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      Cross-Face Nerve Grafting with Infraorbital Nerve Pathway Protection: Anatomic and Histomorphometric Feasibility Study


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          Smiling is an important aspect of emotional expression and social interaction, leaving facial palsy patients with impaired social functioning and decreased overall quality of life. Although there are several techniques available for facial reanimation, staged facial reanimation using donor nerve branches from the contralateral, functioning facial nerve connected to a cross-face nerve graft (CFNG) is the only technique that can reliably reproduce an emotionally spontaneous smile. Although CFNGs provide spontaneity, they typically produce less smile excursion than when the subsequent free functioning muscle flap is innervated with the motor nerve to the masseter muscle. This may be explained in part by the larger number of donor motor axons when using the masseter nerve, as studies have shown that only 20% to 50% of facial nerve donor axons successfully cross the nerve graft to innervate their targets. As demonstrated in our animal studies, increasing the number of donor axons that grow into and traverse the CFNG to innervate the free muscle transfer increases muscle movement, and this phenomenon may provide patients with the benefit of improved smile excursion. We have previously shown in animal studies that sensory nerves, when coapted to a nerve graft, improve axonal growth through the nerve graft and improve muscle excursion. Here, we describe the feasibility of and our experience in translating these results clinically by coapting the distal portion of the CFNG to branches of the infraorbital nerve.

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          The cellular and molecular basis of peripheral nerve regeneration.

          Functional recovery from peripheral nerve injury and repair depends on a multitude of factors, both intrinsic and extrinsic to neurons. Neuronal survival after axotomy is a prerequisite for regeneration and is facilitated by an array of trophic factors from multiple sources, including neurotrophins, neuropoietic cytokines, insulin-like growth factors (IGFs), and glial-cell-line-derived neurotrophic factors (GDNFs). Axotomized neurons must switch from a transmitting mode to a growth mode and express growth-associated proteins, such as GAP-43, tubulin, and actin, as well as an array of novel neuropeptides and cytokines, all of which have the potential to promote axonal regeneration. Axonal sprouts must reach the distal nerve stump at a time when its growth support is optimal. Schwann cells in the distal stump undergo proliferation and phenotypical changes to prepare the local environment to be favorable for axonal regeneration. Schwann cells play an indispensable role in promoting regeneration by increasing their synthesis of surface cell adhesion molecules (CAMs), such as N-CAM, Ng-CAM/L1, N-cadherin, and L2/HNK-1, by elaborating basement membrane that contains many extracellular matrix proteins, such as laminin, fibronectin, and tenascin, and by producing many neurotrophic factors and their receptors. However, the growth support provided by the distal nerve stump and the capacity of the axotomized neurons to regenerate axons may not be sustained indefinitely. Axonal regenerations may be facilitated by new strategies that enhance the growth potential of neurons and optimize the growth support of the distal nerve stump in combination with prompt nerve repair.
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            Contributing factors to poor functional recovery after delayed nerve repair: prolonged denervation.

            The effects of prolonged denervation, independent from those of prolonged axotomy, on the recovery of muscle function were examined in a nerve cross-anastomosis paradigm. The tibialis anterior muscle was denervated for various durations by cutting the common peroneal nerve before a freshly cut tibial nerve was cross-sutured to its distal stump. Nerve regeneration and muscle reinnervation were quantified by means of electrophysiological and histochemical methods. Progressively fewer axons reinnervated the muscle with prolonged denervation; for example, beyond 6 months the mean (+/- SE) motor unit number was 15 +/- 4, which was far fewer than that after immediate nerve suture (137 +/- 21). The poor regeneration after prolonged denervation is not due to inability of the long-term denervated muscle to accept reinnervation because each regenerated axon reinnervated three- to fivefold more muscle fibers than normal. Rather, it is due to progressive deterioration of the intramuscular nerve sheaths because the effects of prolonged denervation were simulated by forcing regenerating axons to grow outside the sheaths. Fewer regenerated axons account for reinnervation of less than 50% of the muscle fibers in each muscle and contribute to the progressive decline in muscle force. Reinnervated muscle fibers failed to fully recover from denervation atrophy: muscle fiber cross-sectional area being 1171 +/- 84 microns2 as compared to 2700 +/- 47 microns2 after immediate nerve suture. Thus, the primary cause of the poor recovery after long-term denervation is a profound reduction in the number of axons that successfully regenerate through the deteriorating intramuscular nerve sheaths. Muscle force capacity is further compromised by the incomplete recovery of muscle fibers from denervation atrophy.
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              Mechanisms of Disease: what factors limit the success of peripheral nerve regeneration in humans?

              Functional recovery after repair of peripheral nerve injury in humans is often suboptimal. Over the past quarter of a century, there have been significant advances in human nerve repair, but most of the developments have been in the optimization of surgical techniques. Despite extensive research, there are no current therapies directed at the molecular mechanisms of nerve regeneration. Multiple interventions have been shown to improve nerve regeneration in small animal models, but have not yet translated into clinical therapies for human nerve injuries. In many rodent models, regeneration occurs over relatively short distances, so the duration of denervation is short. By contrast, in humans, nerves often have to regrow over long distances, and the distal portion of the nerve progressively loses its ability to support regeneration during this process. This can be largely attributed to atrophy of Schwann cells and loss of a Schwann cell basal lamina tube, which results in an extracellular environment that is inhibitory to nerve regeneration. To develop successful molecular therapies for nerve regeneration, we need to generate animal models that can be used to address the following issues: improving the intrinsic ability of neurons to regenerate to increase the speed of axonal outgrowth; preventing loss of basal lamina and chronic denervation changes in the denervated Schwann cells; and overcoming inhibitory cues in the extracellular matrix.

                Author and article information

                Plast Reconstr Surg Glob Open
                Plast Reconstr Surg Glob Open
                Plastic and Reconstructive Surgery Global Open
                Wolters Kluwer Health
                September 2016
                23 September 2016
                : 4
                : 9
                : e1037
                From the [* ]Division of Plastic and Reconstructive Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada; []Division of Plastic and Reconstructive Surgery, University of Toronto, Toronto, Ontario, Canada; and []Department of Surgery, University of Toronto, Toronto, Ontario, Canada.
                Author notes
                Gregory H. Borschel, MD, Division of Plastic and Reconstructive Surgery, The Hospital for Sick Children, 555 University Ave, Toronto ON M5G 1X8, Canada E-mail: gregory.borschel@ 123456sickkids.ca
                Copyright © 2016 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons. All rights reserved.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.

                : 25 May 2016
                : 26 July 2016
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