Current strategies for the chronic stage of spinal cord injury (SCI) had seen little progress. In this report, we present the use of contralateral L5 nerve transfer for the treatment of incomplete SCI patients with unilateral lower limb dysfunction in two male patients. One was diagnosed with L2 vertebral fracture and dislocation combined with coni medullaris injury 10 months prior, and the other was diagnosed with T6 and T7 vertebral fractures with SCI 24 months prior. The patients were treated with decompression surgery within 24 hr after injury. The patients reached a recovery plateau after 6–8 months of spontaneous recovery of locomotion and sustained paralysis in the right leg and were left confined to the wheelchair. The score on the lower‐extremity Fugl‐Meyer assessment (FMA‐LE) was 7 for both patients. The patients were then enrolled, and they underwent half of the anterior root of the contralateral L5 transfer to S1 and S2 to improve lower limb motor function. A posterior approach was performed to expose the L5, S1, and S2 nerve roots. Half of the anterior root of the left L5 was cut, and end‐to‐end neurorrhaphy from the left L5 to the right S1 and S2 was performed subdurally. After the surgery, routine rehabilitation treatments were prescribed. Muscle strength decreased transiently in the donor‐side before recovering within 12 months postoperatively. Muscle strength was significantly improved on the affected side 2 years postoperatively, when the FMA‐LE scores increased to 14 and 15, respectively. The patients regained independent walking ability with crutches. This report suggests that contralateral hemi‐5th‐lumbar nerve transfer is safe and can benefit incomplete SCI patients with unilateral lower limb dysfunction.

Restoring limb movements after central nervous system injury remains a substantial challenge. Recent studies proved that crossing nerve transfer surgery could rebuild physiological connectivity between the contralesional cortex and the paralyzed arm to compensate for the lost function after brain injury. However, the neural mechanism by which this surgery mediates motor recovery remains still unclear. Here, using a clinical mouse model, we showed that this surgery can restore skilled forelimb function in adult mice with unilateral cortical lesion by inducing cortical remapping and promoting corticospinal tract sprouting. After reestablishing the ipsilateral descending pathway, resecting of the artificially rebuilt peripheral nerve did not affect motor improvements. Furthermore, retaining the sensory afferent, but not the motor efferent, of the transferred nerve was sufficient for inducing brain remapping and facilitating motor restoration. Thus, our results demonstrate that surgically rebuilt sensory input triggers neural plasticity for accelerating motor recovery, which provides an approach for treating central nervous system injuries.

No abstract