Cases reported "Amblyopia"

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1/5. amblyopia: a multidisciplinary approach. Proctor lecture.

    Clinically different forms of amblyopia share as common denominators an inability to form well-defined and focused images in one or both eyes and, in the case of unilateral amblyopia, unequal visual input to the brain. This suggests two amblyopiogenic mechanisms which are effective, individually or in unison, in the various forms of amblyopia. The first is lack of adequate visual stimulation during infancy, causing visual deprivation. The second mechanism is based on abnormal binocular interaction. The clinical evidence and data from the animal laboratory will be reviewed in support of this dual etiological concept of amblyopia. An etiological classification of amblyopia suggested in 1972 on hypothetical grounds can be upheld on the basis of information that has accumulated since that time. amblyopia is not a static condition but has a strong dynamic component since its severity can be modified by the type of stimulation received by the sound eye. Special emphases is placed in this lecture on this unique feature which is based on binocular interaction and is similar to the inhibition of afferent visual stimulation during suppression.
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2/5. Visual improvement in amblyopia after visual loss in the dominant eye.

    Partial recovery from amblyopia can occur in animals if the the influence from the dominant eye is removed. This report describes a human, adult amblyope who lost central vision in the dominant eye, and regained useful vision in the amblyopic eye.
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3/5. The lateral geniculate nucleus in human anisometropic amblyopia.

    Experimental amblyopia in animal models causes a reduction of cell sizes in lateral geniculate nucleus (LGN) laminae connected with the amblyopic eye. However, direct evidence that the human amblyopic visual system is affected in a similar manner has been lacking. Histologic study of the LGNs from a patient with ophthalmologically confirmed anisometropic amblyopia shows a decrease of cell sizes in the parvocellular layers innervated by the amblyopic eye. This decrease was more pronounced in laminae receiving crossed fibers. To our knowledge this is the first report about structural alterations in the afferent visual pathway of a human amblyope and the data reaffirm the validity of the monkey model for further study of the basic mechanisms in amblyopia.
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4/5. amblyopia caused by unilateral atropinization.

    Unilateral atropinization is used in infants and children in the treatment of amblyopia (penalization). It is also used to prevent amblyopia in eyes with cataracts involving only the central portions of the lens. It is not generally realized, however, that unilateral atropinization during visual immaturity may actually cause amblyopia. Three reported cases demonstrate this point. Experiments in monkeys raised with unilateral cycloplegia demonstrated shrinkage of cells in the lateral geniculate nucleus and loss of cortical binocularity and of neurons responding to stimulation of the atropinized eye. The clinical data reported in this study, in conjunction with information gleaned from animal models, indicate that caution must be applied when considering prolonged unilateral atropinization of infants and young children.
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5/5. Pattern of ocular dominance columns in human striate cortex in strabismic amblyopia.

    Previous experiments in animals have shown that early unilateral eyelid suture, a model of amblyopia induced by cataract, causes shrinkage of ocular dominance columns serving the deprived eye in the striate cortex. It is unknown whether the ocular dominance columns are affected in amblyopia produced by strabismus. We examined specimens of striate cortex obtained postmortem from a 79-year-old woman with a history of amblyopia in her left eye (20/800) since age 2 from accommodative esotropia. Four years prior to her death, she suffered an ischemic infarct of the left optic disc. This injury to the left optic disc made it possible to label the ocular dominance columns using cytochrome oxidase histochemistry. The pattern of ocular dominance columns was reconstructed throughout most of the right striate cortex. No shrinkage of columns was found. In the left cortex only half the column mosaic was labelled, because the patient had some residual vision in the temporal retina of her left eye. The columns within the labelled portion of the overall mosaic appeared normal. These findings indicate that shrinkage of ocular dominance columns does not occur in humans with amblyopia caused by accommodative esotropia. The ocular dominance columns are probably no longer susceptible to shrinkage at the age when most children with this condition begin to develop amblyopia.
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