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PubMed1993

A simple eyesight screening programme for dental undergraduates: results after 7 years.

This paper reports the results of a simple eyesight screening programme for dental undergraduates which has been used for 7 years. Examinations were performed by orthoptists at a general hospital associated with the dental school. Defects in visual acuity, squints, limitations of convergence, defective stereopsis and colour vision were found. Many students were unaware of their visual defects, and the findings support the continued use of visual screening to identify and encourage those with defects to seek professional treatment at an early opportunity. Many of the defects were correctable or could be improved with help. Those with defective colour-vision were encouraged to seek assistance with shade selection during their clinical careers. The value of visual screening and the significance of the findings are discussed.

Color Vision Defects↗
PubMed2001

Clinical features and a follow-up study in a family with X-linked progressive cone-rod dystrophy.

PURPOSE: To study a large family with X-linked progressive cone-rod dystrophy. METHODS: There were 128 members in the family. Of these, 45 had an ophthalmological examination and 3 gave their permission to use the results of their recent ophthalmological examination. In addition to the usual eye examination, visual fields, colour vision, dark adaptation and electroretinogram (ERG) were examined. RESULTS: Ten affected men aged 6 to 81 years were found in the family. The visual acuities varied from counting fingers (cf) 10 cm to 0.5 in the right eye (RE) and from cf 30 cm to 0.4 in the left eye (LE). The refraction was myopic in all affected members, varying from -1.5 to -24.0 D (RE) and from -2.0 to -20.25 D (LE). In visual functions, central scotomas and concentric constriction in the visual fields, red or red-green defects in colour vision, abnormal cone and rod dark adaptation and affected cone response in ERG were found. The 6 obligate carriers were aged 17 to 77 years. Their visual acuities varied from 0.05 (strabismic amblyopia) to 1.25(RE) and from 0.7 to 1.25 (LE), and refraction from +/-0 to +6.0 D (RE) and from -0.5 to +5.0 D (LE). Their visual fields and colour vision were normal. The non-affected men were aged 13 to 55 years, their visual acuity was normal in both eyes, and refraction varied from -5.0 to +1.5 D (RE) and from -5.5 to +1.75 (LE). The result of the eye examination was normal except in colour vision: two men were congenitally deuteranomalous. The women who were not obligate carriers were aged 10 to 77 years, their visual acuity was from 0.3 to 1.6 in both eyes, and refraction from -5.5 to +4.75 (RE) and from -5.25 to +4.0 (LE). Two women had one amblyopic eye. Otherwise the eye examination was normal. CONCLUSIONS: The clinical diagnosis of X-linked cone dystrophy 1 (COD1) is based on progressive loss of visual acuity, moderate or high myopia, red colour vision defect and affected cone response or cone and rod response in ERG. The future identification of the COD1 gene will confirm the diagnosis of the disease and help in genetic counseling of the family.

Adult↗
PubMed2000

Autosomal dominant cone-rod retinal dystrophy (CORD6) from heterozygous mutation of GUCY2D, which encodes retinal guanylate cyclase.

OBJECTIVE: To describe the clinical features of autosomal dominant cone-rod retinal dystrophy (CRD) in a British family mapping to chromosome 17p12-p13 (CORD6), with a heterozygous mutation (Glu837Asp/ Arg838Ser) of GUCY2D. DESIGN: A prospective, clinical family survey. PATIENTS: Ten affected members of a family with autosomal dominant CRD. METHODS: Full clinical examinations were undertaken. Selected affected family members underwent electrophysiologic evaluation, scotopic static perimetry, dark adaptometry, and color vision assessment. MAIN OUTCOME MEASURES: Clinical appearance and electroretinographic responses. RESULTS: Typical clinical and electroretinographic features of childhood-onset CRD were recorded. In addition, moderate myopia and pendular nystagmus were seen in affected individuals. Color vision assessment in the youngest affected individual showed no color discrimination on a tritan axis, but retention of significant red-green discrimination. Electronegative electroretinogram responses were seen on electrophysiology in the only young family member examined. CONCLUSIONS: The phenotype associated with GUCY2D CRD is clinically distinct from that associated with other dominant CRD loci. Unusual electroretinographic responses may indicate that this mutation of GUCY2D is associated with early defects in photoreceptor synaptic transmission to second-order neurons.

