“…It is now well accepted that changes in spinal cord circuitry, both rostral and caudal to an injury, as well as changes in supraspinal structures underpin spontaneous recovery (Beattie et al, 1997;Rose, 2009, 2011;Fouad et al, 2001;Hill et al, 2001;Lawrence and Kuypers, 1968;Oudega and Perez, 2012;Weidner et al, 2001). Recent experiments using a dual lesion model of SCI in cats have shown that recovery of hindlimb locomotion depends on plasticity in spared descending pathways, and within spinal circuits caudal to the lesion (Barriere et al, 2008;Frigon, 2009;Martinez et al, 2011). Further, anatomical studies in rodent models of incomplete SCI have shown that both intact and damaged axons in the vicinity of a spinal lesion sprout to form new intraspinal circuits (Bareyre et al, 2004;Beattie et al, 1997;Courtine et al, 2008;Fouad et al, 2001;Goldshmit et al, 2008;Goldstein et al, 1997;Onifer et al, 2011;Rank et al, 2014).…”