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PubMed1978

Visual function in acute posterior multifocal placoid pigment epitheliopathy.

We examined a 19-year-old woman with acute posterior multifocal placoid pigment epitheliopathy one week after she noted blurring of central vision. Her corrected visual acuity was R.E.: 6/7.5 (20/25), and L.E.: 6/12 (20/40). The visual fields showed 10-degree pericentral scotomas. A color vision defect and an abnormal Stiles-Crawford effect were present. Dark adaptation showed a delayed time course, with normal final thresholds. The electro-oculogram was subnormal, suggesting widespread abnormality of the retinal pigment epithelium. Active lesions resolved within three weeks, but fluorescein angiography showed characteristic widespread residual changes. Within three weeks, she had normal visual acuity and a normal electro-oculogram. Other tests of visual function showed recovery with a slower time course. By one year, the visual fields, color matching, Stiles-Crawford effect, and dark adaptation were almost normal. Analysis of the color-matching data and Stiles-Crawford effect indicated that the abnormalities of macular function were caused by an underlying lesion of the pigment epithelium and photoreceptors. This caused a physical distortion of the photoreceptor layer and metabolic disfunction of the photoreceptors.

Adult↗
PubMed1979

Brief historical note: the concept of "gonadal dysgenesis".

The history of gonadal by dysgenesis cautions against overinterpretation of data: The streak gonads are neither the result of dysgenesis nor of embryonic origin but represent late fetal/neonatal degeneration; the X-chromatin-negative character of the buccal smear and the frequency of color vision defects did not indicate male sex in the Ullrich-Turner syndrome but rather an XO constitution; severity of dysgenesis did not correlate with risk of gonadal neoplasia but with genotype; the gonadal lesion in the Ullrich-Turner syndrome was not due to a pituitary defect but a primary ovarian lesion; patients with the Noonan syndrome do not have the Turner phenotype. The concept of gonadal dysgenesis, introduced to Kermauner in 1912, has outlived its usefulness. Improved methods of phenotype analysis, family studies, and endocrine and cytogenetic methods have showen it to be causally and pathogenetically heterogeneous and have contributed to a better identification and delineation of the several different genetic entities which it formerly comprised.

Europe↗
PubMed1990

Complicated hereditary spastic paraparesis with cerebral white matter lesions.

A family is described with 5 males in a single generation affected with a previously undescribed complicated form of hereditary spastic paraparesis (HSP). The disease is characterized by speech difficulties, lower limb spasticity and hyper-reflexia, mental retardation, cerebellar ataxia, and tremor. The disease starts in the first decade of life and progresses for 3 to 6 years before stabilizing. Magnetic resonance imaging (MRI) of the brain demonstrates bilateral posterior periventricular white matter lesions. Visual evoked responses are markedly prolonged, but electromyography (EMG) and nerve conduction velocity studies are normal. Three of the 4 living affected members of this pedigree exhibit red-green color vision defects. The presentation of a new complicated hereditary spastic paraparesis syndrome in this pedigree extends our understanding of the variability and heterogenity of this syndrome and suggests an approach for the evaluation of similar families in future genetic studies.

Adolescent↗
PubMed1979

Cerebral color blindness: an acquired defect in hue discrimination.

In contrast to the traditional view that striate visual cortex (area 17) is surrounded by two homogeneous cortical areas (areas 18 and 19), recent studies have shown that mammalian extrastriate visual cortex contains several anatomically and functionally distinct subregions. One such region, the V-4 complex of the rhesus monkey, is highly specialized for the analysis of color information, suggesting that a lesion in a homologous region might produce a defect in color vision while sparing other visual functions. We have studied a patient whose clinical syndrome supports this suggestion: a 44-year-old man with normal color vision suffered two cerebral infarctions that produced first a right and then a left superior homonymous quadrantanopia and also caused prosopagnosia, topographical disorientation, and severely impaired color vision. Computed tomography demonstrated extensive lesions in both inferior occipital lobes in the territories of the lateral branches of the posterior cerebral arteries, involving the lingual and medial occipitotemporal gyri bilaterally; these gyri contain the inferior portion of striate cortex and segments of extrastriate visual cortex. The patient had no difficulty in giving the correct color names associated with common objects presented either verbally or in outline drawings. Standardized testing with the Farnsworth-Munsell 100-hue test, the Nagel anomaloscope, and a method that tests for just-noticeable differences between monochromatic stimuli all showed that the patient's ability to distinguish one color from another was markedly imparied but not totally absent. In contrast, visual acuity, reading, visually guided eye movements, and stereopsis were normal. Cells in the V-4 complex of monkey extrastriate cortex are highly specialized for distinguishing one color from another; the hue discrimination deficit that was demonstrated in this patient with cerebral color blindness indicates that a region or regions with similar function has been damaged.