Adolescent↗
PubMed2004

Molecular genetics of colour vision deficiencies.

Common variation in colour vision exists among both colour normal and colour deficient subjects. Differences at a few amino acid positions that influence the spectra of the L and M cone pigments account for most of this variation. The genes encoding the L and M photopigments are arranged in head-to-tail arrays on the X-chromosome, beginning with the L and followed by one or more M pigment genes. The L and M pigment genes are highly homologous, which predisposed them to unequal crossing over (recombination) resulting in gene deletions and in formation of L/M hybrid genes that encode a variety of pigments with either L-like or M-like spectra that account for the majority of colour vision defects. Only the first two pigment genes of the L/M array are expressed in the retina and, therefore, need to be considered in predicting colour vision. A common single amino acid polymorphism (serine or alanine) at position 180 of the L-pigment plays an important role both in variation in normal colour vision and in the severity of colour vision defects. Blue cone monochromacy is a rare form of colour vision deficiency that results from mutations that abolish function of both the L and M pigment genes. All the above defects are inherited as X-linked recessive traits. Tritanopia is also a rare autosomal dominant colour vision defect caused by mutations in the S pigment gene located on chromosome 7. Total colour blindness (achromatopsia or rod monochromacy) is a rare autosomal recessive trait caused by mutations in genes encoding the proteins of the photoreceptor cation channel or cone transducin that are essential for function of all classes of cone.

Color Vision Defects↗
PubMed1996

Increment threshold and purity discrimination spectral sensitivities of X-chromosome-linked color-defective observers.

The goal of the study was to evaluate spectral opponency in nine X-chromosome-linked color-defective observers. The tasks included increment threshold spectral sensitivity on an achromatic background, heterochromatic flicker photometry, and colorimetric purity discrimination. With a task of heterochromatic flicker photometry, the anomalous trichromatic observers showed spectral sensitivity of the corresponding dichromat. The increment threshold spectral sensitivity and colorimetric purity discrimination data were analyzed using the concept of standard cone photopigment spectral sensitivities for normal and defective vision, and a model that postulates one cone-additive and two cone-antagonistic systems. The model incorporated a shift of the peak spectral sensitivity of the long-wavelength-sensitive (LWS) pigment (for protan observers) or of the middle-wavelength-sensitive (MWS) pigment (for deutan observers). Two dichromats and two anomalous trichromats did not show clear evidence of LWS vs MWS cone antagonism. Five anomalous trichromats showed such cone antagonism. Molecular genetic analysis of the opsin genes is presented for eight of the observers.

Color Vision Defects↗
PubMed1992

A new way to use the Ishihara test.

The Ishihara plates are widely used as a test for colour vision. Originally designed for the purpose of detecting congenital red-green colour blindness, the test also has some value in demonstrating acquired colour vision defects. There are, however, several disadvantages in the present arrangement of the plates. A modification of the test, involving the rearrangement of the order of the plates, is presented which, together with a new recording chart, simplifies both the administration and the interpretation of the test.

Color Perception↗
PubMed1992

The use of colour difference vectors in diagnosing congenital colour vision deficiencies with the Farnsworth-Munsell 100-hue test.

Colour difference vector analysis provides useful and meaningful information in scoring the Farnsworth-Munsell (FM) 100-hue test. However, the FM 100-hue test is limited in its ability to diagnose type and severity of congenital colour vision defect. Type classification for all subjects is incorrect in 21% of cases, and for deuteranomals the misclassification rate is 38%. Visual inspection of the plots yields a similar misclassification rate and classification of plots with few errors (under 180) is generally less reliable. The FM 100-hue test has a limited ability to separate dichromats from anomalous trichromats. A test protocol based on joint D15 and FM 100-hue tests should pass 36% of anomalous trichromats and 26% of all colour defectives yet fail all dichromatic observers. We conclude that administering the FM 100-hue test is of less value than a combination of D15 panels (Standard D15 and L'Anthony's desaturated D15) in the clinical diagnosis of congenital colour defective observers. Our results for the FM 100-hue panel are similar to those reported previously by other investigators.

Adult↗
PubMed2004

[Effect of an early visual encoding defect on attentional function: a study of daltonism using the Stroop test].

