Activities of Cortical Motor Neurons Trigger Electrical Stimulation of Lower Motor Neurons in the Spinal Cord

Restoration of hindlimb locomotion after spinal cord injury (SCI) remains a challenging problem even though functional electrical stimulation (FES) and neuromotor prostheses (NMP) have been investigated in previous studies. In this study, to restore the voluntary movement of paralyzed hindlimb, a circuit was designed that can bypass a lesion to the spinal cord, linking upper motor neurons (UMNs) and lower motor neurons (LMNs) in guinea pigs. An amplifier acquired signals from the primary motor cortex (M1 ) via multi-electrodes array, which triggered a programmed stimulator to generate pulse trains that directly activated LMNs through stimulation electrodes in the spinal cord, hence produced hindlimb movements.;Firstly we used signals from visual cortex (VC), auditory cortex (AC) and medial geniculate body (MGB) respectively to induce hindlimb movement on anaesthetized rats with incomplete SCI. Secondly we acquired signals from hindlimb region of the primary motor cortex (M1HL) to induce contralateral lower limb movement on awake guinea pigs with complete SCI, when animal slowly running on treadmill by their forelimbs. Neural responses of VC, AC or MGB to stimuli of light, sound or electrical current were exactly acquired by the circuit as the frequency of stimuli changed. Twitching of lower limb was observed when up-threshold signals were selected to activate LMNs. In chronic experiments, neural activity of M1HL enabled twitching-like movements of the paraplegic, stimulated hindlimb as animals walked on he treadmill by forelimbs. As shown in supplementary videos, mostly each step of left was followed by movement of left hindlimb, but sometimes followed by none or two. The time lag between forelimb and hindlimb was shortened significantly from 153+/-42 ms to 92+/-23 ms (p<0.01) when the speed of the treadmill was increased from 5.6 cm/s to 11.1 cm/s.;The UMNs were reconnected with LMNs by circuit in transected spinal cord, thus produced hindlimb movement, which electronically bypasses lesion in the spinal cord. Our finding shows the possibility of a novel therapy for functional locomotion recovery of hind limbs in patients with spinal cord injury.;Key words: functional electrical stimulation; lower motor neuron; primary motor cortex; spinal cord injury; upper motor neuron.