Address for correspondence: Ronald J. Tusa, M.D., Ph.D., Yerkes Research Center, 954 Gatewood Rd. NE, Emory University, Atlanta, GA 30322.
Voice: 404-712-0996; fax: 404-712-1927.
rtusa{at}emory.edu
Ann. N.Y. Acad. Sci. 956: 346-360 (2002).
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.
