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PubMed1983

A review of ocular malingering and hysteria for the flight surgeon.

Malingering is the conscious creation of a functional defect or denial of a true defect. Positive malingering is the former, and negative malingering is the latter. Hysteria is similar to malingering except that it is unconscious. Ocular malingering is common among draft evaders. The flight surgeon or military ophthalmologist will more commonly see the negative malingerer in peacetime because of the high physical standards for flying. Wartime creates a sudden shift towards positive malingering, however, for obvious reasons. This paper carefully defines the distinctions between malingering, hysteria, and true disease consistent with the defect claimed. It also provides a systematic approach to history, examination, and special testing of a possible ocular malingerer/hysteric. A number of common ocular complaints are considered separately, including decreased visual acuity, visual field defects, night vision defects, color vision defects, ocular muscle defects, automutilatory defects, opacification of transparent media, blepharospasm, intraocular disease, and asthenopia.

Aerospace Medicine↗
PubMed1989

Color vision defects in adrenomyeloneuropathy.

The relationship between abnormal color vision and adrenomyeloneuropathy (AMN) was investigated in 27 AMN patients and 31 age-matched controls by using the Farnsworth-Munsell 100 Hue test. Twelve (44%) of 27 patients showed test scores significantly above normal. The axes of bipolarity determined by the testing differed widely between the patients with abnormal scores, compatible with the notion that different alterations in visual pigment genes occur in different AMN kindreds. These observations confirm our earlier impression that the frequency of abnormal color vision is increased in these kindreds, and it supports our contentions that (1) AMN (and its companion, adrenoleukodystrophy) are very closely linked to the visual pigment loci at Xq28 and (2) this proximity might provide the opportunity to observe contiguous gene defects.

Adrenal Gland Diseases↗
PubMed1998

Pigment gene expression in protan color vision defects.

We screened 150 male eye donors and identified four who did not have or express L pigment genes, consistent with each of them having a congenital protan color vision defect. One donor was identified as a protanope because he had and expressed a single X-chromosome photopigment gene that encoded an M pigment. Three were categorized as protanomalous because each expressed significant levels of genes specifying two spectrally different M pigments. The first gene in each of the protanomalous arrays was expressed the most and encoded an M pigment that differed in amino acid sequence from M pigments in color normal men.

Base Sequence↗
PubMed1997

[Evaluation of acquired color vision defects by means of the two equation method in primary open-angle glaucoma with normal pressure and in patients from the risk group].

PURPOSE: To evaluate acquired color vision defects in glaucoma patients and glaucoma suspects. MATERIAL AND METHODS: 52 subjects (102 eyes) divided into four groups (with primary open angle glaucoma, normal tension glaucoma, ocular hypertension and with glaucoma-like optic disc) were examined with the IF-2 All-Color Anomaloscope. In all cases both the red-green equation of Rayleigh and the blue-green equation of Moreland were tested and three variables were determined: setting (matching) range (SR), calculated mid point (matching mid point) (CMP) and anomalous quotient (AQ) as compared to control group. RESULTS: No significant changes were found in the variables of the Rayleigh equation. However, in the blue-green equation SR was significantly enlarged in all tested groups and CMP was significantly shifted towards the short wavelength end of the match in first three groups. These results indicate a diminution of the color discriminating sensitivity in the short wavelength half of the visible spectrum and diminution of the blue cone sensitivity in glaucoma patients as well as in ocular hypertension (p < 0.001). In patients with glaucoma-like optic disc the setting range was enlarged in less degree (p < 0.01) without changes in the remaining variables (p > 0.05) what may be indicative of early stage of disease before the perimetric changes. CONCLUSION: Blue-green colour vision testing with the anomaloscope may serve as an additional test in the diagnostics of glaucoma. Glaucoma suspects with blue colour vision disturbances require the most careful investigation and if need be the recommendation of early treatment.

Adolescent↗
PubMed1978

Acquired color vision defects in retrobulbar neuritis.

We used the Farnsworth-Munsell 100 Hue Test to study the incidence of acquired color vision defects in 16 patients with unilateral and and seven patients with bilateral retrobulbar optic neuritis whose visual acuity had recovered to 6/12 (20/40) or better. We recorded the visual-evoked response to a pattern stimulus on the same day. All 30 affected eyes showed an excessive number of errors on Farnsworth-Munsell 100 Hue testing. The number of errors increased with greater residual optic nerve damage. One false-positive and two false-negative visual-evoked responses were found.

Adult↗
PubMed1992

Molecular basis of congenital color vision defects in Chinese patients.

