Visual Processing in Amblyopia: Human Studies
University of California at Berkeley, School of Optometry, Berkeley, CA 94720, USA. Strabismus
04/2006; 14(1):11-9. DOI: 10.1080/09273970500536243
Within the last five years, there have been a number of exciting new advances in our knowledge and understanding of amblyopia. This article reviews recent psychophysical studies of naturally occurring amblyopia in humans. These studies suggest that: 1) There are significant differences in the patterns of visual loss among the clinically defined categories of amblyopes. A key factor in determining the nature of the loss is the presence or absence of binocularity. 2) Dysfunction within the amblyopic visual system first occurs in area V1, and the effects of amblyopia may be amplified downstream. 3) There appears to be substantial neural plasticity in the amblyopic brain beyond the "critical period."
Available from: Marco Milanese
- "Amblyopia is the most common impairment of visual function affecting one eye in adults, with a prevalence of about 1e5% of the total world population (Holmes and Clarke, 2002). This pathology is caused by early abnormal visual experience with a functional imbalance between the two eyes owing to anisometropia, strabismus or congenital cataract, resulting in a dramatic loss of visual acuity in an apparently healthy eye and a broad range of other perceptual abnormalities, including deficits in contrast sensitivity and in stereopsis (Lewis and Maurer, 2005; Levi, 2006). In animal models, amblyopia can be artificially caused by imposing a longterm reduction of inputs from one eye by lid suture (monocular deprivation, MD) (Smith, 1981; Harwerth et al., 1983; Prusky et al., 2000a,b), or by inducing experimental anisometropia or strabismus (Singer et al., 1980; Mitchell et al., 1984; Kiorpes et al., 1998). "
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ABSTRACT: Amblyopia is one of the most common forms of visual impairment, arising from an early functional imbalance between the two eyes. It is currently accepted that, due to a lack of neural plasticity,amblyopia is an untreatable pathology in adults. Environmental enrichment (EE) emerged as a strategy highly effective in restoring plasticity in adult animals, eliciting recovery from amblyopia through a reduction of intracortical inhibition. It is unknown whether single EE components are able to promote plasticity in the adult brain, crucial information for designing new protocols of environmental stimulation suitable for amblyopic human subjects. Here, we assessed the effects of enhanced physical exercise,increased social interaction, visual enrichment or perceptual learning on visual function recovery in adult amblyopic rats. We report a complete rescue of both visual acuity and ocular dominance in exercised rats, in animals exposed to visual enrichment and in animals engaged in perceptual learning.These effects were accompanied by a reduced inhibition/excitation balance in the visual cortex. In contrast, we did not detect any sign of recovery in socially enriched rats or in animals practicing a purely associative visual task. These findings could have a bearing in orienting clinical research in the field of amblyopia therapy.
Available from: Herb Goltz
- "Perceptual deficits associated with amblyopia have been studied extensively (for review see , ); however, the effects of the visual impairments on motor behaviours have not received similar attention. Several recent studies have addressed this gap in the literature by examining the effect of reduced acuity and stereoacuity on eye-hand coordination skills, including block-building, bead-threading, ball-catching  or by using clinical tests to asses visuomotor skills , , . "
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ABSTRACT: Impairment of spatiotemporal visual processing in amblyopia has been studied extensively, but its effects on visuomotor tasks have rarely been examined. Here, we investigate how visual deficits in amblyopia affect motor planning and online control of visually-guided, unconstrained reaching movements.
Thirteen patients with mild amblyopia, 13 with severe amblyopia and 13 visually-normal participants were recruited. Participants reached and touched a visual target during binocular and monocular viewing. Motor planning was assessed by examining spatial variability of the trajectory at 50-100 ms after movement onset. Online control was assessed by examining the endpoint variability and by calculating the coefficient of determination (R(2)) which correlates the spatial position of the limb during the movement to endpoint position.
Patients with amblyopia had reduced precision of the motor plan in all viewing conditions as evidenced by increased variability of the reach early in the trajectory. Endpoint precision was comparable between patients with mild amblyopia and control participants. Patients with severe amblyopia had reduced endpoint precision along azimuth and elevation during amblyopic eye viewing only, and along the depth axis in all viewing conditions. In addition, they had significantly higher R(2) values at 70% of movement time along the elevation and depth axes during amblyopic eye viewing.
Sensory uncertainty due to amblyopia leads to reduced precision of the motor plan. The ability to implement online corrections depends on the severity of the visual deficit, viewing condition, and the axis of the reaching movement. Patients with mild amblyopia used online control effectively to compensate for the reduced precision of the motor plan. In contrast, patients with severe amblyopia were not able to use online control as effectively to amend the limb trajectory especially along the depth axis, which could be due to their abnormal stereopsis.
Available from: ncbi.nlm.nih.gov
- "An extreme example of observers with strong SED is the clinical population with amblyopia. [The amblyopic eye also suffers from a host of visual deficits related to contour integration, spatial and temporal vision, as well as those related to higher level visual functions (e.g., Ciuffreda et al, 1991; Kiorpes & McKee, 1999; Kovacs, 2000; Levi, 2006).] While SED is likely established during early visual development and persists through adulthood, there exists plasticity in the underlying neural circuitries (e.g., Harauzov et al, 2010; Hubel & Wiesel, 1970; Suzuki & Grabowecky, 2007). "
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ABSTRACT: Sensory eye dominance (SED) reflects an imbalance of interocular inhibition in the binocular network. Extending an earlier work (Ooi & He, 2001) that measured global SED within the central 6°, the current study measured SED locally at 17 locations within the central 8° of the binocular visual field. The eccentricities (radius) chosen for this, "binocular perimetry", study were 0° (fovea), 2° and 4°. At each eccentricity, eight concentric locations (polar angle: 0°, 45°, 90°, 135°, 180°, 225°, 270°, and 315°) were tested. The outcome, an SED map, sets up comparison between local SED and other visual functions [monocular contrast threshold, binocular disparity threshold, reaction time to detect depth, the dynamics of binocular rivalry and motor eye dominance]. Our analysis shows that an observer's SED varies gradually across the binocular visual field both in its sign and magnitude. The strong eye channel revealed in the SED measurement does not always have a lower monocular contrast threshold, and does not need to be the motor dominant eye. There exists significant correlation between SED and binocular disparity threshold, and between SED and the response time to detect depth of a random-dot stereogram. A significant correlation is also found between SED and the eye that predominates when viewing an extended duration binocular rivalry stimulus. While it is difficult to attribute casual factors based on correlation analyses, these observations agree with the notion that an imbalance of interocular inhibition, which is largely revealed as SED, is a significant factor impeding binocular visual perception.
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