Amblyopia affects the ON visual pathway more than the OFF (original) (raw)
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The role of local contrast in the visual deficits of humans with naturally occurring amblyopia
Neuroscience Letters, 1992
We measured the positional acuity of amblyopic observers and their sensitivity to the local contrast information which provides the cue for the position judgement. Our results suggest that there exist fundamental differences in the neural losses in humans with strabismic and anisometropic amblyopia. The losses in positional acuity of anisometropic amblyopes may be accounted for on the basis of the reduced contrast sensitivity and increased neural pooling of the underlying visual filters; whereas strabismic amblyopes, like the normal periphery, show an extra loss, which may be accounted for on the basis of scrambling, or jitter in the topographic mapping of information from retina to cortex. Since neurons in the striate cortex of monkeys show precise positional coding [9], it would be of particular interest to examine the positional acuity and local contrast sensitivity in cortical neurons of monkeys with experimental amblyopia using the same stimuli to measure both.
The Amblyopic Deficit and Its Relationship to Geniculo-Cortical Processing Streams
Journal of Neurophysiology, 2010
Amblyopia or lazy eye is the most common cause of uniocular blindness in adults and is caused by a disruption to normal visual development as a consequence of unmatched inputs from the two eyes in early life, arising from a turned eye (strabismus), unequal refractive error (anisometropia), or form deprivation (e.g., cataract). Using high-field functional magnetic resonance imaging in a group of human adults with amblyopia, we previously demonstrated that reduced responses are observable at a thalamic level, that of the lateral geniculate nucleus (LGN). Here we investigate the selectivity of this deficit by using chromatic and achromatic stimuli that are designed to bias stimulation to one or other of the three ascending pathways (the parvocellular, magnocellular, and koniocellular). We find the greatest LGN deficit is for stimuli modulated along the chromatic, L/M cone opponent axis of color space, suggesting a selective loss of parvocellular function in the LGN. We also demonstrate...
Clinical Nutrition, 2006
We investigated neuronal correlates of amblyopic deWcits resulting from early onset strabismus or anisometropia by monitoring individual responses in retinotopically mapped cortical visual areas with functional magnetic resonance imaging (fMRI) in eight psychophysically assessed adult amblyopes. In lower visual areas (V1/V2), grating stimuli presented to the normal and the amblyopic eye evoked strong cortical responses, while responses to the amblyopic eye were progressively reduced in higher areas on the central visual pathway (V3a/VP; V4/V8; lateral occipital complex, LOC). Selective reduction for high spatial frequency gratings was especially obvious in LOC. This suggests that transmission of activity from the amblyopic eye is increasingly impaired while it is relayed towards higher processing levels. Elevated responses in parts of areas V1 and V2 to monocular stimulation of the amblyopic eye might be related to the spatial and temporal distortions experienced by some amblyopic subjects.
Investigative Opthalmology & Visual Science, 2007
The understanding of the site and nature of the cortical processing deficit in human amblyopia awaits the resolution of three fundamental questions about which there is, at present, much controversy: First, is area V1 affected as the present animal models would predict, but some imaging studies argue against? Second, how extensive is the loss of extrastriate function, and does it simply follow as a consequence of an impaired V1 input? Third, does the brain imaging deficit, be it striate or extrastriate, correlate with the welldocumented psychophysical loss?-a fundamental issue on which previous brain imaging studies are divided. METHODS. A spatially broadband stimulus was used to determine the functional MRI responses from the different retinotopically identified visual cortical areas in a group of normal (n ϭ 6) and a group of amblyopic (n ϭ 11) observers. Responses were compared between the amblyopic and fellow fixing eyes of amblyopes and between the dominant and nondominant eyes of normal subjects, in central and peripheral parts of the visual field. Psychophysical acuity and contrast sensitivity was also measured and its correlation with the brain imaging deficit determined. RESULTS. V1 was affected in most but not all cases; the brainimaging deficit involved extensive regions of extrastriate cortex and, at least with the stimuli used in the study, correlated with the V1 loss, suggesting a strong V1 influence; and neither the striate nor the extrastriate deficits correlated with the psychophysical contrast threshold losses at either high or low spatial frequencies. CONCLUSIONS. The results suggest that there are significant suprathreshold processing deficits that are not a consequence of the well-known threshold deficit. Our preoccupation over the past 30 years with the contrast detection deficit in amblyopia limited to the processing within a circumscribed part of V1 may have to be modified to include not only processing deficits for high-contrast stimuli but also the involvement of multiple extrastriate areas.
