Repair and Recovery of Interpositional Nerve Grafts

Techniques used to repair damage to nerves vary according to the nature of the injury to the nerve. Further, advances in various techniques mean that more-recent developments in nerve repair and reconstruction, while fundamentally based on well-established procedures, have evolved to the point where successful outcomes are more common than ever. Despite these advances, however, nerve repair and reconstruction is still a delicate process, and does not always result in a positive outcome. There are a number of factors that can contribute to the outcome of nerve repair and reconstruction; the nature of the injury, the type of technique used to repair it and the anatomical location of the injury site all play significant roles in the outcome of the repair. This paper will examine the basic types of injury to peripheral nerves, the primary approaches to repair and reconstruction of injured nerves, and discuss the amount of time recover can and does take place depending upon the anatomical site of the injury.

Our awareness of the peripheral nervous system (i.e.- nerves outside the brain and spinal cord) date back centuries. Techniques used to repair injuries to peripheral nerves are much more recent, and have evolved rapidly in the last several decades. The approach taken to repairing nerves can range from simple suturing of the epineurium to the grafting of nerve tissue to connect fascicles1. In most cases, appropriate matching of fascicles is imperative; this and other facets of nerve repair and reconstruction will be discussed shortly. Among the primary considerations in choosing an approach to repairing damaged nerves is the extent and nature of the injury. Nerve injuries come in three basic types: compression, stretching, or complete dissection2. Nerves that are crushed or stretched may often be left to heal on their own, or at least a reasonable amount of time may be afforded to such healing before the idea of surgery is considered. Nerves that are stretched beyond their capacity to recover -typically more than 15% of their length- or that are cut, torn, or otherwise dissected are considered to be common candidates for repair and reconstruction2. This does not mean that all damage to peripheral nerves can be repaired, or that all such damage will even be considered for repair. Mitigating factors in considering a nerve injury for repair include the extent of the injury, the anatomical location of the injury, and the amount of time that has passed between the injury and the possible repair3. Even when the conditions are ideal for an attempt at repairing injured nerves, the chances of a positive outcome demonstrating significant recovery of nerve function hovers near 50%4.

The three primary types of nerve damage are classified as neurapraxia, axonotmesis, and neurotmesis2. In neurapraxia, the nerve is compressed or stretched, but axon continuity is maintained. These types of nerve injuries are generally left to heal on their own, and are only treated with surgical options in cases where healing is compromised. Axonotmesis typically involves nerves that are crushed, stretched, or even partially torn to the point that axon continuity is compromised. In axonotmesis some of the supporting and surrounding tissues of the nerve remain intact. The most significant form of nerve damage, neurotmesis, involves the complete cutting, tearing, or other form of dissection to the nerve. In some cases neurotmesis can be repaired by surgically joining the proximal and distal ends of the damaged nerves. In conditions where joining the proximal and distal ends of the damaged nerve would place too much tension on the repair site, it is typically necessary to graft additional tissue into the repair site. The techniques used to perform such a procedure have come a long way in recent years as surgeons and researchers have gained experience and knowledge about what approaches to nerve grafting result in the most positive outcomes5.

The general forms of nerve injury outlined above have degrees within each that further differentiate the seriousness of the injury and what approach, if any, will be taken to treating it2. Axonotmesis is, in fact, subdivided into three distinct types (neurapraxia is Type 1; axonotmesis is Type 2-4; neurotmesis is Type 5). The three different types of axonotmesis are categorized according to the extent of damage to the structures surrounding the axons. In each case, axon continuity is compromised; in Type 2, only the axons are affected; in Type 3 axon and endoneurium continuity is compromised; in Type 4, axon, endoneurium and perineurium continuity are compromised. In each type of axonotmesis the continuity of the epineurium remains intact; when the epineurium is compromised along with the other structures the injury is classified as Type 5, or neurotmesis. Lee and Wolf say the following about injury to and healing of peripheral nerves: “after injury (short of transection), function fails sequentially in the following order: motor, proprioception, touch, temperature, pain, and sympathetic. Recovery occurs sequentially in the reverse order.” For injury involving transaction and surgical repair the rate and extent of recovery will vary widely depending on the site and severity of the injury and other factors.

