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Chea-Su Kee

Publications and source records attributed to Chea-Su Kee.

4 recordsLinked to original sources

Astigmatism in monkeys with experimentally induced myopia or hyperopia.

PURPOSE: Astigmatism is the most common ametropia found in humans and is often associated with large spherical ametropias. However, little is known about the etiology of astigmatism or the reason(s) for the association between spherical and astigmatic refractive errors. This study examines the frequency and characteristics of astigmatism in infant monkeys that developed axial ametropias as a result of altered early visual experience. METHODS: Data were obtained from 112 rhesus monkeys that experienced a variety of lens-rearing regimens that were intended to alter the normal course of emmetropization. These visual manipulations included form deprivation (n = 13); optically imposed defocus (n = 48); and continuous ambient lighting with (n = 6) or without optically imposed defocus (n = 6). In addition, data from 19 control monkeys and 39 infants reared with an optically imposed astigmatism were used for comparison purposes. The lens-rearing period started at approximately 3 weeks of age and ended by 4 to 5 months of age. Refractive development for all monkeys was assessed periodically throughout the treatment and subsequent recovery periods by retinoscopy, keratometry, and A-scan ultrasonography. RESULTS: In contrast to control monkeys, the monkeys that had experimentally induced axial ametropias frequently developed significant amounts of astigmatism (mean refractive astigmatism = 0.37 +/- 0.33 D [control] vs. 1.24 +/- 0.81 D [treated]; two-sample t-test, p < 0.0001), especially when their eyes exhibited relative hyperopic shifts in refractive error. The astigmatism was corneal in origin (Pearson's r; p < 0.001 for total astigmatism and the JO and J45 components), and the axes of the astigmatism were typically oblique and bilaterally mirror symmetric. Interestingly, the astigmatism was not permanent; the majority of the monkeys exhibited substantial reductions in the amount of astigmatism at or near the end of the lens-rearing procedures. CONCLUSIONS: In infant monkeys, visual conditions that alter axial growth can also alter corneal shape. Similarities between the astigmatic errors in our monkeys and some astigmatic errors in humans suggest that vision-dependent changes in eye growth may contribute to astigmatism in humans.

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Peripheral vision can influence eye growth and refractive development in infant monkeys.

PURPOSE: Given the prominence of central vision in humans, it has been assumed that visual signals from the fovea dominate emmetropization. The purpose of this study was to examine the impact of peripheral vision on emmetropization. METHODS: Bilateral, peripheral form deprivation was produced in 12 infant monkeys by rearing them with diffusers that had either 4- or 8-mm apertures centered on the pupils of each eye, to allow 24 degrees or 37 degrees of unrestricted central vision, respectively. At the end of the lens-rearing period, an argon laser was used to ablate the fovea in one eye of each of seven monkeys. Subsequently, all the animals were allowed unrestricted vision. Refractive error and axial dimensions were measured along the pupillary axis by retinoscopy and A-scan ultrasonography, respectively. Control data were obtained from 21 normal monkeys and 3 infants reared with binocular plano lenses. RESULTS: Nine of the 12 treated monkeys had refractive errors that fell outside the 10th- and 90th-percentile limits for the age-matched control subjects, and the average refractive error for the treated animals was more variable and significantly less hyperopic/more myopic (+0.03 +/- 2.39 D vs. +2.39 +/- 0.92 D). The refractive changes were symmetric in the two eyes of a given animal and axial in nature. After lens removal, all the treated monkeys recovered from the induced refractive errors. No interocular differences in the recovery process were observed in the animals with monocular foveal lesions. CONCLUSIONS: On the one hand, the peripheral retina can contribute to emmetropizing responses and to ametropias produced by an abnormal visual experience. On the other hand, unrestricted central vision is not sufficient to ensure normal refractive development, and the fovea is not essential for emmetropizing responses.

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Effects of optically imposed astigmatism on emmetropization in infant monkeys.

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.

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Continuous ambient lighting and lens compensation in infant monkeys.

PURPOSE: Protracted daily lighting cycles do not promote abnormal ocular enlargement in infant monkeys as they do in a variety of avian species. However, observations in humans suggest that ambient lighting at night may reduce the efficiency of the emmetropization process in primates. To test this idea, we investigated the ability of infant monkeys reared with continuous light to compensate for optically imposed changes in refractive error. METHODS: Beginning at about 3 weeks of age, a hyperopic or myopic anisometropia was imposed on 12 infant rhesus monkeys by securing either a -3 D or +3 D lenses in front of one eye and a zero-powered lens in front of the fellow eye. Six of these monkeys were reared with the normal vivarium lights on continuously, whereas the other six lens-reared monkeys were maintained on a 12-h-light/12-h-dark lighting cycle. The ocular effects of the lens-rearing procedures were assessed periodically during the treatment period by cycloplegic retinoscopy, keratometry, and A-scan ultrasonography. RESULTS: Five of six animals in each of the lighting groups demonstrated clear evidence for compensating anisometropic growth. In both lighting groups, eyes that experienced optically imposed hyperopic defocus (-3 D lenses) exhibited faster axial growth rates and became more myopic than their fellow eyes. In contrast, eyes treated with +3 D lenses showed relatively slower axial growth rates and developed more hyperopic refractive errors. The average amount of compensating anisometropia (continuous light, 1.6 +/- 0.5 D vs. control, 2.3 +/- 0.5 D), the structural basis for the refractive errors, and the ability to recover from the induced refractive errors were also not altered by continuous light exposure. CONCLUSION: Ambient lighting at night does not appear to overtly compromise the functional integrity of the vision-dependent mechanisms that regulate emmetropization in higher primates.

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