Back to Annual Meeting Posters
A Ceiling Effect Exists for the Number of Nerves That Will Neurotize a Regenerative Peripheral Nerve Interface Device
Nicklaus S. Carrothers, HS1, Zachary P. French, HS2, Ziya Baghmanli, MD2, Cheryl A. Hassett, BS2, Theodore A. Kung, MD2, Jana D. Moon, BS2, Nicholas B. Langhals, PhD2, Paul S. Cederna, MD2, Melanie G. Urbanchek, PhD2.
1University of Rochester, Rochester, NY, USA, 2University of Michigan, Ann Arbor, MI, USA.
The regenerative peripheral nerve interface (RPNI) has potential for facilitating innate peripheral nerve signal transduction to microcomputers for control of motorized prosthetic limbs. Regenerated RPNI devices recover 20-30% of normally innervated muscle signaling capacity. We reported this for RPNI devices constructed with extensor digitorum longus (EDL) muscle neurotized by the entire peroneal nerve. Our purpose is to determine if providing more nerve fibers for RPNI neurotization increases RPNI signaling capacity.
Rat peroneal nerve has 6,000 nerve fibers, with 600 (10%) classified as myelinated motor while tibial nerve has 13,600 fibers with 1000 (7%) myelinated motor fibers. Fifty-seven rats were assigned to one of six groups varying density of nerve fibers neurotizing RPNI devices. Control EDL and SOL muscles remained innervated by native nerve. RPNI groups were: EDL muscle transfers with entire peroneal neurotization (EDL-RPNI) or SOL muscle transfers neurotized by the entire tibial nerve (SOL-RPNI). Negative controls were denervated EDL muscle (EDL-Den) and SOL muscle (SOL-Den). Recovery times were three to five months. Evoked maximal twitch compound muscle action potentials (CMAP) and maximal muscle contractile force were measured. Control and RPNI group muscles were digested to determine muscle fiber length to whole muscle length (Lf/Lo). Lf/Lo ratios are a factor in calculating physiologic cross sectional area (CSA).
Muscle Lf/Lo increased for EDL-RPNIs but not SOL-RPNI (Table 1). Dividing measured CMAP and force values by CSA normalizes data for comparing EDL and SOL muscles. Though SOL-RPNI devices were neurotized with 40% more motor axons than were implanted in the EDL-RPNI devices, the RPNI signal transduction represented by CMAP, specific CMAP, force and specific force measurements did not differ from EDL-RPNI device signaling (power >0.63) (Table 1). CMAP and specific CMAP signaling for the EDL-RPNI devices were 20% and 17% the Control EDL signals. CMAP and specific CMAP signaling for the SOL-RPNI devices were 27% and 25% the Control SOL signals. Specific CMAP and force deficits usually adjust for muscle atrophy seen with denervation. Muscle atrophy or loss of muscle mass was not observed in this study. CMAP and force measurements correlate strongly (≥ r=0.73, p<0.01) (Table 2).
Providing 40% more neurotizing nerve fibers during RPNI implant did not improve signaling capacity of the RPNI following at least three months of recovery. We believe this represents a ceiling effect on number of nerve fibers needed to neurotize RPNI devices. Both tibial and peroneal nerves contain 10 to 100 times more nerve fibers than innervate native EDL or SOL muscles.
This work was sponsored by the Defense Advanced Research Projects Agency, Grant/Contract No. N66001-11-C-4190.
Back to Annual Meeting Posters