The association between anisometropia, amblyopia, and binocularity in the absence of strabismus.
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PURPOSE: First, to determine if thresholds exist for the development of amblyopia and subnormal binocularity with various types of anisometropia and to confirm or refute existing guidelines for its treatment or observation. Second, to delineate any association between the degree or type of anisometropia and the depth of amblyopia and severity of binocular sensory abnormalities. METHODS: Four hundred eleven (411) patients with various levels of anisometropia, no previous therapy, and no other ocular pathology were evaluated. The effect of anisometropia (both corrected and uncorrected) on monocular acuity and binocular function was examined. RESULTS: Spherical myopic anisometropia (SMA) of > 2 diopters (D) or spherical hypermetropic anisometropia (SHA) of > 1 D results in a statistically significant increase in the incidence of amblyopia and decrease in binocular function when compared to non anisometropic patients. Increasing levels of SMA and SHA beyond these thresholds were also associated with increasing depth (and in the case of SHA, incidence as well) of amblyopia. Cylindrical myopic anisometropia (CMA) or cylindrical hyperopic anisometropia (CHA) of > 1.5 D results in a statistically significant increase in amblyopia and decrease in binocular function. A clinically significant increase in amblyopia occurs with > 1 D of CMA or CHA. Increasing levels of CMA and CHA beyond > 1 D were also associated with an increased incidence (and in the case of SMA, depth as well) of amblyopia. CONCLUSIONS: This study provides guidelines for the treatment or observation of anisometropia and confirms and characterizes the association between the type and degree of anisometropia and the incidence and severity of amblyopia and subnormal binocularity. (+info)
Hyperacuity deficits in anisometropic and strabismic amblyopes with known ages of onset.
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In order to evaluate the influence of etiology of amblyopia and of age at onset of amblyopia on the resulting constellation of spatial vision deficits, resolution/vernier and recognition/resolution acuity ratios were measured in groups of children with either strabismic amblyopia or anisometropic amblyopia with known ages of onset. Strabismic amblyopia with infantile onset (<9 months) and strabismic amblyopia with late onset (18-30 months) were both associated with abnormally low resolution/vernier and abnormally high recognition/resolution acuity ratios. Among amblyopes with infantile onset (<9 months), moderate amblyopia was associated with different resolution/vernier and recognition/resolution acuity ratios in anisometropic and strabismic groups. Infantile amblyopes with poor acuity outcomes included children who initially presented with anisometropia but later developed strabismus and children who initially presented with esotropia but later developed anisometropia; both subgroups with mixed amblyopia had poor resolution/vernier acuity ratios. Data from moderate amblyopes support the hypothesis that anisometropia and strabismus disrupt visual maturation in fundamentally different ways rather than simply at different stages in visual development. (+info)
There appear to be two modes of stereoscopic processing: a conventional linear operation that is dependent on correspondence between local luminance components in the two eyes' views, and a non-linear or second-order processing mode. This second mode may use disparity information provided by particular 'non-Fourier' features of the stimulus such as the contrast envelope. Preliminary results suggest that people who fail standard clinical stereotests are able to extract non-linear disparity information from Gabor stimuli [McColl & Mitchell, 1998. Vision Research, 38, 1889-1900]. Here we evaluate the status of the non-linear mechanism in such individuals by using two types of contrast enveloped stimuli, namely random line and Gabor micropatterns, in a task that requires near/far depth judgements [Ziegler & Hess, 1999. Vision Research, 39, 1491-1507]. Although our sample was small, three of our four subjects who had performed poorly on at least one standard clinical test of stereopsis could perform the task, as well as one 'stereoblind' subject who had failed all four standard clinical tests. The overall results suggest that individuals with stereoanomalies show a diversity of deficits, but some nevertheless can see depth using 'non-linear' mechanisms. (+info)
Sparse-sampling of gratings in the visual cortex of strabismic amblyopes.
