Animal models for visual deprivation-induced strabismus and nystagmus.

Abstract

The development of gaze-stabilizing systems depends on normal vision during infancy. Monkeys reared with binocular lid suture (BLS) for the first 25-40 days of life have strabismus, optokinetic nystagmus deficits, latent nystagmus, and decreased binocular cells in the visual cortex and nucleus of the optic tract. When BLS is extended to 55 days, pendular and congenital nystagmus also occurs. Eyelids in infant monkeys are hairless and thin, but BLS still degrades sensory fusion, motion, and form perception. To determine to what extent these visual properties are critical in the development of normal gaze stabilization, we examined infant monkeys reared with one opaque contact lens over one eye, alternated to the fellow eye every other day (AMO); and monkeys reared in a 3-Hz strobe environment. Monkeys reared with AMO develop strabismus, but have normal optokinetic nystagmus and no spontaneous nystagmus. Area 17 is monocular, but the medial temporal area and the nucleus of the optic tract are binocular. Monkeys reared in strobe light develop pendular nystagmus but not strabismus. We were puzzled by the results of the AMO monkeys until we examined infant monkeys with BLS that were prevented from seeing form through the lids. This was done by leaving the tarsal plate intact behind the eyelid. They developed similar to the AMO monkeys. These results suggest that disruption of sensory fusion during infancy (BLS, AMO) causes strabismus. If strabismus occurs while the monkeys have some form vision from each eye (BLS without tarsal plate), then the nucleus of the optic tract becomes monocular, which causes optokinetic nystagmus deficits and latent nystagmus. Infant monkeys reared without visual motion develop pendular nystagmus.