sutured right eye and closing the left eye. After this reversal, the ocular dominance columns of the initially closed right eye appear practically normal, indicating that anatomical recovery of the initially shrunken columns was induced by opening the right eye and closing the left eye. However, when the right eye is sewn closed beyond the critical period, the columns of the right eye do not reexpand if the right eye is opened and the left eye closed.

Eyelid suturing in the baby macaque is a good model for visual deprivation amblyopia. In children, this condition can be caused by any dense opacity of the ocular media or occlusion by the eyelid. Visual deprivation can rapidly cause profound amblyopia.

Amblyopia in children also has other causes. Optical defocus resulting from anisometropia causes the cortical neurons driven by the defocused eye to be less sensitive (particularly to higher spatial frequencies because they are most affected by blur) and to send out a weaker signal. This results in reduced binocular activity. Anisometropic amblyopia has a later-onset critical period than strabismic amblyopia and requires a prolonged period of unilateral blur. Meridional (astigmatic) amblyopia does not develop during the first year of life and may not develop until age 3.

Strabismus can be artificially created in monkeys by the sectioning of an extraocular muscle. Alternating fixation develops in some monkeys after this procedure; they maintain normal acuity in each eye. Examination of the striate cortex reveals cells with normal receptive fields and an equal number of cells responsive to stimulation of either eye. However, the cortex is bereft of binocular cells (see Fig 6-3). After 1 extraocular muscle is cut, some monkeys do not alternately fixate but constantly fixate with the same eye, and amblyopia develops in the deviating eye. An important factor in the development of strabismic amblyopia is interocular suppression due to uncorrelated images in the 2 eyes. Strabismus causes abnormal input to the striate cortex by preventing the synchronous firing of correlated images from the 2 foveae. Another factor is the optical defocus of the deviated eye. The dominant eye is focused on the object of regard, while the deviated eye is pointed in a different direction; for the deviated eye, the object may be too near or too far to be in focus. Either mechanism can cause asynchrony or inhibition of 1 set of signals in the striate cortex. The critical period for development of strabismic amblyopia begins at approximately 4 months of age, during the time of ocular dominance segregation and sensitivity to binocular correlation.

Abnormal sensory input alone is sufficient to alter the normal anatomy of the visual cortex. Other areas of the cerebral cortex may also depend on sensory stimulation to form the proper anatomical circuits necessary for normal adult visual function. This notion underscores the importance of providing children with a stimulating sensory environment.

Abnormalities of Binocular Vision

When a manifest deviation of the eyes occurs, the corresponding retinal elements of the eyes are no longer directed at the same object. This places the patient at risk for 2 distinct visual phenomena: visual confusion and diplopia.

Visual Confusion

Visual confusion is the simultaneous perception of 2 different objects projected onto corresponding retinal areas. The 2 foveal areas are physiologically incapable of simultaneous perception of dissimilar objects. The closest foveal equivalent is retinal rivalry, wherein the 2 perceived images rapidly alternate (Fig 6-4). Confusion may be a phenomenon of extrafoveal retinal areas only. Clinically significant visual confusion is rare.