Comparative studies provide a model describing how abnormal binocular interactions in the cortex and midbrain could disturb the development of optokinetic nystagmus (OKN) and control of fixational eye movements in amblyopia and strabismus. Cortical projections to the pretectum that mediate the control of temporal OKN for the ipsilateral eye are functionally suppressed by a subcortical projection to the pretectum mediating nasal OKN for the contralateral eye. The reduced cortical projection to the pretectal nucleus of the optic tract (NOT) causes a marked attenuation of the OKN response to temporal target motion and a smaller reduction of the OKN response to nasal movement during monocular stimulation. Subcortical binocular suppression may occur in clinical patients with amblyopia and account for their permanent reduction of the slow phase gain of OKN when either the amblyopic or nonamblyopic eye is stimulated. Reduced cortical projections to the NOT may also cause slow drifts of both eyes during attempted steady monocular fixation to occur to the side of the covered eye (latent nystagmus). The horizontal directional drift bias subsequently interacts with monocular pursuit tracking eye movements by adding to nasal and subtracting from temporal eye movements. Similar disturbances of eye fixation, OKN, and pursuit tracking in the vertical meridian suggest an analogous scheme for direct (subcortical) and indirect (cortical) projections to subcortical nuclei controlling downward and upward eye movements, respectively. These anomalies are primarily of the optokinetic and not the pursuit system because amblyopic eyes do not have an abnormally long build-up of optokinetic slow phase velocity which would be symptomatic of a pursuit anomaly. These disturbances of OKN are permanent and appear to result from abnormal binocular stimulation during a critical period for visuo-motor development.