Signal Amplification of the MC-RPNI for Exoskeleton Control following Volumetric Muscle Loss (VML) Injury
Katherine L Burke, MD1, Ipek Berberoglu, BS1, Brandon J Lin, BS1, Paul S Cederna, M.D.2 and Stephen WP Kemp, Ph.D.1, 1University of Michigan, Ann Arbor, MI, 2Plastic Surgery, University of Michigan, Ann Arbor, MI
Introduction: Volumetric muscle loss (VML) is the traumatic or surgical loss of skeletal muscle beyond the inherent regenerative capacity of the body, leading to permanent severe functional impairments in these patients. Currently, treatment for VML includes free muscle flaps as well as physical rehabilitation, however, neither adequately results in full functional restoration of the affected extremity. Recently, exoskeletons have been developed as promising devices for restoration of function for patients with motor extremity impairment, such as those with VML. Despite advancements in wearable exoskeleton technology, an adequate interface for exoskeleton control does not currently exist. To overcome this problem, we have developed the Muscle Cuff Regenerative Peripheral Nerve Interface (MC-RPNI), a construct composed of a free muscle graft wrapped circumferentially around an intact peripheral nerve. The MC-RPNI regenerates and reinnervates through collateral sprouting from intact axons within the encompassed nerve, enabling the construct to amplify efferent motor action potentials by several magnitudes. This signal amplification allows for higher fidelity signaling and motor intention detection. Here, we investigated the ability of the MC-RPNI to amplify signaling necessary for intuitive control of an exoskeleton device in a rat model of VML injury.
Methods: Twenty-four male Lewis rats were randomly assigned to one of four groups (n=6): 1.) VML injury, 2.) VML injury with MC-RPNI (3) negative control (complete resection of tibialis anterior (TA) muscle) with MC-RPNI, and (4) positive control (no injury) with MC-RPNI. VML injury was created with a 6 mm punch biopsy of the middle third of the TA. Two months following injury, MC-RPNIs were implanted around the common peroneal (CP) nerve. Endpoint testing was performed after a three-month construct maturation period, including in vivo electrophysiologic analyses and muscle force testing. MC-RPNI and TA were then harvested for histologic analyses.
Results: MC-RPNI constructs remained viable over the three-month maturation period in all animal subjects. Electrophysiologic analysis conducted in vivo demonstrated that the MC-RPNIs in all groups amplified physiologic CP nerve signaling and generated recordable compound muscle action potentials (CMAPs). Furthermore, muscle force testing demonstrated neural-evoked strength deficits of the TA muscle in VML injury groups, validating the model.
Conclusions: These findings demonstrate that the MC-RPNI is capable of amplifying neuronal signals from peripheral nerves to large, recordable EMG signals in the setting of VML. As such, the MC-RPNI has promising potential as a biologic neural interface to facilitate accurate exoskeleton control for functional restoration for individuals with VML injury.
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