Recovery of voluntary motor function after incomplete spinal cord injuries is attributed to a variety of physiological mechanisms, such as resolution of conduction block in injured axons, and neuroplasticity mechanisms in spared axons. To better understand these recovery mechanisms, we have examined motor recovery in one type of incomplete cord injury, the Brown-Sequard Syndrome. This syndrome is observed in patients with unilateral injury of the spinal cord and is manifested as asymmetric weakness and painjtemperature sensory loss contralateral to the weakest extremity. We have followed the course of motor recovery in two patients and reviewed the literature in an additional 59. Common features of this motor recovery include: 1) recovery of ipsilateralproximal extensor muscles before ipsilateral distal flexors, 2) recovery of any weakness in the extremity with pain/temperature sensory loss before the opposite extremity, and 3) recovery of voluntary motor strength and a functional gait by 1 to 6 months. We discuss these observations with respect to three hypotheses to explain motor recovery and suggest that neuroplasticity mechanisms functioning in spared descending axons may mediate much of the observed recovery after Brown-Sequard cord lesions.