The Perceptual Consequences of Interocular Suppression in Amblyopia
Investigative Opthalmology & Visual Science, 2011
PURPOSE. It is known that information from an amblyopic eye can be strongly suppressed when both eyes are open. The authors investigated the way in which suppression influences the relative perception of suprathreshold contrast and luminance between a person's eyes under dichoptic viewing conditions. METHODS. Stimuli consisted of four patches of luminance or four patches containing gratings. Two patches were presented to each eye. Ten amblyopes with mild suppression (six strabismic, three anisometropic and strabismic, and one deprivation; mean age, 34.5 years) and three control observers with normal vision (mean age, 33.0 years) matched the appearance of the stimuli presented to each eye. The match involved manipulation of either luminance or contrast. RESULTS. Amblyopes with mild suppression decreased stimulus luminance in the fellow fixing eye or increased luminance in the amblyopic eye to achieve a match (mean matching luminance, 21.1 and 39.6 cd/m 2 for the fellow fixing eye and the amblyopic eye, respectively; standard luminance, 30 cd/m 2). This interocular mismatch was also observed when luminance was variable and contrast was kept constant (mean matching luminance, 22.8 cd/m 2 for the fellow fixing eye). On the other hand, the amblyopic eye showed no loss of perceived contrast. There was little or no mismatch between the two eyes of control participants with normal binocular vision. CONCLUSIONS. Amblyopes have monocular deficits in contrast perception but dichoptic deficits in luminance perception, suggesting that suppression in its mild form involves luminance processing.
Human brain …, 2009
The processing deficit in amblyopia is not restricted to just high spatial frequencies but also involves low-medium spatial frequency processing, for suprathreshold stimuli with a broad orientational bandwidth. This is the case in all three forms of amblyopia; strabismic, anisometropic, and deprivation. Here we use both a random block design and a phase-encoded design to ascertain (1) the extent to which fMRI activation is reduced at low-mid spatial frequencies in different visual areas, (2) how accurately spatial frequency is mapped across the amblyopic cortex. We report a loss of function to suprathreshold low-medium spatial frequency stimuli that involves more than just area VI, suggesting a diffuse loss in spatial frequency processing in a number of different cortical areas. An analysis of the fidelity of the spatial frequency cortical map reveals that many voxels lose their spatial frequency preference when driven by the amblyopic eye, suggesting a broader tuning for spatial frequency for neurons driven by the amblyopic eye within this low-mid spatial frequency range.
Strabismic amblyopia. Part 2. Neural processing
Clinical and Experimental Optometry
This is the second of a two-part survey of current literature concerning strabismic amblyopia. The aim of this review is to bring the optometric community up to date on the status of scientific research into strabismic amblyopia. Part 1 in this series discussed research into strabismic amblyopia from the viewpoint of psychophysical experiments, which investigate both spatial and temporal behavioural deficits accompanying strabismic amblyopia. These include deficits in contrast sensitivity, spatial localisation, fixation, ocular motility, accommodation, crowding, attention, motion perception and temporal processing. Part 2 concerns neural processing in regards to strabismic amblyopia. It discusses current understanding of more fundamental aspects of central processing of visual information and in particular current theories regarding neural sites and mechanisms involved in amblyopia.
Spatial interactions reveal inhibitory cortical networks in human amblyopia
Vision Research, 2005
Humans with amblyopia have a well-documented loss of sensitivity for first-order, or luminance defined, visual information. Recent studies show that they also display a specific loss of sensitivity for second-order, or contrast defined, visual information; a type of image structure encoded by neurons found predominantly in visual area A18/V2. In the present study, we investigate whether amblyopia disrupts the normal architecture of spatial interactions in V2 by determining the contrast detection threshold of a second-order target in the presence of second-order flanking stimuli. Adjacent flanks facilitated second-order detectability in normal observers. However, in marked contrast, they suppressed detection in each eye of the majority of amblyopic observers. Furthermore, strabismic observers with no loss of visual acuity show a similar pattern of detection suppression. We speculate that amblyopia results in predominantly inhibitory cortical interactions between second-order neurons.