The evoked potential (EP) over primary somatosensory cortex (SI) was monitored before and after a complete lesion of the primate dorsal column (DC) pathway on one side. The EP was elicited by electrocutaneous or mechanical stimulation of either foot, and was recorded from the contralateral cortical surface for periods of up to 3 months after the lesion. The amplitudes of the three major peaks (P20, N50, and P90) of the cortical somatosensory EP were significantly reduced following interruption of the contralateral DC. Over weeks following the lesion, there was a significant increase in amplitude of the P90 component of the EP that was not evident in the other peaks. The postlesion increases in P90 amplitude were correlated with improved performance on a task that required grasping with either foot, suggesting that behavioral recovery from a DC lesion results in part from neural plasticity, as opposed to a simple relearning of the task.