Abstract

The problem of the pathophysiology of strabismic amblyopia may be approached from a number of points of view. Since this type of amblyopia is characterized by the absence of ophthalmoscopically demonstrable organic pathologic defects in the retina, many investigators have considered that the decrease in visual acuity results from an active inhibition in the visual cortex. Others have placed the seat of the inhibitory process in the retina itself. Still others have felt that in strabismic amblyopia there is a disturbance of the higher visual functions which results in an inability to integrate a sensed form into a meaningful percept. vom Hofe 1 in 1930 first hinted at this possibility. Testing the visual acuity of amblyopic eyes with various simple geometric forms (rectangle, cross, circle, etc.), he reported that the responses of some of his patients were reminiscent of the behavior of the patients with traumatic lesions of the occipital

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