Plastic Surgery Research Council
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PSRC 60th Annual Meeting

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Neonatal Nerve Injury Past Postnatal Day 5 Results in Significant Neuronal Death and Persistence of Functional Deficits in the Rat
Joseph Catapano, MD, Stephen Kemp, PhD, Tessa Gordon, PhD, Gregory Borschel, MD, FACS, FAPP.
University of Toronto, Toronto, ON, Canada.

PURPOSE:
In obstetrical brachial plexus injuries, the nerves of newborns are stretched and sometimes ruptured. These injuries can be devastating, with more than 25% of infants being left with permanent neurological deficits and potentially chronic pain in the future. Unlike adults, peripheral nerve crush injuries in neonates have demonstrated significant retrograde neuronal death after injury, robbing the nervous system of crucial regenerative components. Loss of viable neurons has been largely overlooked as a cause of morbidity following proximal nerve injuries in newborns. Previous studies have suggested that neonatal susceptibility to motor neuron death after crush injury does not extend past postnatal day 5 (P5) and the time-course of sensory neuron death is poorly understood. We sought to further examine central motor and sensory neuron survival in neonatal crush injuries after P5 and to assess axonal regeneration and functional recovery of behavior and muscle parameters following injury.
METHODS:
Groups underwent sciatic nerve crush injury at post-natal day 3, 5, 7 or 30. Following neonatal crush injury, animals were returned to their cages. Weights were monitored for 1 month, at which point all animals underwent retrograde labeling of the sciatic nerve with FluorGold (FG). A 5mm section of sciatic nerve distal to the original injury site was harvested for histomorphometry and analysis of axonal regeneration. Functional and behavioural recovery was tested using SFI (Sciatic Functional Index), muscle twitch and tetanic force analysis, motor unit number estimation (MUNE) and wet muscle weights.
RESULTS:
Following sciatic crush injury at P3, the number of retrogradely labeled motoneurons was reduced to approximately 35% in comparison to uninjured animals. Animals injured at P5 and P7 also displayed statistically significant lower neuron numbers than uninjured controls. All animals injured were found to have significantly lower dorsal root ganglion (DRG) counts than controls. Functionally, only animals injured at P30 were able to recover normal walking track SFI values 1 month after injury. Similar results were seen for extensor digitorum longus (EDL) muscle twitch/tetanic force analysis, MUNE and wet muscle weights.
CONCLUSION:
Animals in both the P5 and P7 nerve injury groups displayed significant neuron loss and decreased functional recovery following nerve injury, suggesting that neuron loss remains a cause of disability following injury beyond P5 and treatments targeted to rescue neurons after injury may continue to be of benefit past this time.


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