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At least 253 records · Page 14Linked to original sources
PubMed2003

[Disorders of color vision].

This review gives a summary of all colour vision disorders (dyschromatopsias) and diagnostic methods and tests. Colour vision is inadequately treated in current literature with regard to the choice of diagnostic methods and the interpretation of results for a single disorder, which contributes to wrong dyschromatopsia diagnosing seen every day in specialist practice. Examination for colour disorders is usually outpatient and is carried out by ophthalmology or neurology departments or occupational health services under the supervision of an ophthalmologist to prevent misinterpretation of results and wrong occupational choices. The problem is very serious, and proper education should be able to provide guidelines for correct and early diagnosis of dyschromatopsia. As the examination is not well defined, it is very important to set unique criteria in diagnosing any single colour vision disorder.

Color Perception Tests↗
PubMedDate not supplied

Central disorders of vision in humans.

Over the past 20 years, researchers have discovered over 30 separate visual areas in the cortex of the macaque monkey that exhibit specific responses to visual and environmental stimuli. Many of these areas are homologous to regions of the human visual cortex, and numerous syndromes involving these areas are described in the neurologic and ophthalmic literature. The focus of this review is the anatomy and physiology of these higher cortical visual areas, with special emphasis on their relevance to syndromes in humans. The early visual system processes information primarily by way of two separate systems: parvocellular and magnocellular. Thus, even at this early stage, visual information is functionally segregated. We will trace this segregation to downstream areas involved in increasingly complex visual processing and discuss the results of lesions in these areas in humans. An understanding of these areas is important, as many of these patients will first seek the attention of the ophthalmologist, often with vague, poorly defined complaints that may be difficult to specifically define.

Animals↗
PubMed1999

Genetic disorders of vision revealed by a behavioral screen of 400 essential loci in zebrafish.

We examined optokinetic and optomotor responses of 450 zebrafish mutants, which were isolated previously based on defects in organ formation, tissue patterning, pigmentation, axon guidance, or other visible phenotypes. These strains carry single point mutations in >400 essential loci. We asked which fraction of the mutants develop blindness or other types of impairments specific to the visual system. Twelve mutants failed to respond in either one or both of our assays. Subsequent histological and electroretinographic analysis revealed unique deficits at various stages of the visual pathway, including lens degeneration (bumper), melanin deficiency (sandy), lack of ganglion cells (lakritz), ipsilateral misrouting of axons (belladonna), optic-nerve disorganization (grumpy and sleepy), inner nuclear layer or outer plexiform layer malfunction (noir, dropje, and possibly steifftier), and disruption of retinotectal impulse activity (macho and blumenkohl). Surprisingly, mutants with abnormally large or small eyes or severe wiring defects frequently exhibit no discernible behavioral deficits. In addition, we identified 13 blind mutants that display outer-retina dystrophy, making this syndrome the single-most common cause of inherited blindness in zebrafish. Our screen showed that a significant fraction (approximately 5%) of the essential loci also participate in visual functions but did not reveal any systematic genetic linkage to particular morphological traits. The mutations uncovered by our behavioral assays provide distinct entry points for the study of visual pathways and set the stage for a genetic dissection of vertebrate vision.

Albinism↗
PubMed2003

Developmental disorders of vision.

This review of developmental disorders of vision focuses on only a few of the many disorders that disrupt visual development. Given the enormity of the human visual system in the primate brain and complexity of visual development, however, there are likely hundreds or thousands of types of disorders affecting high-level vision. The rapid progress seen in developmental dyslexia and WMS demonstrates the possibilities and difficulties inherent in researching such disorders, and the authors hope that similar progress will be made for congenital prosopagnosia and other disorders in the near future.

Brain↗
PubMed2003

Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are.

As ophthalmologists we need a basic model of how the higher visual system works and its common disorders. This presentation aims to provide an outline of such a model. Our ability to survey a visual scene, locate and recognise an object of interest, move towards it and pick it up, recruits a number of complex cognitive higher visual pathways, all of which are susceptible to damage. The visual map in the mind needs to be co-located with reality and is primarily plotted by the posterior parietal lobes, which interact with the frontal lobes to choose the object of interest. Neck and extraocular muscle proprioceptors are probably responsible for maintaining this co-location when the head and eyes move with respect to the body, and synchronous input from both eyes is needed for correct localisation of moving targets. Recognition of what is being looked at is brought about by comparing the visual input with the "image libraries" in the temporal lobes. Once an object is recognised, its choice is mediated by parietal and frontal lobe tissue. The parietal lobes determine the visual coordinates and plan the visually guided movement of the limbs to pick it up, and the frontal lobes participate in making the choice. The connection between the occipital lobes and the parietal lobes is known as the dorsal stream, and the connection between the occipital lobes and the temporal lobes, comprises the ventral stream. Both disorders of neck and extraocular muscle proprioception, and disorders leading to asynchronous input along the two optic nerves are "peripheral" causes of impaired visually guided movement, while bilateral damage to the parietal lobes can result in central impairment of visually guided movement, or optic ataxia. Damage to the temporal lobes can result in impaired recognition, problems with route finding and poor visual memory. Spontaneous activity in the temporal lobes can result in formed visual hallucinations, in patients with impaired central visual function, particularly the elderly. Deficits in cognitive visual function can occur in different combinations in both children and adults depending on the nature and distribution of the underlying brain damage. In young children the potential for recovery can lead to significant improvement in parietal lobe function with time. Patients with these disorders need an understanding of their deficits and a structured positive approach to their rehabilitation.

Adult↗
PubMed1997

Psychogenic disorders of vision in childhood ("visual conversion reactions"): perspectives from adolescence: a research note.

Fifteen adolescents who had exhibited psychogenic disorders of vision in childhood were compared with a control group of adolescents who had experienced childhood visual dysfunction of organic origin. The principal modes of assessment were clinical interviews, the Parental Bonding Instrument (PBI), and self-report measures concerning specific personality traits. Adolescents who had previously presented with psychogenic disorder were more likely to (1) report having experienced school difficulties and the loss of a significant figure at the time of presentation, (2) rate their mothers as over-involved on the PBI and (3) report adjustment difficulties and obsessional personality traits in adolescence.

Adolescent↗