This study describes the neural mechanisms of spinal cord stimulation (SCS), which is utilized to restore voluntary movement in people with paralysis, enabling the brain to regain control over spinal motoneurons. Previously, SCS has been shown to restore movement in individuals with spinal cord injury and stroke, but it's never been proven. By combining computational modeling, monkey electrophysiology, and human recordings, the researchers conclude that recovery. The residual supraspinal drive produces a small depolarization that’s not enough to generate movement but raises the membrane potential close to threshold. When subthreshold EPSPs occur, they can be transformed into action potentials. This shows that motor neurons fire in similar patterns at 100 Hz SCS pulse intervals in simulations and in monkeys. This pattern creates two distinct parameter regions: a voluntary one, in which SCS impulses become suprathreshold only with supraspinal input, and an involuntary regime, in which SCS alone drives motoneurons and overrides voluntary control. They also show that the voluntary regime shrinks dramatically as lesion severity increases, meaning severe injury leaves a very narrow window of SCS parameters that allow genuine volitional control. These predictions were validated in electrophysiological experiments. In anesthetized monkeys, pairing internal capsule stimulation with SCS increased SCS-evoked reflexes by up to 285%, demonstrating that corticospinal inputs facilitate SCS-mediated EPSPs. Similarly, in humans with paralysis, motor units show a response to SCS with a 40-100% of spikes in stimulation pulses. These results help clarify the mechanism by which SCS and residual brain activity interact to restore voluntary movement.