Normal fixation of eccentric targets*

Sansbury, Richard V.; Skavenski, Alexander A.; Haddad, Genevieve M.; Steinman, Robert M.

doi:10.1364/josa.63.000612

Cited by 57 publications

(38 citation statements)

References 8 publications

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“…Results of Sansbury et al (1973) support this idea. In their experienced normal subjects, as error signals were generated by more peripheral retinal regions, small increases (a few minutes of arc) in drift magnitude were found.…”

Section: Discussionmentioning

confidence: 58%

Increased drift in amblyopic eyes.

Ciuffreda¹,

Kenyon²,

Stark³

1980

British Journal of Ophthalmology

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Reports are conflicting on the presence of increased drift in amblyopic eyes. Furthermore, the individual effects of either amblyopia or strabismus alone on ocular drift have not been systematically investigated. We therefore used a photoelectric method to record horizontal eye position during monocular and binocular fixation in patients having amblyopia without strabismus, intermittent strabismus, or constant strabismus amblyopia. Our principal finding was increased drift amplitude (up to 3 5 degrees) and velocity (up to 3 0 degrees per second) in amblyopic eyes during monocular fixation. While increased drift was found 75 % of the time in amblyopia without strabismus and 50% of the time in constant strabismus amblyopia, it was found only 20% of the time in intermittent strabismus. Amblyopic drift could be either error-producing or error-correcting in nature. Increased drift was not present during monocular fixation with the dominant eye or during binocular fixation in any of our 16 patients. We therefore conclude that amblyopia and not strabismus is a necessary condition for the presence of markedly increased fixational drift. Increased drift amplitude but not velocity may adversely affect visual acuity in the amblyopic eye.

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Section: Discussionmentioning

confidence: 58%

Increased drift in amblyopic eyes.

Ciuffreda¹,

Kenyon²,

Stark³

1980

British Journal of Ophthalmology

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“…It has been shown that participants with normal vision who endeavor to fixate on a peripheral target exhibit a substantial decrease in fixation stability. Sansbury et al (1973) developed a paradigm for comparing stability of central fixation and peripheral fixation at about 10 deg. Fixation was 3-4 times less stable with peripheral fixation.…”

Section: Preferred Retinal Locus (Prl)mentioning

confidence: 99%

Functional and cortical adaptations to central vision loss

2005

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Age-related macular degeneration (AMD), affecting the retina, afflicts one out of ten people aged 80 years or older in the United States. AMD often results in vision loss to the central 15-20 deg of the visual field (i.e. central scotoma), and frequently afflicts both eyes. In most cases, when the central scotoma includes the fovea, patients will adopt an eccentric preferred retinal locus (PRL) for fixation. The onset of a central scotoma results in the absence of retinal inputs to corresponding regions of retinotopically mapped visual cortex. Animal studies have shown evidence for reorganization in adult mammals for such cortical areas following experimentally induced central scotomata. However, it is still unknown whether reorganization occurs in primary visual cortex (V1) of AMD patients. Nor is it known whether the adoption of a PRL corresponds to changes to the retinotopic mapping of V1. Two recent advances hold out the promise for addressing these issues and for contributing to the rehabilitation of AMD patients: improved methods for assessing visual function across the fields of AMD patients using the scanning laser ophthalmoscope, and the advent of brain-imaging methods for studying retinotopic mapping in humans. For the most part, specialists in these two areas come from different disciplines and communities, with few opportunities to interact. The purpose of this review is to summarize key findings on both the clinical and neuroscience issues related to questions about visual adaptation in AMD patients.

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“…These fixational eye movements include ''microsaccades,'' small ballistic unidirectional eye movements that are generated at random intervals in all directions. Fixational eye movements, including microsaccades, have been correlated with stimulus visibility (5)(6)(7)(8), and in a previous paper we showed that microsaccades increase the probability of firing in area V-1 cells by moving their receptive fields over stationary stimuli (9). Here we ask whether microsaccades might also induce an increase in neural activity at an earlier level, in the neurons of the lateral geniculate nucleus (LGN).…”

mentioning

confidence: 91%

The function of bursts of spikes during visual fixation in the awake primate lateral geniculate nucleus and primary visual cortex

Martínez-Conde

Macknik

Hubel

2002

Proc. Natl. Acad. Sci. U.S.A.

226

197

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When images are stabilized on the retina, visual perception fades. During voluntary visual fixation, however, constantly occurring small eye movements, including microsaccades, prevent this fading. We previously showed that microsaccades generated bursty firing in the primary visual cortex (area V-1) in the presence of stationary stimuli. Here we examine the neural activity generated by microsaccades in the lateral geniculate nucleus (LGN), and in the area V-1 of the awake monkey, for various functionally relevant stimulus parameters. During visual fixation, microsaccades drove LGN neurons by moving their receptive fields across a stationary stimulus, offering a likely explanation of how microsaccades block fading during normal fixation. Bursts of spikes in the LGN and area V-1 were associated more closely than lone spikes with preceding microsaccades, suggesting that bursts are more reliable than are lone spikes as neural signals for visibility. In area V-1, microsaccadegenerated activity, and the number of spikes per burst, was maximal when the bar stimulus centered over a receptive field matched the cell's optimal orientation. This suggested burst size as a neural code for stimuli optimality (and not solely stimuli visibility). As expected, burst size did not vary with stimulus orientation in the LGN. To address the effectiveness of microsaccades in generating neural activity, we compared activity correlated with microsaccades to activity correlated with flashing bars. Onset responses to flashes were about 7 times larger than the responses to the same stimulus moved across the cells' receptive fields by microsaccades, perhaps because of the relative abruptness of flashes. When the visual world is stabilized on the retina, visual perception fades as a consequence of neural adaptation (1-4). But during normal vision we move our eyes involuntarily every few hundred milliseconds, even as we try to fixate our gaze on a small stimulus, preventing retinal stabilization and the associated fading of visibility. These fixational eye movements include ''microsaccades,'' small ballistic unidirectional eye movements that are generated at random intervals in all directions. Fixational eye movements, including microsaccades, have been correlated with stimulus visibility (5-8), and in a previous paper we showed that microsaccades increase the probability of firing in area V-1 cells by moving their receptive fields over stationary stimuli (9). Here we ask whether microsaccades might also induce an increase in neural activity at an earlier level, in the neurons of the lateral geniculate nucleus (LGN). We also ask how effective microsaccades are in generating neural activity by comparing them with previously characterized and well known visual stimuli, flashing bars. Finally, because transient neural firing (i.e., bursts of spikes) has been proposed as a neural code for the visibility of a stimulus (9-12), we also ask here whether bursts of spikes are used by the visual system to encode the salience of a stimulus. To answer thi...

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Normal fixation of eccentric targets*

Cited by 57 publications

References 8 publications

Increased drift in amblyopic eyes.

Increased drift in amblyopic eyes.

Functional and cortical adaptations to central vision loss

The function of bursts of spikes during visual fixation in the awake primate lateral geniculate nucleus and primary visual cortex

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