Clinical optokinetic nystagmus asymmetry in treated esotropes.

Abstract

Monocular optokinetic nystagmus (OKN) asymmetry is associated with disruption of early binocular visual development. Three groups of treated esotropic patients and a group of normal controls were evaluated for the presence of clinically detectable monocular OKN asymmetry. Clinical assessment of monocular OKN asymmetry was performed by observing eye movements in response to a hand-held rotating drum. Asymmetry was quantitated on a scale of 0 to +3 OKN asymmetry. Clinical OKN asymmetry was evaluated in the following groups of patients: those with congenital esotropia treated with very early surgery achieving high-grade stereo acuity (group 1); those with congenital esotropia treated with late surgery achieving no stereopsis (group 2); those with acquired esotropia achieving high-grade stereo acuity after treatment with spectacle correction (group 3); and normal controls (group 4). Two of the three patients in group 1 showed +3 OKN asymmetry despite having high-grade stereo acuity; the third one, who was surgically aligned earliest (13 weeks), demonstrated +1 OKN asymmetry. This patient achieved orthotropia, 40 seconds stereo acuity, perfect Randot stereo acuity, and had no dissociated vertical deviation or latent nystagmus. All 10 patients in group 2 (those with late alignment-after 1 year-and no stereo acuity) showed +3 OKN asymmetry. All four patients in group 3 (those with acquired hypermetropic esotropia and high-grade stereo acuity after treatment) and all 10 patients in the normal control group showed no OKN asymmetry. Clinically obvious monocular OKN asymmetry can occur in patients with congenital esotropia who are aligned early and develop high-grade stereo acuity. Even brief periods of strabismus during the early period of binocular motor development can result in persistent OKN asymmetry. This suggests that binocular motor processing may develop distinct from, and prior to, the development of high-grade stereo acuity. OKN asymmetry appears to be a clinical sign of an insult to early binocular motor development.