Unilateral sensorimotor cortical lesions in newborn rats result in the development of an anomalous ipsilateral corticospinal tract originating from the opposite unablated hemisphere. Intracortical microstimulation of the intact hemisphere in adult rats that sustained such lesions demonstrated a reduction in current threshold levels needed to evoke ipsilateral forelimb movements. Disruption of the low-threshold ipsilateral movements by medullary pyramidotomy as observed in the present study suggests that these movements were mediated by the anomalous ipsilateral corticospinal tract fibers which traverse the medullary pyramid.