Adult↗
PubMed1986

Cone function and cone interaction in hereditary degenerations of the central retina.

Spectral sensitivity functions and the transient decrease of sensitivity to short wavelengths after the offset of yellow light (transient tritanopia) were measured by increment threshold techniques in patients suffering from hereditary macular degenerations. Color vision defects were determined by arrangement tests and the anomaloscope. Central areolar choroidal dystrophy was found to produce a mild protan defect and to reduce foveal spectral sensitivity throughout the visible spectrum by a factor of 100; it also abolishes transient tritanopia. Electroretinogram (ERG) was normal, electrooculogram (EOG) subnormal. Stargardt's disease, despite numerous fluorescent macular spots, does not abolish transient tritanopia nor does it reduce spectral sensitivity, although scotopic matches were performed on the Nagel anomaloscope. Only in severe, advanced cases was transient tritanopia reduced and spectral sensitivity found to follow the absorption spectrum of rods. Routine ERGs and EOGs were normal. Vitelliform macular degeneration, despite the ophthalmoscopically pronounced dystrophic macula, produced only very small changes in spectral sensitivity and transient tritanopia, although a widened matching range on the Nagel anomaloscope and electrophysiological abnormalities were found. Apparently damage of the retinal circuit which connects long and short wavelength-sensitive cones, caused by hereditary conditions, is different from that caused by retinotoxic drugs.

Adult↗
PubMed1991

Difficulty differentiating Leber's from dominant optic neuropathy in a patient with remote visual loss.

A 31-year-old man who inexplicably lost vision as a child was referred for evaluation of bilateral optic atrophy. Other family members had also suffered unexplained visual loss. He had asymmetric impairment of visual acuity, central scotomas, and optic disc pallor. He also had a tritan color vision defect and excavation of the temporal portion of his optic discs, two features that were consistent with autosomal dominant optic atrophy. However, examination of the mitochondrial DNA of the proband and of two of his relatives revealed a mutation at nucleotide 11778, known to be associated with Leber's hereditary optic neuropathy. This case illustrates the difficulty physicians may encounter when trying to clinically differentiate Leber's from dominant optic atrophy in patients with remote visual loss, and it emphasizes the importance of obtaining a molecular assay for a mitochondrial mutation in cases of ambiguously classified hereditary optic neuropathy.

Adult↗
PubMed1990

Distinguishing between clinical impairments due to optic nerve or macular disease.

Many optic neuropathies and subtle maculopathies may have similar clinical presentations. This represents a challenge to the ophthalmologist to distinguish between the two on clinical grounds. These patients may not have obvious signs and their symptoms may be ambiguous. For example, a young man presenting with optic neuritis may have similar complaints to one suffering from central serous retinopathy. Several general principles can be used to distinguish between optic neuropathies and maculopathies. Additionally, specific psychophysical tests can be of help. The most important aspect of the history is in establishing the tempo of onset, duration and resolution of the symptoms. Optic nerve lesions often produce symptoms described as dimness or grayness, whereas macular lesions usually reduce visual acuity and produce metamorphopsia. The clinical examination requires comparing optic nerve function studies (afferent pupillary defects, color vision and brightness sense) to visual acuity. Additionally, assessing the central visual field especially through Amsler grid testing or threshold Amsler grid testing is very useful. Certain psychophysical tests can be performed in the office. Threshold amsler grid testing, photostress testing, contrast sensitivity, and the Pulfrich phenomena can all be put to advantage in distinguishing between optic neuropathies and maculopathies.

