Search PubMedSearch

PubMed · 7088177

Hyperacuity and amblyopia.

Abstract

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.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D M Levi, S Klein. 1982-07-15. Hyperacuity and amblyopia.. https://doi.org/10.1038/298268a0

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Genome-Wide and Rare Variant Association Studies of Amblyopia in Admixed American and African Ancestry Groups.

OBJECTIVE: To identify genetic variants associated with amblyopia in African (AFR) and Admixed American (AMR) ancestry groups, expanding on previous studies conducted in European ancestry. DESIGN: Retrospective ancestry-stratified genome-wide association study (GWAS) and gene-level rare variant association study (RVAS). PARTICIPANTS: Participants in the All of Us Research Program from AFR and AMR ancestry groups who had whole-genome sequencing available. Cases and controls were distinguished based on the presence of International Classification of Diseases 9/10/SNOMED diagnosis codes for amblyopia in electronic health records. This yielded ancestry-stratified subsets of 269 cases and 71 585 controls of AMR ancestry and 366 cases and 79 460 controls of AFR ancestry. METHODS: Stratified logistic regression models were adjusted for age, biological sex, and the top 10 principal components of genomic ancestry. GWAS was limited to common variants (minor allele frequency &#x2265;1%), and RVAS was limited to rare variants with coding sequence-altering effects (minor allele frequency >1%, exonic only, excluding synonymous variants) aggregated at the gene level using the SKAT algorithm. Downstream analyses of the significant variants were performed using KEGG and GO pathway analysis and STRING database queries for protein-protein interactions and gene-gene interactions. MAIN OUTCOME MEASURES: Single-nucleotide polymorphisms were determined to have genome-wide significance if P < 5e-8 in the GWAS, and genes were determined to have significant association with amblyopia in the RVAS if P < 8.0 &#xd7; 10-4. RESULTS: In the AMR GWAS, 245 unique single-nucleotide polymorphisms mapping to 97 distinct loci were identified, notably within neurodevelopmental and axonal guidance genes, including ROBO1, SEMA4B, PTPRD, NRXN1, and CAMK2D. The AFR GWAS identified 11 significant variants corresponding to 6 loci mapping primarily to long noncoding RNAs and pseudogenes. The AMR RVAS identified 15 genes, including axonal transport genes (KIF1B and KIF7) and growth factor signaling genes (EGF, ERBIN, and AKAP17A). The AFR RVAS identified a single gene, DLG2, which encodes the postsynaptic protein PSD-93, which promotes the closure of the sensitive period of neuroplasticity for vision in early childhood. CONCLUSIONS: Genetic risk architectures for amblyopia differ across ancestries but fundamentally converge on neurodevelopmental signaling, cortical synapse assembly, and sensitive period plasticity rather than ocular structural dynamics. FINANCIAL DISCLOSURE(S): The authors have no proprietary or commercial interest in any materials discussed in this article.

Amblyopia

Neuronal correlates of amblyopia in the visual cortex of macaque monkeys with experimental strabismus and anisometropia.

Amblyopia is a developmental disorder of pattern vision. After surgical creation of esotropic strabismus in the first weeks of life or after wearing -10 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.

Amblyopia