Schonauer et al discuss the evolution of nerve grafting, noting that grafting was long thought to be inferior to direct repair until advances in technique and approach produced positive outcomes that were sometimes equal to or greater than those achieved through direct repair. Because direct repair was thought for so long to be superior to grafting, surgeons often went to great lengths to make such direct repair possible, and to ameliorate or eliminate the application of tension on the repair site6. In some cases extensive surgical procedures, including the removal of bone to shorten the repair site, were undertaken in an effort to minimize such tension. Further complicating the issue of grafting is that there are two sites of anastomosis across which axon continuity must be restored (at the proximal and distal ends of the injured nerve that are being bridged by the grafted tissue). Relatively recent advances in the approaches to grafting have resulted in more positive outcomes, leading surgeons to more frequently consider grafting as an alternative to direct repair of damaged nerves7.

Most of the advances in grafting have come about from simple trial-and-error; older techniques and approaches have sometimes been supplanted by new approaches as different techniques have produced greater positive outcomes7. For many years the prevailing wisdom guiding nerve grafting was to use the thickest possible donor nerve; the problem with this approach was that the rate of revascularization tends to be in inverse proportion to the thickness of the donor nerve4. In more recent years surgeons have had success in choosing thinner grafts that still facilitate the growth of axon and other structural continuity while allowing for easier revascularization of the affected tissue.

For both direct repair and nerve grafting it is typically necessary to prepare the proximal and distal sites of the damaged nerve8. Changes to the damaged portions of the injured nerves begin soon after injury; in some cases these changes can facilitate healing and in others they can hinder it. Wallerian degeneration, for example, begins in the distal portion of a severed nerve within hours or days of the time of injury2. Such degeneration involves changes to the axons that must be removed prior to direct repair or grafting. The proximal end of the injury site undergoes a different set of changes; this includes the development of a growth cone at the tip of the damaged axion. This growth cone is “a specialized motile exploring apparatus”2 that seeks out new paths for the spontaneous healing and regeneration of damaged nerve tissue.

For many years it was believed that it was best to allow several weeks to pass for Wallerian degeneration to take place before attempting to surgically repair danged nerves; more recently, researchers have determined that more immediate repair results in better outcomes4. The site of the surgery must be adequately prepared; this includes ensuring the site is properly vascularized, that the skeletal and muscle structures are strong and stable, and that the distal and proximal ends of the transected nerve have had damaged tissue cut away to allow the proper development of axon continuity2. In larger, multifascicular nerves, it is typically necessary to take care to properly match the fascicles and other nerve structures9. Nerves that are “mixed-function”9 and contain fascicles that control, for example, various motor functions must be properly matched to ensure that reinnervation results in the renewal of such motor functions. In cases where fascicles are poorly or improperly matched it may be impossible to restore sensory and motor function, obviating the primary purposes of surgical repair9.

The rate and extent to which damaged nerves can heal on their own or recover after surgery depend on a number of factors. Nerves that are injured by stretching may simply recover on their own after the force that caused the stretching is removed. Nerves that are stretched beyond their capacity to heal on their own may need to be repaired by surgical means. In cases where a nerve is compressed, it may be necessary to perform surgery not on the nerve, but o the area around it that is causing the compression. For nerves that are damaged to the point where surgical repair or grafting is necessary, the need to address the problem quickly is determined by the extent and nature of the injury, as well as the primary function of the affected nerve(s). Sensory nerves can be repaired even many years after being damaged, while nerves associated with motor function –i.e. nerves where muscle is the target organ- must typically be repaired in a relatively short time if motor function is to be restored2.

The anatomical site of a nerve injury will also determine, at least in part, how well and how quickly the damaged nerve will recover after surgery. Typically, the more distal the injury the greater the amount of time it will take to heal. Sasmor13 cites the example of facial paralysis in infancy resulting from facial nerve compression during childbirth. Such paralysis typically reverses itself with several weeks or months after birth; such recovery time is brief in part because the distance from the brain to the involved peripheral nerves is so short. Nerve damage that takes place in, for example, the hand, will likely take longer to heal (and may result in less-than-complete sensory or motor function) than damage that is more proximal to the central nervous system9.

Although the rate and extent of recovery of peripheral nerves after grafting are affected by a number of factors, the general physiology remains the same. The recovery and healing of post-surgical damaged nerves involves a complex set of processes; generally speaking, however, healing and recovery is determined by the precision with which the nerve has been repaired and the ability of the surrounding tissue to produce nerve growth factor and otherwise support recovery10. The choice of whether to perform a direct repair or to choose an interpositional graft is usually made based on the amount of tension that will be placed on the repair site6. Some minor amount of tension has been found to speed repair over a tension-free repair; generally, however, anything beyond the most minimal tension will result in a poor outcome6. In such instances, or in cases where the proximal and distal ends of the damaged nerve must be removed to an extent that leaves too large a gap, it typically becomes necessary to repair the site by grafting.

