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Muscle Cuff Regenerative Peripheral Nerve Interface (MC-RPNI) for Exoskeleton Control Following Nerve Injury During the Early Postnatal Developmental Period in Rats
Katherine L Burke, MD1; Erin Guy, BS1; Jennifer C Lee, MSE1; Gabriela Cinotto, MD1; Nash P Hamill, BS1; Paul S Cederna, MD2; Stephen WP Kemp, PhD1
1University of Michigan, Ann Arbor, MI; 2Plastic Surgery, University of Michigan, Ann Arbor, MI

INTRODUCTION: Brachial plexus birth injuries (BPBI) occur in approximately 0.9 per 1000 live births in the United States and often result in devastating, life-long disabilities of affected children. In contrast to the process of regeneration and repair following nerve injuries in adults, neonatal nerve injuries lead to massive motor and sensory neuron death due to loss of functional contact between nerve terminals and their targets, in addition to the inability of immature Schwann cells in the injured nerve to sustain regeneration. Robotic exoskeletons have become a promising modality for restoration of function for individuals with extremity weakness, however, current user-intention detection processes remain suboptimal. To address this problem, we developed the Muscle Cuff Regenerative Peripheral Nerve Interface (MC-RPNI), consisting of a free muscle graft wrapped circumferentially around an intact peripheral nerve. Following reinnervation by collateral axonal sprouting, the MC-RPNI amplifies efferent motor action potentials by several magnitudes, allowing for higher fidelity signaling and detection of motor intention. The purpose of this study was to utilize the MC-RPNI in a rat model of neonatal nerve injury to amplify neuronal signaling necessary for intuitive control of an exoskeleton device.
METHODS: Forty-two Lewis rats were randomly assigned to one of seven groups (n=6/group) (see Table 1). Animals underwent nerve injuries on postnatal day 3 and MC-RPNI implantation was performed at 2 months of age. Behavioral testing was performed serially for 18 weeks to assess functional recovery and pain. After three months, in vivo electrophysiologic analyses were conducted to evaluate signaling capabilities of the MC-RPNI.
RESULTS: All neonatal nerve injury groups displayed impaired functional recovery following injury, demonstrating the persistence of severe deficits during this early postnatal developmental period. Following MC-RPNI implantation, mechanical or cold hypersensitivity did not develop in any group, indicating the MC-RPNI construct does not cause compressive neuropathy or chronic neuropathic pain. MC-RPNI constructs remained viable over the three-month period and demonstrated regeneration, revascularization, and reinnervation. Furthermore, MC-RPNIs generated amplified CMAP signals in all groups.
CONCLUSION: MC-RPNIs are capable of amplifying neuronal signals from peripheral nerves injured in the early postnatal period. The results of this study support the MC-RPNIís potential to serve as a biologic interface to facilitate accurate exoskeleton control in the setting of traumatic nerve injury with limited distal muscle reinnervation.


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