A Caprine Model of a Novel Amputation Paradigm for Bi-directional Neural Control of a Bionic Limb
Tyler R. Clites, BS, Matthew J. Carty, MD, Hugh M. Herr, PhD.
MIT, Cambridge, MA, USA.
PURPOSE - No significant changes have been made to limb amputation surgical paradigms since the Civil War era. Traditional approaches are plagued by poor nerve treatment, which leads to neuromas and phantom pain, and complicates neural communication with advanced limb prostheses. In this study we present a caprine model of the Linked Residual Musculature Peripheral Nerve Interface (LRM-PNI), a surgical approach designed to reduce phantom pain and improve bi-directional neural control of a bionic limb. The key advancement in this architecture is the surgical coaptation of natively-innervated agonist-antagonist muscle pairs within the residuum. The benefits of this approach are two-fold. First, preservation of the mechanical coupling between agonist contraction and antagonist stretch allows physiologically-relevant muscle state feedback from a prosthesis through mechanical activation of native mechanoreceptors within these linked muscles. Second, by preserving functionality of these native mechanoreceptors, we limit the presence of non-meaningful phantom sensation, including phantom pain. We hypothesize that these advancements will allow for afferent proprioceptive sensation of a limb prosthesis through native neural pathways, which is crucial in both reflexive and volitional lower extremity control during gait.
METHODS - A transtibial amputation was performed on the hindlimb of a goat, during which the lateral tarsal tunnel from the amputated ankle was grafted transversely to the medial surface of the tibia, serving as a “synovial pulley”. Distal ends of the lateral gastrocnemius and tibialis cranialis were then coapted to either end of this synovial pulley, allowing coupled motion of the agonist-antagonist muscle pair (see figure). The residual musculature was sensorized with implantable epimysial and intramuscular electrodes, as well as sonomicrometry crystals. Over a two-month period, electromyography and muscle-state measurements were recorded from the residuum while the animal ambulated without a prosthesis, and fluoroscopic evaluations of coupled motion in the presence of artificial muscle stimulation were carried out under anesthesia. The animal was then sacrificed, and the residuum was examined.
RESULTS - Electromyography from residual musculature during gait indicate that the animal continued to send neural commands to the coapted agonist-antagonist muscle pair in the absence of a prosthetic limb device. Muscle-state measurements and fluoroscopic evaluations show clear coupled motion of the agonist-antagonist pair in the presence of both natural neural commands and artificial muscle stimulation. Integrated EMG from the agonist muscle was cross-correlated against muscle state recordings from the antagonist; it was determined that the average time delay from agonist muscle activation to antagonist muscle stretch was 93 ms, with a correlation coefficient of .73. Post-mortem examination of the residual tissues showed no signs of necrosis and no abundance of scarring.
CONCLUSIONS - These findings indicate that the LRM-PNI architecture has the potential to provide coupled motion of agonist-antagonist muscle pairs, as in the pre-amputation physiological milieu. Guided by these findings, it is our expectation that further development of the LRM-PNI architecture will improve bi-directional neural control of advanced limb prostheses.
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