Nerve transfers have been used in the past decades by reconstructive surgeons to treat upper extremity injuries [ 1 – 4 ]. In this application, peripheral nerves are transferred to new target muscles to either restore muscle function following nerve damages [ 4 , 5 ], restore hand function in tetraplegia, or to improve the control of myoelectric prostheses by targeted muscle reinnervation (TMR) [ 6 – 8 ]. Clinical studies have shown that nerve transfers provide exceptional outcomes in terms of regeneration [ 9 , 10 ], but limited quantities of donor nerves sometimes prevent better overall extremity function [ 11 ]. As little is known about the neurophysiological effects of nerve transfers, detailed experimental investigations may identify possibilities to refine this treatment. Currently, the standard neuromuscular experimental model is the rat hindlimb, which provides a large anatomy and many available studies on methodology or techniques [ 12 – 14 ]. However, 81 % of all nerve damages in humans occur in the upper extremity [ 15 ] and significant anatomical and physiological differences exist compared with the lower extremity. The same applies to nerve transfers, which are almost exclusively used in the upper extremity to restore critical hand function but rarely in the lower extremity. Important for functional outcomes is the application of nerve transfers that take synergistic function and axon ratio between donor and recipient into account. Correct axon ratio is crucial for the successful reinnervation of a high number of muscle fibers and thus muscle functionality [ 16 ]. The synergistic function between donor and recipient facilitates cortical recognition of the new innervation pattern by the patient [ 17 ]. This process of reintegrating lost muscle function via new nerve connections is in any case demanding but highly complicated if donor nerves are transferred to antagonistic muscles [ 5 , 18 ].
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Bergmeister et al. (2016) studied this question.
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