Amblyopia is usually defined as a deficit in optotype (Snellen) acuity with no detectable organic cause. We asked whether this visual abnormality is completely characterized by the deficit in optotype acuity, or whether it has distinct forms that are determined by the conditions associated with the acuity loss, such as strabismus or anisometropia. To decide this issue, we measured optotype acuity, Vernier acuity, grating acuity, contrast sensitivity, and binocular function in 427 adults with amblyopia or with risk factors for amblyopia and in a comparison group of 68 normal observers. Optotype acuity accounts for much of the variance in Vernier and grating acuity, and somewhat less of the variance in contrast sensitivity. Nevertheless, there are differences in the patterns of visual loss among the clinically defined categories, particularly between strabismic and anisometropic categories. We used factor analysis to create a succinct representation of our measurement space. This analysis revealed two main dimensions of variation in the visual performance of our abnormal sample, one related to the visual acuity measures (optotype, Vernier, and grating acuity) and the other related to the contrast sensitivity measures (Pelli-Robson and edge contrast sensitivity). Representing our data in this space reveals distinctive distributions of visual loss for different patient categories, and suggests that two consequences of the associated conditions--reduced resolution and loss of binocularity--determine the pattern of visual deficit. Non-binocular observers with mild-to-moderate acuity deficits have, on average, better monocular contrast sensitivity than do binocular observers with the same acuity loss. Despite their superior contrast sensitivity, non-binocular observers typically have poorer optotype acuity and Vernier acuity, at a given level of grating acuity, than those with residual binocular function.

/pdf/the-pattern-of-visual-deficits-in-amblyopia-2m0tukeh9i.pdf

The pattern of visual deficits in amblyopia.

Vernier acuity, crowding and amblyopia

Amblyopia is a developmental disorder of pattern vision. After surgical creation of esotropic strabismus in the first weeks of life or after wearing 210 diopter contact lenses in one eye to simulate anisometropia during the first months of life, macaques often develop amblyopia. We studied the response properties of visual cortex neurons in six amblyopic macaques; three monkeys were anisometropic, and three were strabismic. In all monkeys, cortical binocularity was reduced. In anisometropes, the amblyopic eye influenced a relatively small proportion of cortical neurons; in strabismics, the influence of the two eyes was more nearly equal. The severity of amblyopia was related to the relative strength of the input of the amblyopic eye to the cortex only for the more seriously affected amblyopes. Measurements of the spatial frequency tuning and contrast sensitivity of cortical neurons showed few differences between the eyes for the three less severe amblyopes (two strabismic and one anisometropic). In the three more severely affected animals (one strabismic and two anisometropic), the optimal spatial frequency and spatial resolution of cortical neurons driven by the amblyopic eye were substantially and significantly lower than for neurons driven by the nonamblyopic eye. There were no reliable differences in neuronal contrast sensitivity between the eyes. A sample of neurons recorded from cortex representing the peripheral visual field showed no interocular differences, suggesting that the effects of amblyopia were more pronounced in portions of the cortex subserving foveal vision. Qualitatively, abnormalities in both the eye dominance and spatial properties of visual cortex neurons were related on a case-by-case basis to the depth of amblyopia. Quantitative analysis suggests, however, that these abnormalities alone do not explain the full range of visual deficits in amblyopia. Studies of extrastriate cortical areas may uncover further abnormalities that explain these deficits.

/pdf/neuronal-correlates-of-amblyopia-in-the-visual-cortex-of-4u91uu4pvb.pdf

Neuronal Correlates of Amblyopia in the Visual Cortex of Macaque Monkeys with Experimental Strabismus and Anisometropia

To further our understanding of the cortical deficit in strabismic amblyopia, we measured, compared and mapped functional magnetic resonance imaging (fMRI) activation between the fixing and fellow amblyopic eyes of ten strabismic amblyopes. Of specific concern was whether the function of any visual area was spared in strabismic amblyopia, as recently suggested by both positron emission tomography (PET) and fMRI studies, and whether there was a close relationship between the fMRI response and known psychophysical deficits. To answer these questions we measured the psychophysical deficit in each subject and used stimuli whose relationship to the psychophysical deficit was known. We observed that stimuli that were well within the amblyopic passband did produce reduced fMRI activation, even in visual area V1. This suggests that V1 is anomalous in amblyopia. A similar level of reduction was observed in V2. In two subjects, we found that stimuli outside the amblyopic passband produced activation in visual area V3A. We did not find a close relationship between the fMRI response reduction in amblyopia and either of the known psychophysical deficits even though the fMRI response reduction in amblyopia did covary with stimulus spatial frequency.

/pdf/the-cortical-deficit-in-humans-with-strabismic-amblyopia-48pgvfv2ks.pdf

The cortical deficit in humans with strabismic amblyopia.

The most frequent cause of visual loss in childhood is functional amblyopia, an abnormality of visual acuity usually associated with either anisometropia (unequal refractive errors) or strabismus (turned eye) during early development. The usual clinical investigation of the visual acuity of amblyopes involves discrimination of the high contrast letters of a Snellen chart; however, there are other aspects of acuity, for example, grating acuity (the high spatial frequency limit of vision) and Vernier acuity (the smaller perceptible misalignment). Because of the extreme precision of Vernier acuity compared with either grafting or Snellen acuity, it is considered to be a form of hyperacuity which requires very precise positional information. In an effort to understand the nature of the neural abnormalities which cause the reduced acuity of amblyopes, we have measured here the Vernier acuity of amblyopic observers using an extended Vernier grating stimulus, and compared these results with their Snellen acuity and grating acuity. The results showed that different acuity losses are associated wih anisometropic versus strabismic amblyopia. When scaled with respect to their grating acuity, anisometropic amblyopes, like normals, showed hyperacuity, even at high spatial frequencies, while strabismic amblyopes showed severe losses in Vernier acuity. Snellen letter acuity showed a similar deficit relative to grating acuity in strabismic but not in anisometropic amblyopes. Contrary to some previous theories which have considered that all forms of amblyopia share a common neural basis, these results strongly support the view that different neural losses are associated with amblyopias of different aetiologies.

Hyperacuity and amblyopia

Differences in the neural basis of human amblyopias: The effect of mean luminance

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Differences in the neural basis of human amblyopias: The effect of mean luminance