The general purpose of grafting nerve tissue into a damaged nerve is to facilitate the development of new axon continuity. A fundamental component of ensuring the rapid and adequate healing of the graft site is revascularization; the more quickly and fully the site is revascularized, the more quickly and completely nerve function can be restored3. Revascularization is the first step in the recovery and healing of grafted nerves, and it is critical to ensure a successful outcome. Subsequent to the revascularization process, new axon continuity develops within the grafted tissue, with the most positive outcome being full or nearly-full restoration of sensory or motor activity. This recovery can take weeks or months, depending on such factors as the type of nerve that was injured, the age of the patient, and the degree to which the fascicles were properly matched5. Mixed-function nerve bundles that drive both sensory and motor function may take longer to recover, and poorly matched fascicles may result in incomplete recovery.

While the recovery rates of different types of injury and repair vary, the process is more or less the same. A properly vascularized area will serve as the site of sprouting angiogenesis, wherein microcappilaries will develop in the site, feeding blood, nerve growth factor, and other supporting functions to the grafted tissue11. It is important to minimize the production of scar tissue and to eliminate as much damaged tissue as possible before surgery to ensure that the newly-growing nerve cells can easily grow to connect the damaged nerve ends15. As healing continues, sensory functions typically return quickly, while the reinnervation of muscle tissue needed to restore motor function may take more time13. Full recovery of sensory and motor function is not always possible, but minimizing the exacerbating effects of time and damage may result in more positive outcomes. It is impossible to accurately predict how long recovery will take, with the time needed for recovery ranging from weeks to years depending on the nature and extent of the injury, the proficiency of the surgical repair, and the age and condition of the patient.




  1. Noaman, Hassan H. “intech.” Surgical Treatment of Peripheral Nerve Injury. N.p., n.d. Web. 1 Feb. 2013. <>.


  1. Lee, Steve K., and Scott W. Wolfe. “Peripheral Nerve Injury and Repair.” Journal of the American Academy of Orthopaedic Surgeons4 (2000): n. pag. Web. 1 Feb. 2013.


  1. Kalia, Susheel et al. Cellulose Fibers: Bio- and Nano-Polymer Composites ; Green Chemistry and Technology. Berlin, Germany: Springer, 2011. Print.


  1. Laschke, Matthew, et al. “Inosculation: connecting the life-sustaining pipelines.” Tissue Engineering, Part B: Reviews4 (2009): 435. Web. 1 Feb. 2013.


  1. Midha, Rajiv, and Eric L. Zager. Surgery of Peripheral Nerves: A Case-Based Approach. New York, NY: Thieme, 2008. Print.


  1. Greco, Giovanni N. Tissue Engineering Research Trends. New York, NY: Nova Science Publishers, 2008. Print.


  1. Meyer, Ulrich. Fundamentals of Tissue Engineering and Regenerative Medicine. Berlin, Germany: Springer, 2009. Print.


  1. Kondo, K., et al. “+ – Reconstruction of the intratempor… [Acta Otolaryngol Suppl. 2007] – PubMed – NCBI.” National Center for Biotechnology Information. N.p., n.d. Web. 1 Feb. 2013. <>.


  1. Hentz, Vincent R, and Robert A. Chase. Hand Surgery: A Clinical Atlas. Philadelphia, Pa: W.B. Saunders, 2001. Print.


  1. Levine, Marci, et al. “Nerve growth factor is expressed in rat femoral vein.” Journal of Oral and Maxillofacial Surgery7 (2002): 729-733. Print.


  1. Newton, Charles D, and David M. Nunamaker. Textbook of Small Animal Orthopaedics. Philadelphia, PA: Lippincott, 1985. Print.


  1. Dumitrescu-Ionescu, Doina. “Journal of medicine and life | Reconstructive microsurgery of peripheral nerves.” Journal of medicine and life | Home. N.p., n.d. Web. 2 Feb. 2013. <>.


  1. Heijke, G. et al. “Processed Porcine Collagen Tubing Versus Conventional Suturing In Peripheral Nerve Reconstruction: A Study In Rabbits.” Microsurgery3 (2001): n. pag. Web. 16 May 2001.



  1. “Nerve Injury, Nerve Reconstruction, and Recovery of Nerve Function.” Riversong Plastic Surgery | Newburyport, MA | Anna Jaques Hospital | Michele Sasmor, MD. N.p., n.d. Web. 1 Feb. 2013. <>.


  1. Schonauer, Fabrizio, et al. “Peripheral Nerve Reconstruction with Autologous Grafts.” intech. N.p., n.d. Web. 1 Feb. 2013.