Abstract
Peripheral nerve injuries, associated with significant morbidity, can benefit from electrical stimulation (ES), as demonstrated in animal studies through improved axonal growth. This study combined the clinical gold standard of isograft repair in a rat model of sciatic nerve injury to evaluate the effects of intraoperative ES on functional tests and histology. Forty rats underwent a surgically induced gap injury to the right sciatic nerve and subsequent repair with an isograft. Half of these rats were randomly selected to receive 10 min of intraoperative ES. Functional testing, including response time to a heat stimulus and motor functional tests, were conducted.Histology of the sciatic nerves and gastrocnemius muscles were analyzed after 6 and 12 weeks of recovery. Rats that underwent ES treatment showed incremental improvements in motor function between weeks 2 and 12, with a significantly higher push-off response than the no-ES controls after 6 weeks. Although no differences were detected between groups in the sensory testing, significant improvements over time were noted in the ES group. Histology parameters, sciatic nerve measures, and gastrocnemius muscle weights demonstrated nerve recovery over time for both the ES and no-ES control groups. Although ES promoted improvements in motor function comparable to that in previous studies, the benefits of intraoperative ES were not detectable in other metrics of this rat model of peripheral nerve injury. Future work is needed to optimize sensory testing in the rodent injury model and compare electrical activity of collagen scaffolds to native tissue to detect differences.
Highlights
Peripheral nerve injury is a prevalent clinical challenge associated with high treatment costs and a significant impact on quality of life.[1]
Electrical activity naturally occurring in the peripheral nerves has sparked many research questions to investigate how exogenous electrical therapy can be used to encourage nerve growth after injury
The literature shows that intraoperative electrical stimulation (ES) influences nerve regeneration through increased neurite length, directional alignment of growing neurites, and the upregulation of biochemical factors to support growth.[5,6,9,27,28]
Summary
Peripheral nerve injury is a prevalent clinical challenge associated with high treatment costs and a significant impact on quality of life.[1]. Within 12–24 months of nerve injury, the target neuromuscular end plate loses its integrity and the adjacent muscle tissue undergoes irreversible fibrotic changes. Sensory end organs can last up to 3 years after a peripheral nerve injury, which allows for sensory function to be recovered even though muscle function may be lost.[2,3] Despite technological advances, the gold standard for bridging nerve-gap defects in the clinic remains the use of an autograft that provides the optimal native environment and scaffolding for axon regeneration.[2,3,4] repair with autografts is held to the 1 mm/day regeneration speed in humans; improvements in techniques to achieve healing prior to neuromuscular junction death continue to be investigated
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