Spinal cord injury (SCI) often results in life-long sensorimotor impairment. Spontaneous recovery from SCI is limited, as supraspinal fibers cannot spontaneously regenerate to form functional networks below the level of injury. Despite this, animal models and humans exhibit many motor behaviors indicative of recovery when electrical stimulation is applied epidurally to the dorsal aspect of the lumbar spinal cord. In 1976, epidural stimulation was introduced to alleviate spasticity in Multiple Sclerosis. Since then, epidural electrical stimulation (EES) has been demonstrated to improve voluntary mobility across the knee and/or ankle in several SCI patients, highlighting its utility in enhancing motor activation. The mechanisms that EES induces to drive these improvements in sensorimotor function remain largely unknown. In this review, we discuss several sensorimotor plasticity mechanisms that we hypothesize may enable epidural stimulation to promote recovery, including changes in local lumbar circuitry, propriospinal interneurons, and the internal model. Finally, we discuss genetic tools for afferent modulation as an emerging method to facilitate the search for the mechanisms of action.

脊髓损伤（SCI）通常会导致终生感觉运动障碍。 SCI 的自发恢复是有限的，因为脊髓上纤维不能自发再生以形成损伤水平以下的功能网络。尽管如此，当对腰脊髓背侧进行硬膜外电刺激时，动物模型和人类表现出许多表明恢复的运动行为。 1976 年，硬膜外刺激被引入以缓解多发性硬化症的痉挛状态。此后，硬膜外电刺激 (EES) 已被证明可以改善几名 SCI 患者的膝盖和/或踝关节的自主活动能力，突显了其在增强运动激活方面的效用。 EES 诱导的感觉运动功能改善的机制在很大程度上仍然未知。在这篇综述中，我们讨论了几种感觉运动可塑性机制，我们假设这些机制可能使硬膜外刺激促进恢复，包括局部腰椎回路、本体脊髓中间神经元和内部模型的变化。最后，我们讨论传入调节的遗传工具作为一种新兴方法，以促进作用机制的研究。