that anisometropia frequently developed after onset of strabismus in esotropic cases in contrast to exotropic cases. An increasing refractive error in the deviating esotropic eye could be combined with an emmetropisation of the fixating eye. (+info)
Effects of optically imposed astigmatism on emmetropization in infant monkeys.
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PURPOSE: Although astigmatism is prevalent during early infancy, the influence of astigmatism on early refractive development is unclear. This study was undertaken to determine the effects of astigmatism on emmetropization in monkeys. METHODS: Infant rhesus monkeys (n = 39) were exposed to optically simulated astigmatism in one or both eyes from approximately 1 to 4 months of age. With-the-rule, against-the-rule, and oblique astigmatisms were optically simulated by appropriately orienting the principal meridians of the spherocylindrical treatment lenses (+1.50 -3.00 D x 90 degrees, 180 degrees, 45 degrees, or 135 degrees; i.e., +1.50 and -1.50 D powers in the two principal meridians). Refractive development was assessed every 2 to 3 weeks by cycloplegic retinoscopy, keratometry and corneal videotopography, and A-scan ultrasonography. Data from 19 control monkeys, including 3 animals that were reared with binocular plano lenses, were used for comparison purposes. RESULTS: Most of the cylinder-lens-reared monkeys, regardless of the orientation of the imposed astigmatism, showed clear signs of either hyperopic or myopic growth compared with control monkeys. The distributions of refractive error and vitreous chamber depth both showed bimodal patterns that differed from normal by amounts equivalent to the optical powers of the principal meridians of the treatment lenses. More frequently, refractive development was biased toward the eye's least-hyperopic focal plane. The refractive changes were mainly axial. After lens removal, the lens-reared monkeys recovered and as a group exhibited refractive errors and axial dimensions similar to those in control monkeys. CONCLUSIONS: In the presence of significant amounts of astigmatism, emmetropization is directed toward one of the two focal planes associated with the astigmatic principal meridians and not the circle of least confusion. These results suggest that the mechanisms responsible for emmetropization are insensitive to stimulus orientation and the global form of the retinal image. It appears that emmetropization seeks out the image plane that contains the maximum effective contrast integrated across spatial frequency and stimulus orientation. (+info)
Association of ocular dominance and anisometropic myopia.
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PURPOSE: To determine the association between ocular dominance and degree of myopia in patients with anisometropia. METHODS: Fifty-five subjects with anisometropic myopia were recruited. None of them had amblyopia. Refractive error and axial length were measured in each subject. Ocular dominance was determined using the hole-in-the-card test and convergence near-point test. RESULTS: There was a threshold level of anisometropia (1.75 D) beyond which the dominant eye was always more myopic than the nondominant eye. Of the 33 subjects with anisometropia of < or =1.75 D, the dominant eye was more myopic in 17 (51.5%) subjects. Dominant eyes, determined by the hole-in-the-card test, had a significantly greater myopic spherical equivalent (-5.27 +/- 2.45 D) than nondominant eyes (-3.94 +/- 3.10 D; P < 0.001). Dominant eyes also had a longer axial length than nondominant eyes (25.15 +/- 0.96 mm vs. 24.69 +/- 1.17 mm, respectively; P < 0.001). The difference was more evident in those subjects with higher anisometropia (>1.75 D), but was not significant in those with lower anisometropia (< or =1.75 D). Similar results were obtained using the convergence near-point test. CONCLUSIONS: The present study shows that the dominant eye has a greater degree of myopia than the nondominant eye in subjects with anisometropic myopia. Taking ocular dominance into account in the design of randomized clinical trails to assess the efficacy of myopia interventions may provide useful information. (+info)
Ocular dominance column width and contrast sensitivity in monkeys reared with strabismus or anisometropia.
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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. (+info)
Compensation for experimentally induced hyperopic anisometropia in adolescent monkeys.