Diagnosis, Differential↗
PubMed1987

Ability of deutan color defectives to perform simulated air traffic control tasks.

Air traffic controllers perform a variety of tasks which require them to identify, discriminate, and name colors. Qualification standards for this occupation require applicants and incumbents to have normal color vision. The validity of this standard has been questioned and is currently under review. In this study, 22 deutans and 78 normals were tested on a set of tasks which simulated critical tasks performed daily by air traffic controllers. The four tasks included discriminating red from black pencil marks on flight progress strips, color-naming of 1 degree and 0.1 degree discs, and identification of colored line segments embedded in a multicolored background. Deutans classified as mild were found to perform all tasks as well as normals. Moderate deutans performed only the large disc color-naming task as well as normals, whereas severe deutans performed none of the tasks as well as normals. Different methods for scoring the color vision tests were explored to determine their value as predictors of task performance. The D-15 relative error score was found to be the single best predictor of performance on the tasks (r-square = 0.602). It is concluded that mild deutan color defectives have adequate color vision for safe performance of several critical air traffic control tasks. Moderate and severe deutans do not. In addition, the results of several methods for scoring color vision tests can be used to predict group, but not individual, performance with high reliability.

Aviation↗
PubMed1988

A new perimetric color vision analyzer.

A new apparatus was developed for mapping the extrafoveal color vision, the perimetric color vision analyzer. A yellow test object with varying degrees of saturation is presented on a cathode ray tube color display in a random sequence at one of 10 points around the fixation spot. The background is a mosaic pattern consisting of gray spots of the same size and shape as the test object, with various luminances. Background patterns with or without a test object are presented alternately. The subject is instructed to press a key when he detects a yellow object in the background pattern. The luminance of the test object is in the same range as the background gray spots. Since the luminance of background spots is changed synchronously at random when the test object appears, the subject can detect the test object only by the difference in color saturation. The results show the color contrast sensitivity at every designated point in the central visual field. The clinical application of the perimetric color vision analyzer revealed extrafoveal color defects which could not be evaluated with conventional color vision tests. It also showed that in some chorioretinal and optic nerve disorders the topographic pattern of color contrast sensitivity disagrees with that of luminance contrast sensitivity measured with automated static perimetry.

Adult↗
PubMed1992

Vision defects in albinism.

We have examined the possible presence of color vision anomalies in 9 individuals (17 eyes, 1 blind) with fundus findings suggesting ocular albinism using the Ishihara plates, the 28-hue Roth test, and the Davico anomaloscope. Results indicate that four of these individuals show no sign of the anomalies expected in an albino in either of the two eyes. Of the remaining cases, two are simple deuteranomals in both eyes, according to Pickford's classification criteria. The rest have protanomaly; however, in these the deviation toward red appears in both eyes in only one subject, whereas in the other two subjects it appears in only one eye, their binocular color vision being basically normal. Our study shows that a large proportion of these albinos have photophobia, pendular nystagmus, strabismus, noticeable refractive errors (astigmatism and high myopia), and poor visual acuity [usually less than 6/30 (20/100) with correction]. The measurement of contrast sensitivity function (CSF) indicates that the frequency of 12 cpd cannot be perceived, even in binocular vision.

Adolescent↗
PubMed1979

The ability of color defectives to judge signal lights at sea.

Measures were made of the ability of color-defective men to judge correctly the colors of navigation lights (red, green, or white) presented to them at night under realistic sea conditions. Eighty-one color-defective men were employed; they were categorized as to type and degree of defect using a battery of five color-vision tests. While the average performance of the color-defective men was considerably poorer than that of 24 color normals, there were large individual differences within each category of defect. Attempts to account for these differences in performance by variations in acuity, intelligence, and motivation failed. The extent to which the data can be accounted for by modern color-vision theory is discussed.

Color Vision Defects↗