Other studies have shown that the application of tail nerve electrical stimulation (TNES) in rats with spinal cord contusion could promote the recovery of spontaneous locomotor function. In a previous study, we found that medium‐frequency electrical stimulation of the tail root of rats with transection SCI could effectively protect neurons in the L1–L5 segment of the spinal cord and prevent muscle atrophy in the hindlimbs.
Therefore, it is of great significance to identify non‐invasive, safe and effective stimulation protocols that can activate the CPG and motor neural circuits in the spinal cord. However, the application of EES and ISMS requires electrode implantation these techniques produce certain side effects and can only be applied in certain circumstances, thus limiting their clinical application. These treatments act via the central pattern generator (CPG). However, the implementation of these programs requires the prevention of neuronal apoptosis and alleviation of atrophy in the muscles of the paralyzed limbs.īoth EES and direct intra‐spinal micro‐stimulation (ISMS) at the lumbosacral spinal cord have been proven to induce walking and produce electromyograms (EMGs) after high‐level SCI. Subsequently, the researchers conducted a series of studies on the brain–computer interface and spinal cord epidural electrical stimulation (EES) and demonstrated that electrical stimulation of the spinal cord at a certain frequency could re‐initiate limb movement in the absence of inputs from the brain. An exciting development was the recent research from Courtine et al, who reported that electrical stimulation of the spinal cord below the level of the injured segments could induce limb movement. However, even after decades of research, there has been no breakthrough in locomotor function recovery. Hence, these pathological processes are considered crucial obstacles in the reconstruction of locomotor function.Īt present, the treatment for SCI focuses on cell transplantation and tissue engineering, both of which aim to promote regeneration of the corticospinal tract (CST) and other brain‐derived nerve axons or facilitate the formation of new neural circuits at the injury site to relay neural information and eventually restore innervation to the paralyzed limbs. These processes can subsequently develop into irreversible atrophy of muscles in the paralyzed limbs. Transected spinal cord injury (SCI) may induce the loss of innervation in the spinal cord below the injury area, thus resulting in the loss of locomotor function.Īlthough spinal cord tissue below the level of the injured segments may be relatively intact, the long‐term loss of excitatory input from the brain can lead to functional silencing of neurons, cell body atrophy, and apoptosis.