1/96. Complete sparing of high-contrast color input to motion perception in cortical color blindness.It is widely held that color and motion are processed by separate parallel pathways in the visual system, but this view is difficult to reconcile with the fact that motion can be detected in equiluminant stimuli that are defined by color alone. To examine the relationship between color and motion, we tested three patients who had lost their color vision following cortical damage (central achromatopsia). Despite their profound loss in the subjective experience of color and their inability to detect the motion of faint colors, all three subjects showed surprisingly strong responses to high-contrast, moving color stimuli--equal in all respects to the performance of subjects with normal color vision. The pathway from opponent-color detectors in the retina to the motion analysis areas must therefore be independent of the damaged color centers in the occipitotemporal area. It is probably also independent of the motion analysis area MT/V5, because the contribution of color to motion detection in these patients is much stronger than the color response of monkey area MT.- - - - - - - - - - ranking = 1keywords = visual, contrast (Clic here for more details about this article) |
2/96. A locus for autosomal recessive achromatopsia on human chromosome 8q.Autosomal recessive achromatopsia is a rare disorder characterized by total absent color vision, nystagmus, photophobia, and visual impairment, frequently leading to 'legal blindness'. The primary defect is at the photoreceptor level, with retinal cones being absent or defective. The first locus for this disorder was mapped to chromosome 2q11. Here, we confirm the genetic mapping of a locus discovered in our studies of a kindred with Irish ancestry, but no known consanguinity, in which 5 of 12 children are affected. We have mapped the locus in this disorder in this family to chromosome 8q. Available data now narrow the region containing the putative gene to 1.2 cM.- - - - - - - - - - ranking = 0.69100480204673keywords = visual (Clic here for more details about this article) |
3/96. Toxic optic neuropathy after concomitant use of melatonin, zoloft, and a high-protein diet.melatonin is a neuromodulating hormone found in the pineal gland and retina. It is involved in light-dark circadian rhythms and mediates retinal processes in a manner antagonistic to that of dopamine. Zoloft (sertraline) is an antidepressant drug that blocks the reuptake of serotonin at the neural synapse. serotonin is the natural precursor of melatonin. A 42-year-old woman sought treatment for visual acuity loss, dyschromatopsia, and altered light adaptation. Neuro-ophthalmologic examination was otherwise normal except for evolving bilateral cecocentral scotomas. She had taken Zoloft for 4 years and began a high-protein diet with melatonin supplementation 2 weeks before onset of visual symptoms. visual acuity and color vision improved within 2 months after melatonin and the high-protein diet were discontinued. Combined use of melatonin, Zoloft, and a high-protein diet may have resulted in melatonin/dopamine imbalance in the retina, manifesting as a toxic optic neuropathy. physicians and patients should be alerted to this potential drug interaction.- - - - - - - - - - ranking = 1.3820096040935keywords = visual (Clic here for more details about this article) |
4/96. Hemianopic colour blindness.A man developed cortical blindness after cerebral infarction in the distribution of both posterior cerebral arteries. When he recovered from this condition, he was found to be colour blind in the left visual field, but not in the right. This unusual situation resulted in apparently contradictory performances on hemifield and free-field tasks of colour discrimination, naming, and recognition. The contradictions may be explained by interhemispheric competition between a hemisphere which could discriminate colours and a hemisphere which was colour blind.- - - - - - - - - - ranking = 0.69100480204673keywords = visual (Clic here for more details about this article) |
5/96. An acquired color defect of the opponent-color system.An acquired unilateral color defect in a 22-year-old man has been investigated with standard clinical tests and by using techniques which, it is thought, test specifically for the sensitivity of the luminance and opponent-color systems. The spectral sensitivity of the defective left eye, using 1 degree 200 ms. test flashes on a white background, has a single broad peak at about 550 nm. and resembles the photopic luminosity curve; in contrast, the normal curve, measured in the same conditions, has three peaks at about 440, 520, and 600 nm. However, the subject's spectral sensitivity curve for detecting 20 Hz. flicker is quite normal and is similar to his curve for 200 ms. flashes. It has recently been proposed that the three peaks of the normal curve for 200 ms. flashes reflect the activity of the opponent-color system, whereas the single peak for flicker detection is related to the luminance system. The preceding observations may thus be interpreted in terms of a specific loss of the subject's opponent-color system and this would explain his poor color discrimination. His luminance system appears to be normal, and evidence is presented for the maintained function of red- and green-sensitive (but not blue-sensitive) cones. The spectral sensitivity of the subject's right eye is nearly normal, suggesting a precortical origin of the defect; however, there seems to be some abnormality in this eye, indicating a less developed form of the same defect.- - - - - - - - - - ranking = 6.4927514701908keywords = sensitivity, contrast (Clic here for more details about this article) |
6/96. Rod monochromatism -- an incomplete form.An incomplete form of rod monochromatism is described in a young man with normal visual acuity and absence of nystagmus or photophobia. ERG showed normal threshold sensitivity in white and blue lights but virtual absence of the first portion of response in red light. The sensory threshold curve lacked the typical rod-cone discontinuity, whereas the curve after full dark adaptation was normal. It is suggested that the condition is due to atypical disfunction of the cones.- - - - - - - - - - ranking = 2.2987429096968keywords = sensitivity, visual (Clic here for more details about this article) |