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Strabismic amblyopes show losses in positional acuity that cannot be explained by their resolution or contrast sensitivities. One hypothesis for these losses is a reduction in the density of cortical neurons that are driven by the amblyopic eye (cortical undersampling). The question this study addressed was whether the foveal representation of the amblyopic eye is undersampled in the cortex of strabismic amblyopes. In order to assess spatial sampling psychophysically, we recorded the perceived orientation of a stationary grating as a function of grating orientation and frequency in three strabismic amblyopes. To ensure high retinal contrast, the grating was imaged on the fovea of each observer using a laser interferometer. We found that the strabismic amblyopes misperceived the orientation of the grating at spatial frequencies that are a factor of two to six lower than the sampling frequency of the foveal cones. Since the retina and LGN in strabismic amblyopes are presumably normal, this result suggests sparse cortical sampling in the foveal representation of the amblyopic eye. Undersampling by cortical neurons may contribute to the spatial distortions present in strabismic amblyopic eyes. (+info)
The neural deficit in strabismic amblyopia: sampling considerations.
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In order to understand the nature of the neural loss in strabismic amblyopia, we have applied a technique which has been used in the normal periphery to psychophysically probe the sampling properties of the neuronal population. We ask whether there is a 'sampling' deficit and if so whether it is based on either an absolute loss of neurons (i.e. spatial undersampling) or an irregular arrangement of a normal number of neurons (i.e. irregular sampling). Our results suggest that neural pooling restricts the spatial frequency region where sampling considerations are important to a very small part of the visible high spatial frequency range. Within this limited region, irregular sampling rather than spatial undersampling is the greater contributor to the strabismic amblyope deficit. (+info)
The orientation discrimination deficit in strabismic amblyopia depends upon stimulus bandwidth.
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We show that the previously reported orientation deficit in amblyopia (Skottun, B. C., Bradley, A., & Freeman, R. D. (1986). Orientation discrimination in amblyopia. Investigative Ophthalmology and Visual Science, 30, 532-537) also occurs for arrays of randomly positioned Gabor micropatterns for which explanations based on either neural disarray or local neural interactions would not hold. Furthermore, when using Gabors, we show that the deficit varies with the spatial frequency and orientational bandwidth of the stimuli used to measure it. We discuss two competing explanations for this, one based on a broader underlying detector bandwidth in amblyopia (both orientation and spatial frequency) and the other based on a selective deficit of first-order, as opposed to second-order orientation processing in strabismic amblyopia. Our results favour the latter interpretation. (+info)
Factors limiting contrast sensitivity in experimentally amblyopic macaque monkeys.
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Contrast detection is impaired in amblyopes. To understand the contrast processing deficit in amblyopia, we studied the effects of masking noise on contrast threshold in amblyopic macaque monkeys. Amblyopia developed as a result of either experimentally induced strabismus or anisometropia. We used random spatiotemporal broadband noise of varying contrast power to mask the detection of sinusoidal grating patches. We compared masking in the amblyopic and non-amblyopic eyes. From the masking functions, we calculated equivalent noise contrast (the noise power at which detection threshold was elevated by square root of 2) and signal-to-noise ratio (the ratio of threshold contrast to noise contrast at high noise power). The relation between contrast threshold and masking noise level was similar for amblyopic and non-amblyopic eyes. Although in most cases there was some elevation in equivalent noise for amblyopic compared to fellow eyes, signal-to-noise ratio showed greater variation with the extent of amblyopia. These results support the idea that the contrast detection deficit in amblyopia is a cortical deficit. (+info)
A new test of contour integration deficits in patients with a history of disrupted binocular experience during visual development.
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Previous studies have suggested that the integration of orientation information across space is impaired in amblyopia. We developed a method for quantifying orientation-domain processing using a test format that is suitable for clinical application. The test comprises a graded series of cards where each card includes a closed path (contour) of high contrast Gabor signals embedded in a random background of Gabor signals. Contour visibility in both normals and patients with histories of abnormal binocular vision depends jointly on the spacing of elements on the contour as well as background element density. Strabismic amblyopes show significant degradation of performance compared to normals. Small but significant losses in sensitivity were also observed in a group of non-amblyopic strabismus patients. Threshold measurements made with contrast reducing diffusers indicated that the amblyopic loss is not due to the reduced contrast sensitivity of the amblyopic eye. An abnormal pattern of long-range connectivity between spatial filters or a loss of such connectivity appears to be the primary source of contour integration deficits in amblyopia and strabismus. (+info)