The Stroop color-word test is often used to assess attentional function. In this study we investigated whether dyschromatopsia affects the results of this test, and in that case which are the attentional consequences of this color-vision trouble. Event-related potentials were recorded on 19 dyschromatopsic subjects when submitted to a video-displayed Stroop test, and compared to those of 19 control subjects. Results showed that reaction times of dyschromatopsic subjects, although generally longer than those of controls, had normal interference and facilitation effects. Potentials evoked by neutral stimulations were delayed for P2 and P3 waves, and those evoked by word-containing stimulations showed delays for N2b (N320) and P3 waves. The premotor potential appeared modified in dyschromatopsic patients, whereas error negativities, or correct response negativities were identical to those of control subjects. We conclude that dyschromatopsia affects negatively the performance in the Stroop test, at sensory levels which are reflected by evoked potentials, but without important consequences on attentional function. In particular, dyschromatopsia did not alter significantly the attentional focusing on the chromatic aspects of the stimulus.

Adult↗
PubMed1992

Late onset dominant cone dystrophy with early blue cone involvement.

A dominant cone dystrophy spanning seven generations was found in a pedigree from the Netherlands. The onset of the decline of visual acuity started after the age of 20, while a near complete absence of blue cone function (a so-called tritan defect) already existed before the presence of any ophthalmological abnormalities.

Adolescent↗
PubMed2002

Keratoconus associated with cone-rod dystrophy: a case report.

A 31-year-old man with bilateral keratoconus associated with apical corneal scarring underwent uneventful penetrating keratoplasty in his left eye. Postoperatively his best-corrected visual acuity did not improve beyond 20/120. Examination of the fundus revealed features suggestive of bull's eye maculopathy. On performing an electroretinogram study of both eyes, grossly delayed implicit time with reduced amplitudes of the rod response and extinguished cone waveforms were noted, indicating cone-rod dystrophy. Color blindness was also noted on testing with Ishihara's pseudoisochromatic plates. Genetic counseling showed this to be an isolated defect with negative family history. Preoperative electrophysiologic studies may have a prognostic role in these cases.

Adult↗
PubMed1991

A family with acquired and inherited blue-yellow axis.

The pedigree of a family with a blue-yellow axis in the Farnsworth 100-Hue is reported. The fact that a blue-yellow axis corresponds to an inherited defect in 6 subjects and to an acquired defect in 1 subject is discussed. Methodological conditions necessary for making the differential diagnosis between an inherited and an acquired blue-yellow defect are recalled.

Adult↗
PubMed1983

Visual fields: simplified screening and recording procedures.

In some cases, visual field screening must be greatly simplified in order to obtain clinically useful information. This becomes possible when specific techniques are used for anomalies such as relative central scotoma, hemianopsia, and glaucomatous field defects. A working knowledge of visual pathway anatomy and function enables the optometrist to efficiently screen for these disorders by confrontation with red test objects, with pseudoisochromatic plates, and with the tangent screen. After the type of field defect has been determined by initial screening, recording its parameters with the tangent screen follows easily.

Color Perception Tests↗
PubMed2002

Protan colour vision deficiency and road accidents.

BACKGROUND: Protans are precluded from holding a commercial driver's licence in Australia because they have a substantially reduced ability to see red lights and have more road accidents involving signal lights. This exclusion has been in place since 1994 but is likely to be abandoned following a current review of medical standards for commercial drivers. This paper reviews the level of risk of road accidents due to protan colour vision deficiency. It also addresses the question of whether it is fair to regard all protans as having a higher risk of road accident because some protans might have a sensitivity to red light that is as good as that of some people with normal colour vision. METHODS: Data of two studies by Verriest and co-workers are re-analysed to estimate the degree of overlap of the protan and colour normal distributions of sensitivity to red light. RESULTS: Field trial data show that protans have a very reduced visual range for red signals compared to colour normal observers but there is considerable variability among both classes of observers and the distributions do overlap. However, some variability is due to differences in observers' choices of a detection criterion, their speed of response and the measurement method. A laboratory study of the spectral sensitivity of protan and colour normal subjects that largely removes these sources' variability shows that all protans have a sensitivity to red light that is less than that of the least sensitive colour normal. CONCLUSION: It is reasonable to conclude that all protans, regardless of the severity of their defect, have a lesser ability to see red signals than colour vision normal observers and for that reason will have a higher risk of road accident.

Accidents, Traffic↗