Cases reported "Color Vision Defects"

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11/161. Familial congenital monochromatism, cataracts, and sensorineural deafness.

    Two sisters had diagnoses of congenital monochromatism, cataracts, bilateral nonprogressive sensorineural deafness, and hyperinsulinism in both, and labyrinthine dysfunction in one. This recessively inherited condition is added to the growing number of syndromes in which one of the features may be a disturbance of hypothalamic function. ( info)

12/161. 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. ( info)

13/161. A typical case study correcting color deficiency.

    Within one month after visiting his optometrist, a 14-year-old color deficient vocational high school student was able to sufficiently improve his color discrimination and his perception of objects which blend with their background, so as to continue with his study in electronics. The three prescribed sessions were adequate and the student was very pleased with his color improvement. ( info)

14/161. The luminance fall in anomaloscope examination: clinical examples.

    PURPOSE: The evaluation of the anomaloscope slope quotient in patients with acquired colour vision deficiency. methods: Two patients with Stargardt's disease in combination with protanomaly and deuteranomaly, respectively, were selected and also 3 patients with a presumed dominant optic atrophy of the protan type. The anomaloscope examination was performed according to the Linksz procedure. The luminance fall was calculated as the slope quotient SQ:Y units luminance fall per X units width of the matching range. RESULTS: The SQ of the 2 Stargardt patients was steeper than the SQ of congenital colour vision defectives, especially at the red end of the anomaloscope green-red mixture scale, indicating pathologic scotopization superimposed on the congenital deficiency. In optic atrophy of the protan type the SQ was flatter than in congenital deficiency, indicating that this deficiency has nothing to do with congenital protan deficiency. CONCLUSION: Calculation of the slope quotient SQ is helpful for the diagnosis of acquired colour vision deficiency, especially when the subject also has a congenital colour vision deficiency or is supposed to have such a deficiency. ( info)

15/161. Neurological deficits in solvent-exposed painters: a syndrome including impaired colour vision, cognitive defects, tremor and loss of vibration sensation.

    Five individuals are described who had participated in a study of former dockyard painters. All had worked between 16 years and 45 years as industrial painters, much of the time inside ships. All underwent structured neurological examination, colour vision testing (allowing calculation of a colour confusion index corrected for age and alcohol), and detailed psychometric testing. An occupational history sufficient to allow estimation of past exposure to solvents was taken. All gave a history of exposure to high concentrations of solvents at work, and several described episodes of acute narcosis. All showed neurological deficits and some had overt neurological disease, although in no case had this previously been linked to their work. The most striking features, sufficient to constitute a syndrome, were acquired blue-yellow colour vision deficits, coarse tremor, impaired vibration sensation in the legs and cognitive impairment. Their estimated cumulative exposures to solvents ranged between the equivalent of 13 and 37 calendar years working at the occupational exposure Standard concentration (OES years). This study for the first time gives an indication of the concentrations of solvents likely to lead to serious neurological disease in humans. It serves as a reminder to physicians to take an occupational history from patients with obscure neurological or psychological impairment. ( info)

16/161. 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. ( info)

17/161. Macular dystrophy with protan genotype and phenotype studied with cone type specific ERGs.

    PURPOSE: To determine the L- and M-cone driven ERG responses in a male patient with macular dystrophy and a protan phenotype. methods: We measured large field ERG thresholds to stimuli which modulated exclusively the L- or the M-cones or the two in various combinations (both in-phase and in counterphase). In none of the stimuli, the S-cones were modulated. Additionally, standard and multifocal ERGs were measured. Analysis of the L- and M-cone pigment genes was performed by means of PCR, RFLP analysis and dna sequencing techniques. RESULTS: Macular dystrophy was revealed by the markedly abnormal multifocal ERGs in presence of near normal standard ERGs. The large field ERG responses were exclusively driven by the M-cones with enlarged thresholds when compared with otherwise normal protanopes. In addition, the M-cone driven ERG response phases were abnormal. Pigment gene analysis confirmed a protan genotype with the presence of a single 5'red/3'green hybrid pigment gene. CONCLUSIONS: Our novel stimulus technique allows a reliable analysis of the separate cone pathways even in cases with macular dysfunction. The increased thresholds and the abnormal phase behavior of the M-cone driven ERGs reflect altered mechanisms of the retinal physiology in this patient. The data strongly suggest that the macular dystrophy and the protanopia have independent origins. ( info)

18/161. 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. ( info)

19/161. 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. ( info)

20/161. 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. ( info)
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