Developmental changes in optokinetic mechanisms in the absence of unilateral cortical control

Animal models suggest that the asymmetry of monocular optokinetic nystagmus (OKN) in young infants can be explained by a direct pathway from retina to the midbrain nucleus of the optic tract. However, earlier studies with hemispherectomized infants showed no evidence for OKN responses towards the damaged cortex that could be ascribed to this subcortical pathway. In longitudinal testing of two infants with very extensive unilateral cortical damage, we have now shown that OKN responses in both directions do occur before 10 months of age. OKN towards the damaged cortex, indicating functioning of the direct pathways in the absence of cortical control, drops out in the later development. The neural circuitry responsible for OKN in humans appears to undergo a plastic reorganization.