Visual Development, Diagnosis, and Treatment of the Pediatric Patient
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So with this many options and opportunities available, why not take a closer look to see what you can get today? Results 1 - 50 of for Optometry Books. ISBN: Contact lenses: A handbook for patients by Roth, H. Visual Optics, Vol. Deprivation happens when eye diseases prevent the light stimulus from reaching the retina, thus forestalling the normal visual process.
It also may occur due to anatomic deficits of the retina or optic nerve, or abnormal movement disorders of the eye nystagmus. When it occurs during the critical period of visual development, it can cause amblyopia. The main diseases that cause this are congenital cataract, blepharoptosis, nystagmus disorders, optic nerve coloboma and hypoplasia, retinal disorders, persistent fetal vasculature; other disease processes can also result in amblyopia. Amblyopia caused by deprivation was the first type studied in works of Hubel and Wiesel in the s.
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The authors demonstrated that suturing the eyelids of cats deprived their eyes from receiving visual stimuli, which led to innumerable anatomical and functional changes in the cortical visual pathways. The authors found that these changes were more drastic the earlier, the more intense, and the more prolonged the deprivation. Studies with cats 18 and monkeys 10, have shown that the primary alteration of monocular visual deprivation is a change to the cortical ocular dominance columns.
In cats, during the most sensitive phase of the critical period, a day of deprivation leads to a slight reduction in vision. Two to 3 days lead to a proportionally much more severe visual reduction, whereas deprivations of more than 6 to 10 days lead to full shift of the cells from the ocular dominance column to the side of the opposing eye, with severe reduction of vision. In addition to changes in V1, amblyopia is associated with morphological changes in CGL. The effect of late eye closure has also been studied.
Thus, the effect of deprivation on the size of the bands of the cortical ocular dominance columns was greatly reduced when closure occurred after 10 weeks of age. Therefore, 3 months would be the end of the critical period of cortical changes in a monkey, which would correspond to approximately 18 months of life in a human. Not only is brain structure different among species, but deprivation studied in animal models is known and controlled, whereas in most cases involving children, there will be varied clinical pictures and multiple associated factors to amblyopia. The ideal period to treat the causes of deprivation in humans is within the first six months of life; after that, the chance to ensure the effectiveness of treatment and achieve normal results decreases rapidly.
For instance, dense bilateral cataracts not treated by 3 months of age will almost assuredly lead to the development of nystagmus, which will severely limit visual acuity permanently. Deprivation amblyopia causes profound anatomical changes in visual circuitry and has the greatest impact on visual acuity and all other visual functions. Anisometropia is a difference in the state of refraction of at least 1 diopter between 2 eyes.
The most common type of anisometropia seems to vary with the age, ethnicity, and ocular pathologies of the analyzed sample. Hypermetropic anisometropia is the most likely type to cause amblyopia, since the retina of the more ametropic eye never receives a clear and defined image: The fovea of the good eye is focused and there will be no stimulus of accommodative effort to adjust the focus of the more hyperopic eye.
In myopic anisometropia, the more ametropic eye can be used for near vision, preventing the same levels of amblyopia as seen with hyperopia. Anisometropia may be considered a moderate form of deprivation of visual stimulus, since the more ametropic eye is deprived of receiving a good-quality stimulus in retina. Anatomical and functional changes similar to deprivation are therefore expected in amblyopia caused by anisometropia.
In cases of anisometropia as well as in deprivation, there is a partial "disconnection" of the affected eye in the primary visual cortex, leading to abnormal neuronal competition. While in normal animals most cortical neurons respond to stimulation of 2 eyes, in animals that were subjected to occlusion or blurring of the image of one eye, the proportion of cortical neurons responding to stimuli of the affected eye is much smaller. There is also clear evidence of neural acuity deficit in anisometropia and deprivation. That is, cortical neurons that still respond to stimuli of the affected eye tend to have diffuse and insensitive receptive fields and, therefore, generate worse spatial resolution and contrast sensitivity.
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The severity of amblyopia is not directly related to the magnitude of the refractive degree itself but to the amount of anisometropia between the 2 eyes. Despite differences in the inputs received from each eye, in anisometropia both eyes receive congruent images; that is, unlike strabismus there is no stimulation of non-corresponding retinal areas. The suppression is mainly foveal, but the periphery continues to fuse images. Anisometropic amblyopia is often associated with microtropia, leading to a mixed mechanism of visual disturbance.