7/96. Leber hereditary optic neuropathy associated with antiretroviral therapy for human immunodeficiency virus infection.PURPOSE: Antiretroviral therapy has reduced the morbidity and mortality associated with human immunodeficiency virus (hiv) infection. However, side effects are increasingly recognized, including a commonly reported toxic mitochondrial myopathy. We report such a case of Leber hereditary optic neuropathy in a patient with antiretroviral therapy for hiv infection and speculate on a possible toxic etiologic role in the development of Leber hereditary optic neuropathy by a shared mitochondrial mechanism. methods: Case Report. Bilateral optic disk abnormalities observed in a 38-year-old hiv positive man with a family history of Leber hereditary optic neuropathy were documented with fundus photography, color vision testing, and visual field testing. Mitochondrial dna testing was used to confirm the genetic predisposition to Leber hereditary optic neuropathy. RESULTS: Progressive bilateral optic nerve pallor temporally associated with the administration of antiretroviral medication was observed. Diagnostic testing revealed progressive visual field and color vision loss as well as a mitochondrial dna mutation consistent with Leber hereditary optic neuropathy. CONCLUSION: Antiretroviral therapy may be associated with the onset of Leber hereditary optic neuropathy in genetically predisposed patients.- - - - - - - - - - ranking = 1.3820096040935keywords = visual (Clic here for more details about this article) |
8/96. Disc excavation in dominant optic atrophy: differentiation from normal tension glaucoma.OBJECTIVE: In patients with dominant optic atrophy (DOA, Kjer type), excavation of the optic nerve develops, and these patients may be misdiagnosed as having normal tension glaucoma (NTG). This study examined disc morphologic features in patients with DOA and explored features that help distinguish this condition from NTG. DESIGN: Noncomparative, observational case series. PARTICIPANTS: patients with DOA who were seen at the Duke University eye Center between 1987 and 1996 and who had bilateral optic nerve photographs. methods: Retrospective chart review of the results of visual acuity testing, visual field testing by Goldmann perimetry, color vision testing, intraocular pressure measurement, and observation of bilateral optic nerve photographs. MAIN OUTCOME MEASURES: Appearance of the optic disc and peripapillary zone in patients with DOA. RESULTS: Nine patients were identified. The mean age at the time of evaluation was 28 years (range, 11-62 years). Most patients had a mild to moderate reduction in visual acuity. color vision as tested with Hardy-Rand-Rittler plates was reduced (4.0/10 /- 4.2/10). A cup-to-disc ratio of more than 0.5 was observed in at least one eye of eight patients. A temporal wedge-shaped area of excavation was observed in 14 of the 18 eyes studied. Moderate to severe temporal pallor was observed in all of the eyes. pallor of the remaining (noncupped) neuroretinal rim was also observed consistently, ranging from mild to moderate. A gray crescent and some degree of peripapillary atrophy were noted in all eyes. CONCLUSIONS: Several clinical features, including early age of onset, preferential loss of central vision, sparing of the peripheral fields, pallor of the remaining neuroretinal rim, and a family history of unexplained visual loss or optic atrophy, help to distinguish patients with DOA from those with NTG.- - - - - - - - - - ranking = 2.7640192081869keywords = visual (Clic here for more details about this article) |
9/96. Localization of hemiachromatopsia.Impaired color perception with relative preservation of form vision (achromatopsia) caused by cerebral lesions was first described over a century ago. However, for many years some researchers questioned the existence of an area of cerebral cortex apart from the primary visual cortex specialized in color processing. The development of sophisticated structural and functional neuroimaging techniques has allowed verification of the cortical structures important in color perception. We describe a case of a patient with impaired color perception in one hemifield of vision (hemiachromatopsia) and compare the localization of the lesion with previous cases described in the literature. These cases show that lesions of the ventromedial occipital cortex can impair color perception and leave form vision intact.- - - - - - - - - - ranking = 0.69100480204673keywords = visual (Clic here for more details about this article) |
10/96. A disorder of colour perception associated with abnormal colour after-images: a defect of the primary visual cortex.A 64 year old woman with posterior cortical atrophy secondary to probable Alzheimer's disease is described. Her presenting symptom was of seeing objects as abnormally coloured after prior exposure to a coloured stimulus. Formal testing disclosed that the patient experienced colour after-images of abnormal latency, duration, and amplitude.The demonstration of prolonged colour after-images in a patient with a cortical disease process provides strong evidence that the generation of colour after-images is mediated at least in part by the visual cortex. A mechanism for the generation of colour after-images is proposed in which abnormal prolongation of the images results from excessive rebound inhibition of previously excited wavelength selective neurons in V1. This may occur as a consequence of the relative sparing of inhibitory interneurons in V1 in the context of the degeneration of excitatory neurons that occurs in Alzheimer's disease.- - - - - - - - - - ranking = 3.4550240102337keywords = visual (Clic here for more details about this article) |
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