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PURPOSE: Early in life, the optical demand associated with the eye's effective refractive state regulates emmetropization in many species, including primates. However, the potential role of optical demand and/or defocus in the genesis of common refractive errors, like myopia, that normally develop much later in life is not known. The purpose of this study was to determine whether chronic optical defocus alters refractive development in monkeys at ages corresponding to when myopia typically develops in children. METHODS: A hyperopic anisometropia was produced in seven adolescent rhesus monkeys by photorefractive keratectomy (PRK) with an excimer laser. Standard treatment algorithms for correcting myopia in humans were used to selectively flatten the central cornea of one eye thereby producing relative hyperopic refractive errors in the treated eyes. The laser ablation zones were 5.0 mm in diameter and centered on the monkeys' pupils. The laser procedures were performed when the monkeys were 2 to 2.5 years old, which corresponded to onset ages between approximately 8 and 10 human years. The ocular effects of the induced anisometropia were assessed by corneal topography, retinoscopy, and A-scan ultrasonography. RESULTS: By approximately 30 days after PRK, the experimentally induced refractive errors had stabilized and the treated eyes were between +0.75 and +2.25 D more hyperopic than their fellow eyes. Subsequently, over the next 300 to 400 days, six of the seven monkeys showed systematic reductions in the degree of anisometropia. Although some regression in corneal power occurred, the compensating refractive changes were primarily due to relative interocular differences in vitreous chamber growth. CONCLUSIONS: Vision-dependent mechanisms that are sensitive to refractive error are still active in adolescent primates and probably play a role in maintaining stable refractive errors in the two eyes. Consequently, conditions that result in consistent hyperopic defocus could potentially contribute to the development of juvenile onset myopia in children. (+info)
Spatial-frequency-dependent changes in cortical activation before and after patching in amblyopic children.
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PURPOSE: To examine the cortical response under transient stimulus conditions in amblyopic children before and after eye patching. To determine whether improvement in acuity is associated with spatial-frequency-dependent changes in specific peaks of the cortical response. METHODS: Visual evoked potentials (VEPs) to check reversal (163-18 arc min) and onset of sine wave gratings (0.5-4 cyc/deg) were measured in 24 amblyopic children (<7 years of age) before eye patching. VEPs were repeated in nine subjects with 20/40 or better acuity after patching. Age, severity of amblyopia, and VEP amplitudes of positive peak (P)100, P1, and negative peak (N)2 were analyzed by multivariate statistics. RESULTS: Before patching, the amblyopic eye showed decreasing amplitude with increasing spatial frequencies (P < 0.05) when compared with the nonamblyopic eye. Reduced amplitudes occurred at frequencies well below acuity. Latencies were mildly prolonged. After patching, amplitudes increased in the amblyopic eye across all spatial frequencies (ANCOVA; P < 0.0001 for each peak). However, a spatial-frequency-dependent increase in amplitude was significant only for a late negative peak (N2). The patched eye showed no significant changes. CONCLUSIONS: Recovery of acuity after eye patching is associated with an overall increase in cortical activation across a wide range of spatial frequencies below the acuity threshold. A spatial-frequency-dependent increase in a late negative peak suggests that the cortical generator of this peak demonstrates plasticity of acuity recovery. (+info)
Effects of photorefractive keratectomy-induced defocus on emmetropization of infant rhesus monkeys.
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PURPOSE: To investigate whether photorefractive keratectomy (PRK) performed in infant primates can modify emmetropization and therefore could be used to study mechanisms of refractive error development. METHODS: Six healthy rhesus monkeys ranging in age from 2 to 3 months were randomly divided into two groups (n = 3 each). Anisometropia was induced in each animal by performing PRK on one eye. Hyperopic anisometropia was induced in group A monkeys by flattening the cornea of the right eye, whereas myopic anisometropia was produced in group B monkeys by steepening the cornea of the right eye. Corneal morphology and topography, refractive status, and axial growth were evaluated over a 5-month observation period. RESULTS: All the PRK-treated corneas were re-epithelialized and transparent within 3 days after surgery. Subsequently, all the surgically treated eyes exhibited interocular alterations in axial growth rate that were appropriate to compensate for the PRK-induced anisometropia. Specifically, vitreous chamber elongation rates were faster in the eyes with induced hyperopias than in their fellow eyes (0.63 +/- 0.05 mm vs. 0.40 +/- 0.09 mm), but slower in the eyes with induced myopia than in their fellow eyes (0.58 +/- 0.13 mm vs. 0.73 +/-0.10 mm). In some animals, the recovery from the induced anisometropia was facilitated by interocular differences in the rate of corneal flattening. However, the rates of corneal flattening in the treated eyes and their fellow eyes were not significantly different. CONCLUSIONS: PRK-induced defocus predictably alters axial growth rate and the normal course of emmetropization in developing eyes. Thus, PRK is a useful alternative to current methods used to impose experimental refractive errors in laboratory animals. These results also indicate that refractive surgery performed in childhood may affect normal growth of the eye, resulting in decreased predictability of future refractive status. (+info)