Peripheral nerve injuries are very common. Although peripheral nerve fibres having the potential to regenerate, the rate of growth is no more than 1 mm/day in the human. That, coupled with the long distance to reach target in proximal nerve injury, is often translated to poor clinical outcome. In situations where there is complete disruption of the nerve trunk, the additional time required for the regenerating axons to cross the injury site can be very substantial. That results in further delays and even worse functional recovery. Therefore, there is a great need for novel treatment modalities to expedite nerve growth and functional return. Post-surgical electrical stimulation to the proximal nerve stump has been shown to accelerate functional recovery in animal models for several decades. However, the underlying mechanisms of this are only becoming better understood in the new millennium. Up-regulation of neurotrophic factors such as BDNF in Schwann cells, along with downstream intermediaries including cAMP play a key role in speeding up the extension of growth cones across the injury site. Indeed, in NGF 4/5 knockout mice and BDNF/TrkB deficient mice, the acceleration effect of electrical stimulation is abolished. Sensory and motor nerve fibres respond to ES differently. Although motor nerve fibres show positive response to a wide range of stimulation durations from as long as several weeks to as short as an hour, the optimum window of stimulation duration for sensory nerve fibres is much narrower. While robust acceleration occurs with 1 hour of electrical stimulation, the accelerated growth becomes increasingly attenuated with long periods of stimulation. This is likely due to intrinsic differences in motor and sensory nerve fibres. For example, polysialic acid was shown to be critical in determining motor axons’ capacity for accelerated regeneration after electrical stimulation. The beneficial effects of electrical stimulation of the proximal nerve stump only occur in motoneurons that are capable of up-regulating polysialic acid. Conversely, the benefits of stimulation were completely abolished if polysialic acid was removed from the regenerating axons. A second critical downstream effector in preferential motor nerve reinnervation is HNK-1 glycan that is exclusively expressed by motor axons. Enhancement of HNK-1 expression was not seen in TrkB deficient mice in whom preferential motor reinnervation does not occur. Electrical stimulation has also been shown to improve specific path finding for regenerating sensory nerve fibres. However, the precise mechanism for that has not been established. With promising results shown in animal studies, the same brief post-surgical electrical stimulation paradigm has been applied clinically to patients with severe axon loss injury. These include severe compressive median neuropathy in carpal tunnel syndrome and compressive ulnar neuropathy at the elbow. In those studies, significantly greater motor nerve reinnervation and better functional outcomes were found in the treatment group that received 1 hour 20 Hz continuous electrical stimulation. The same benefits on sensory nerve regeneration were also recently shown in patients with digital nerve laceration. These clinical translational studies open the door to test the effects of brief electrical stimulation to devastating proximal peripheral nerve conditions such as injury to the brachial plexus that often carry poor outcomes with conventional treatments.