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A Novel Biologic Nerve Interface For Exoskeleton Control In The Setting Of Peripheral Nerve Compromise
Jennifer Lee, MD, Shelby Svientek, MD, Justin Wisely, BS, Amir Dehdashtian, MD MS, Paul Cederna, MD, Stephen Kemp, PhD.
University of Michigan, Ann Arbor, MI, USA.

Purpose: Advanced exoskeletons have been developed as assistive devices for those individuals with extremity weakness. Unfortunately, they are rarely utilized secondary to inadequate human-machine interfacing capabilities. To address this limitation, we have developed the Muscle Cuff Regenerative Peripheral Nerve Interface (MC-RPNI) which consists of a free skeletal muscle graft wrapped around an intact peripheral nerve. Over time, the MC-RPNI regenerates and becomes reinnervated and has the ability to amplify efferent motor action potentials to facilitate accurate and discrete exoskeleton control. The primary objective of this experiment was to determine if the MC-RPNI can amplify nerve signals in a nerve injury model without adversely impacting the function of distally-innervated muscles.
Methods: Rats were randomly assigned to five groups (n=6/group): (1) MC-RPNI; (2) nerve injury with distal MC-RPNI; (3) nerve injury with proximal MC-RPNI; (4) nerve injury; and (5) sham. Nerve injuries were created by resecting 50% of the common peroneal nerve’s diameter over a length of 15mm. MC-RPNIs were fabricated by harvesting and trimming the contralateral extensor digitorum longus (EDL) muscle to a length of 10mm and securing it to the nerve circumferentially with sutures. The MC-RPNI was placed distal (Group 2) or proximal (Group 3) to the nerve injury or centrally (Group 1) on the peroneal nerve. At three months, rats underwent electrophysiological analysis and muscle-force testing.
Results: All MC-RPNIs remained viable and demonstrated appropriate regeneration and reinnervation on histology and IHC (Figure 1). Peroneal nerve motor action potential amplitudes measured 71.8+/-18.3µV for injured nerves and 120.1+/-17.6µV for intact nerves. Average CMAPs were 5.1+/-0.8mV in MC-RPNIs located proximal to the nerve-injury and 2.9+/-0.4mV in those located distally, producing signal amplification of 38x and 53x, respectively. Although the MC-RPNI had no impact on distal muscle function in non-nerve-injured groups (EDL maximal tetanus: controls=2900+/-118mN; MC-RPNIs=2658+/-166mN), its location in rats with nerve-injury did have an effect. For those with the MC-RPNI located distally, EDL maximal tetanus (2223.9+/-201.5mN) was similar to those obtained from nerve-injury only rats (1932.2+/-96.0mN). However, for those rats with the MC-RPNI placed proximally, maximal tetanus (1233.2+/-184.7mN) was significantly lower.
Conclusion: When placed distal to nerve injury, the MC-RPNI has the ability to amplify injured peripheral nerve signals by several magnitudes while avoiding further functional impairment of distally-innervated muscle. However, muscle impairment can result if the MC-RPNI is placed proximal to a nerve-injury. Thus, it is important to consider the location of the nerve-injury when designing MC-RPNI interventions for the control of exoskeleton devices.


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