Rj. Tusa et al., Gaze-stabilizing deficits and latent nystagmus in monkeys with brief, early-onset visual deprivation: Eye movement recordings, J NEUROPHYS, 86(2), 2001, pp. 651-661
The normal development and the capacity to calibrate gaze-stabilizing syste
ms may depend on normal vision during infancy. At the end of 1 yr of dark r
earing, cats have gaze-stabilizing deficits similar to that of the newborn
human infant including decreased monocular optokinetic nystagmus (OKN) in t
he nasal to temporal (N-T) direction and decreased velocity storage in the
vestibuloocular reflex (VOR). The purpose of this study is to determine to
what extent restricted vision during the first 2 mo of life in monkeys affe
cts the development of gaze-stabilizing systems. The eyelids of both eyes w
ere sutured closed in three rhesus monkeys (Macaca mulatta) at birth. Eyeli
ds were opened at 25 days in one monkey and 40 and 55 days in the other two
animals. Eye movements were recorded from each eye using scleral search co
ils. The VOR, OKN, and fixation were examined at 6 and 12 mo of age. We als
o examined ocular alignment, refraction, and visual acuity in these animals
. At 1 yr of age, visual acuity ranged from 0.3 to 0.6 LogMAR (20/40-20/80)
. All animals showed a defect in monocular OKN in the N-T direction. The ve
locity-storage component of OKN (i.e., OKAN) was the most impaired. All ani
mals had a mild reduction in VOR gain but had a normal time constant. The a
nimals deprived for 40 and 55 days had a persistent strabismus. All animals
showed a nystagmus similar to latent nystagmus (LN) in human subjects. The
amount of LN and OKN defect correlated positively with the duration of dep
rivation. In addition, the animal deprived for 55 days demonstrated a patte
rn of nystagmus similar to congenital nystagmus in human subjects. We found
that restricted visual input during the first 2 mo of life impairs certain
gaze-stabilizing systems and causes LN in primates.