Our results demonstrated that EMS using a moderate stimulation paradigm immediately following nerve transection and repair enhances electrophysiological and behavioral recovery.

In contrast to adult rat nerve injury models, neonatal sciatic nerve crush leads to massive motor and sensory neuron death. Death of these neurons results from both the loss of functional contact between the nerve terminals and their targets, and the inability of immature Schwann cells in the distal stump of the injured nerve to sustain regeneration. However, current dogma holds that little to no motoneuron death occurs in response to nerve crush at postnatal day 5 (P5). The purpose of the current study was to fully characterize the extent of motor and sensory neuronal death and functional recovery following sciatic nerve crush at mid-thigh level in rats at postnatal days 3-30 (P3-P30), and then compare this to adult injured animals. Following nerve crush at P3, motoneuron numbers were reduced to 35% of that of naïve uninjured animals. Animals in the P5 and P7 group also displayed statistically fewer motoneurons than naïve animals. Animals that were injured at P30 or earlier displayed statistically lower sensory neuron counts in the dorsal root ganglion than naïve controls. Surprisingly, complete behavioral recovery was observed exclusively in the P30 and adult injured groups. Similar results were observed in muscle twitch/tetanic force analysis, motor unit number estimation and wet muscle weights. Rats in both the P5 and P7 injury groups displayed significant neuronal death and impaired functional recovery following injury, challenging current dogma and suggesting that severe deficits persist following nerve injury during this early postnatal developmental period. These findings have important implications concerning the timing of neonatal nerve injury in rats.

No abstract

Proximal neonatal nerve injuries, such as obstetric brachial plexus injury, produce significant retrograde neuronal death after injury. High-dose N-acetylcysteine significantly increases motor neuron survival, which may improve functional outcomes after obstetrical brachial plexus injury.

Treating partially or completely denervated muscle following nerve injury using electrical muscle stimulation has been met with much controversy. Previous studies have shown that chronic electrical muscle stimulation or neuromuscular activity leads to impaired reinnervation of muscle end plates. In this study we investigated the use of a moderate stimulation paradigm delivered daily over a 2 week period and the effects on functional recovery and reinnervation. Rat gastrocnemius muscle was denervated by complete tibial nerve transection and immediately repaired using epineurial sutures. Electrical muscle stimulation was carried out 5 days per week in 1 hour sessions. Our results show that numbers of motoneurons reinnervating muscle and reinnervated endplates were significantly higher in animals that received daily muscle stimulation compared to those without stimulation. Other functional measurements such as muscle force, weight, and contractile properties were no different between groups. Our results provide evidence that the improved reinnervation may be due to antidromic depolarization of axons proximal to the repair site.

No abstract