Applying Southern blot hybridization, the structures of the red pigment gene (RPG) and the green pigment gene (GPG) were analyzed in 43 Chinese patients with red-green color vision defects, including 3 female cases of deuteranopia. The same analysis was carried out in 4 normal relatives and 3 carriers from 3 affected families, as well as in 11 normal controls. Among the 43 patients, abnormalities of the RPG were detected in all 19 protans, and abnormalities of the GPG were found in 14 of the 24 deutans. In about 80% of the protans and deutans, an alteration of exon 5 in RPG or GPG was discovered. All 19 protans had anomalous RPG and in one protan the normal RPG was replaced by a 5' red-3' green hybrid gene. However, no protans showed deletion of the whole RPG. Some deutans had no GPG; some had a 5' green-3' red hybrid gene with or without the GPG. The exon 5 of RPG and GPG was amplified by polymerase chain reaction (PCR) and the amplified fragments were further analyzed by RsaI digestion. The results of PCR were identical to those of nucleic acid hybridization. PCR will be a useful tool in prenatal diagnosis and genetic counseling.

Adolescent↗
PubMed1994

A study of spectral electroretinogram of color vision defects due to macular diseases.

Studies of spectral electroretinograms in central serous retinopathy (CSR) and hereditary macular degeneration (HMD) showed that the b-wave amplitudes of most wavelengths of CSR were significantly decreased as compared with normal controls, and those of HMD were obviously lower than the normal values. Patients of HMD with type-A color vision defects (CVD) had primarily a reduction of b-wave amplitudes in the full spectrum of 480-620 nm, and patients with type-I CVD a reduction of b-wave amplitudes wave-lengths of 480-560 nm. These differences might reflect differences in damages to the medium-and long-wave length.

Adolescent↗
PubMed1981

Color vision defects in retinitis pigmentosa.

Sixty-seven patients with retinitis pigmentosa underwent color vision testing with the Nagel anomaloscope and Farnsworth-Munsell (FM) 100-hue test. Results showed both similarities and differences among different genetic types. The presence of an atrophic-appearing foveal lesion found in individual cases served as a reliable indicator of performance on color vision testing as did a reduction in visual acuity to less than 20/30. When no foveal lesion was apparent in patients with visual acuity better than 20/30, patients with autosomal dominant disease showed superior performance on color vision testing when compared to autosomal recessive, X-linked recessive, and isolated cases. Regardless of genetic type, the FM 100-hue test was more sensitive in detecting poor color vision performance than the Nagel anomaloscope.

Adolescent↗
PubMed1993

[A study of spectral electroretinograms of color vision defects due to macular diseases].

Studies of spectral electroretinograms in central serous chorioretinopathy (CSC) and hereditary macular degeneration (HMD) found that the b-wave amplitudes of CSC for most wavelengths were significantly decreased as compared with normal controls, and the b-wave amplitudes of HMD for most wavelengths were obviously lower than the normal values. Patients of HMD with type-A color vision defects (CVD) showed primarily a reduction of b-wave amplitudes for the full spectrum of 480-620 nm, and patients with type-I CVD a reduction of b-wave amplitudes for wavelengths of 480-560 nm. These differences might reflect differences in damages to the medium-and long-wave length cones.

Adolescent↗
PubMed1998

Severity of color vision defects: electroretinographic (ERG), molecular and behavioral studies.

Earlier research on phenotype/genotype relationships in color vision has shown imperfect predictability of color matching from the photopigment spectral sensitivities inferred from molecular genetic analysis. We previously observed that not all of the genes of the X-chromosome linked photopigment gene locus are expressed in the retina. Since sequence analysis of DNA does not necessarily reveal which of the genes are expressed into photopigments, we used ERG spectral sensitivities and adaptation measurements to assess expressed photopigment complement. Many deuteranomalous subjects had L, M, and L-M hybrid genes. The ERG results showed that M pigment is not present in measurable quantities in deutan subjects. Using these results to determine gene expression improved the correlations between inferred pigment separation and color matching. Furthermore, we found a subject who had normal L and M genes and normal proximal promoter sequences, yet he had a single photopigment (M) by ERG and tested as a protanope. These results demonstrate the utility of ERG measurements in studies of molecular genetics of color vision deficiencies, and further support the conclusion that not all genes are expressed in color deficient subjects. In particular, deuteranomaly requires a presently unknown mechanism of selective expression which excludes normal M genes and allows expression of L-M hybrid genes in one cone type, and the normal L in another.

Adaptation, Ocular↗