PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1891830

Visual resolution limits in human albinism.

R V Abadi·E Pascal
View original source ↗Export metadata ↓

Abstract

The effects of the involuntary ocular oscillations on visual resolution was examined in 22 albinos and 11 idiopaths with congenital nystagmus. The idiopaths showed a linear relationship between the proportion of the slow phase spent at low velocities (less than or equal to deg/sec) and the log of the minimum angle of resolution; such that long dwell times were compatible with good resolution. For the albinos there appeared to be a critical duration of low retinal slip velocities above which there was no improvement in acuity. This supports the contention that factors other than the congenital nystagmus limit visual resolution in the albino.

Explore related subjects

Albinism, OcularAlbinism, OculocutaneousEye MovementsFixation, OcularHumansNystagmus, PathologicTime FactorsVisual AcuityComparative StudyJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R V Abadi, E Pascal. 1991. Visual resolution limits in human albinism.. https://doi.org/10.1016/0042-6989(91)90063-b

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

KEEP EXPLORING

Related citations

PubMed1998

Two spectral types of retinal light damage occur in albino as well as in pigmented rat: no essential role for melanin.

Earlier we showed that two spectral types of retinal damage occur in the pigmented rat. In the present study we investigated whether the same is true for albino rats. When investigating this issue we implicitly investigated the role of melanin in both damage types. An albinotic (Wistar) and a pigmented (Long Evans) strain of rats were used. Under anesthesia, a small part of the retina was irradiated at either 380 nm or at 470 nm. Three days later, the retina was analysed by funduscopy and prepared for light microscopy. Funduscopy showed no signs of damage in the albinotic retina. In the pigmented retina a decoloration of the fundus was noticed after irradiations starting from retinal doses of 0.6+/-0.1 J cm-2 at 380 nm, and from 489+/-71 J cm-2 at 470 nm. By light microscopy, retinal damage was found in the albino retina. The histologic manifestations at 380 nm differed from those at 470 nm. Irradiation at 380 nm at a dose of 0. 5-0.9 J cm-2 damaged a few scattered photoreceptor cells. At doses of 1.2-1.6 J cm-2 all rods were damaged, while the other retinal layers showed no changes. These findings were similar to those found at 380 nm in the pigmented rat. At 470 nm, damage was found most prominently in the retinal pigment epithelium. These cells showed swelling and an increased number of dark inclusions. Threshold damage occurred at doses of 250-500 J cm-2. Again, the pathology in the pigmented rat was highly similar to that in the albino rat. The results show that both spectral damage types occur in albino as well as in pigmented retina. Therefore, melanin plays no crucial role in these light damage types.

Albinism, Ocular↗
PubMed1998

The retinal pigment epithelium as a developmental regulator of the neural retina.

Melanin-related agents regulate the development of the mammalian neural retina, because in albinos there are a range of retinal deficits including abnormal connections between the eye and brain, an underdeveloped central retina and a rod deficit. These deficits may arise because gradients of retinal development in the albino are delayed and the retina is abnormally proliferative, but also goes through a subsequent period of excessive cell death. This may be caused by a reduction in ocular DOPA in albinos as this is in the synthetic pathway of melanin and is a known cell cycle regulator.

Albinism, Ocular↗
PubMed1998

OA1 mutations and deletions in X-linked ocular albinism.

X-linked ocular albinism (OA1), Nettleship-Falls type, is characterized by decreased ocular pigmentation, foveal hypoplasia, nystagmus, photodysphoria, and reduced visual acuity. Affected males usually demonstrate melanin macroglobules on skin biopsy. We now report results of deletion and mutation screening of the full-length OA1 gene in 29 unrelated North American and Australian X-linked ocular albinism (OA) probands, including five with additional, nonocular phenotypic abnormalities (Schnur et al. 1994). We detected 13 intragenic gene deletions, including 3 of exon 1, 2 of exon 2, 2 of exon 4, and 6 others, which span exons 2-8. Eight new missense mutations were identified, which cluster within exons 1, 2, 3, and 6 in conserved and/or putative transmembrane domains of the protein. There was also a splice acceptor-site mutation, a nonsense mutation, a single base deletion, and a previously reported 17-bp exon 1 deletion. All patients with nonocular phenotypic abnormalities had detectable mutations. In summary, 26 (approximately 90%) of 29 probands had detectable alterations of OA1, thus confirming that OA1 is the major locus for X-linked OA.

Albinism, Ocular↗