Abstract

The so-called infantile strabismus syndrome consists of (1) strabismus, (2) a defect of temporally-directed pursuit and optokinetic tracking in monocular viewing, and (3) latent nystagmus (LN). The following causal relationship between these three phenomena is suggested. Firstly, infantile strabismus impairs the development of binocularity in the visual cortex. Secondly, the reduced binocularity prevents oculomotor maturation: The nasal-temporal asymmetry in pursuit and optokinetic nystagmus (OKN) that is a normal feature in the first few months of life remains as a permanent defect. Finally, the asymmetry in the smooth tracking systems produces LN. — The impairment of temporally-directed tracking cannot be due to a defect in the retino-cortical pathway because the patients can perceive temporally-directed object motion, and distinguish various velocities. Rather, the visual cortex seems to lack the ability to transmit temporally-directed object motion to the premotor structures of the brainstem if binocularity has failed to develop in the first months of life. — The nystagmus of patients with infantile strabismus often has a gaze-paretic component. The pathophysiological relationship of this component with the above-mentioned three signs of infantile strabismus is not yet clear. — Dissociated vertical divergence (DVD) is another phenomenon that frequently occurs together with early onset strabismus. As is the case in LN, DVD also depends on the balance of inputs coming through the right and left eyes. Otherwise, nothing is known of the pathogenesis of DVD.

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