Amblyopia by pure anisometropia is the one with the best prognosis, with sometimes surprising recovery of VA with the use of adequate correction alone, and even in later treatments. Strabismus is a deviation of one eye with loss of eye parallelism. As a result, the eyes do not receive equal images, leading the visual system to adapt to this change.
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This adaptive mechanism avoids diplopia, but it causes a restructuring of the visual cortical circuits in the visual cortex that in turn causes amblyopia. In strabismic amblyopia, the cortical ocular dominance columns remain structured, even in cases of moderate amblyopia.
Only in cases of deep amblyopia are there reports of alteration of dominance columns. Although the cortical cellular apparatus is relatively preserved, many functional changes occur in the visual system.
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There is active and deep suppression of the dominant eye over the deviating eye, retinal correspondence is completely lost, and cellular interactions are altered. Tychesen and colleagues have shown many visual function alterations in monkeys with strabismus, as well as loss of V1 binocular connections. The animals exposed to only 3 weeks of decorrelation recovered these functions.
Other studies have shown that excitatory interactions for the deviating eye remain deactivated, but inhibitory ones do not, even after correction of the position of the deviating eye, indicating active cortical suppression and an imbalance between the cortical cellular columns. Strabismus causes change in or loss of connectivity to the cortical spatial information pathways, altering the spatial summation and side inhibitions of received stimuli and, consequently, preventing the integration of contours and shapes.
A distortion of the spatial vision occurs that interferes with numerous discriminatory visual tasks including visual acuity, Vernier visual acuity alignment accuracy , and crowding. In strabismus there is no binocular facilitation for any type of stimulus; the suppression is constant and strong and is probably a modified form of suppression of binocular rivalry.
Thus, it is suppression that leads to amblyopia in an individual who has strabismus and not vice versa, because the inactivity of the system may interfere with the process of synaptic development. In strabismus, the different stimuli received by the eyes prevent normal image fusion, compromising binocular vision and summation and the ability to discriminate disparity and depth of vision with altered stereoscopic visual acuity stereopsis and even postural stability. Contrast sensitivity in strabismic amblyopia is less affected than in amblyopia due to deprivation or anisometropia, with change mainly to high spatial frequencies.
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Amblyopia caused by strabismus therefore has a major impact on visual acuity and binocular vision, and contrast sensitivity is relatively sparing. Amblyopia is considered mixed when caused by 2 amblyogenic factors. Combination of anisometropic and strabismic amblyopia is common, especially in partially accommodative esotropia, microtropia, and monofixation syndrome. Clinically, mixed amblyopia is more severe with similar deficits of visual functions, there is an exacerbation of visual acuity loss and contrast sensitivity and typically an extinction of stereopsia.
The magnitude of the impact on each visual function will depend on the concomitant onset or at different times of each ocular change. A study comparing visual acuity, Vernier acuity, grating acuity, contrast sensitivity, and binocular function of adults with amblyopia of different etiologies 11 categories with normal subjects revealed 2 main dimensions of variation of visual performance on subjects with amblyopia: one related to visual acuity measures optotypes, Vernier, and grids and the other related to contrast sensitivity measurements Pelli-Robson and edge contrast sensitivity.
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Figure 1. Amblyopia Map: The figure shows the mean locations of the 11 clinically defined subject categories in the two-factor space. The diagonal bars show one standard error of the mean measured along the principal axes of the elliptical distributions. Reprinted with permission from McKee et al. Amblyopia is, therefore, a neural disorder resulting from abnormal brain stimulation during the critical period of visual development. As shown by several studies, the striate cortex V1 is the main cortical area affected by amblyopia.
Amblyopes have decreased binocular neurons and decreased neurons responsible for the amblyopic eye in V1 in addition to active binocular suppression. Despite the well-known visual processing deficits, recent work has shown that amblyopic patients present alterations in visual processing of high-order cortical functions 88 such as deficiency in movement integration, 89 perception and processing of shape and global contour, 13, altered perception of alignment Vernier acuity , and symmetry.
Recent evidence shows that the perceptual impact of amblyopia extends even beyond vision to multisensory processing. These high-order deficits are also found in the fellow eye 72, and during binocular vision.