eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Trauma
Facial Nerve Repair
Updated: Jun 29, 2009
Introduction
Facial paralysis has many causes, and the etiology determines the likelihood of spontaneous return of function, as in most cases of idiopathic facial paralysis (Bell palsy). The transected or severely damaged nerve requires repair in order to achieve a satisfactory return of function. The problem remains a frustrating one because residual weakness and synkinesis is an inevitable component of the healing process. Nonetheless, most patients benefit greatly from modern techniques of repair.
The surgical anatomy and landmarks of the facial nerve.
History of the Procedure
The history of nerve repair dates back to Galen, who discussed the possibility of nerve regeneration in 200 AD. Paul of Arginia performed the first documented suture repair in 600 AD. The work of Waller in the 1850s was crucial to the understanding of peripheral nerve degeneration and regeneration. By the 1930s, Balance and Duel were reporting their results with facial nerve grafting. Lathrop and Myers advanced these techniques during World War II. In 1970, Scaramella described the technique of cross-face nerve grafting, further modified by Anderl.
Today, repair of the facial nerve involves several choices of procedures. These include direct repair, cable nerve grafting, and nerve crossover techniques. Facial nerve decompression for cases of intact but damaged nerves and procedures of facial reanimation distinct from the repair of the facial nerve are discussed elsewhere in this journal (see Dynamic Reanimation for Facial Paralysis).
Problem
Paralysis of the facial nerve is a cause of significant functional and aesthetic compromise. Functional concerns primarily involve adequate protection of the eye, with a real risk of exposure keratitis if not properly addressed. In addition, swallowing, drooling, and speech difficulties may arise. The degree of suffering these patients feel, however, is often far greater than these functional problems alone would produce. Patients with facial paralysis, especially younger ones, may experience tremendous psychosocial distress about their condition. Poor self-image and difficulty interacting with peers and family members can be devastating.
Repair of the facial nerve is generally a concern in cases of permanent complete facial paralysis. This may involve all or selected branches of the facial nerve. Frustration arises in the difficulty often found in achieving an excellent result. Synkinesis and hypofunction are an expected result, and these problems are among the challenges to be overcome with future improved techniques.
Etiology
The causes of facial paralysis are many. They may be divided into congenital, neoplastic, traumatic, inflammatory, and idiopathic.
Congenital facial paralysis, such as in the well-described although poorly understood Möbius syndrome, is uncommon.
Idiopathic facial paralysis (Bell palsy) makes up the most common type. These cases are often thought to be the result of virally induced inflammation of the nerve resulting in compromise of function, swelling, and vascular compromise. Facial nerve repair is uncommonly required because most of these patients regain function spontaneously. When paralysis is permanent, some advocate facial nerve decompression in selected cases. This article focuses on cases requiring various nerve grafting techniques, rather than procedures of decompression.
Traumatic injuries, which include blunt and penetrating trauma, as well as iatrogenic injury during surgery, comprise the next most common category. The site of injury to the facial nerve may be intracranial, intratemporal, or external to the stylomastoid foramen. Acoustic neuroma surgery is an example of a disease process and procedure that puts the facial nerve at risk, in this case in the cerebellopontine angle. Any of these sites of injury may be amenable to techniques of facial nerve repair, with the exception of injuries near the root entry zone of the nerve, in which case the length of facial nerve stump available to repair may be inadequate.
Neoplastic causes of facial paralysis commonly involve tumors of the parotid gland, typically malignant. Facial nerve schwannomas, acoustic neuromas, and neoplasms of the brain are among the less common causes of facial paralysis. Inflammatory and infectious causes of facial paralysis can occur. Infectious agents implicated include virally mediated conditions such as herpes zoster (eg, Ramsey Hunt syndrome), mumps, Coxsackie virus, and mononucleosis. Bacterial infections include sequelae of otitis media and Lyme disease.
Inflammatory conditions include sarcoidosis.
Pathophysiology
The facial nerve undergoes degeneration of the distal segment after significant injury, as described by Waller. Sunderland classified the degree of injury into 5 types. These 5 degrees describe the pathophysiologic events associated with each of the disorders described above that may affect the nerve.
First-degree injury is referred to as neurapraxia, in which a physiologic block is produced by increased intraneural pressure. An example is by external compression. The covering layers of the nerve (ie, endoneurium, perineurium, epineurium) are not disrupted, and the nerve is capable of stimulation. Full return of function without synkinesis is observed.
Second-degree injury involves a similar mechanism, but the compression is unrelieved and results in degeneration of the nerve axons. This is termed axonotmesis, and again, excellent return is expected, although recovery may take several months. Nerve stimulation is compromised, so distinguishing this from axonotmesis is difficult. Degrees 3 through 5 involve loss of endoneural, perineural, and epineural tubes, respectively. Fourth- and fifth-degree injuries imply partial or complete transection of the nerve. Regeneration is incomplete, and synkinesis is inevitable. Repair of the facial nerve is generally performed in cases of complete paralysis.
Presentation
History reveals the cause of the facial paralysis and is extremely important in treatment planning. The signs and symptoms of facial paralysis are obvious. The House-Brackman grading scale for facial paralysis is used to objectively describe the degree of paresis or paralysis. Patients demonstrate a lack of tone in addition to no movement on the affected side.
Of particular importance is the inability to adequately protect the eye. This should be assessed by careful inspection for signs of exposure keratitis, ability to close the eye, and the presence or absence of a Bell phenomenon. Questioning of partners and family members can reveal the adequacy of eye closure during sleep. Measures to protect the eye (eg, lubricants, artificial tears, eye taping at night) must be instituted as appropriate.
Indications
Facial nerve repair is an option for facial paralysis without a reasonable likelihood of spontaneous return of function. Essential in determining whether repair is indicated are the cause of the paralysis and the duration of time since the injury. Some general principles are helpful. In general, transected nerves produce the best result when reapproximated. This produces an intact motor nerve supply from the facial motor nucleus in the pons to the muscle endpoint and is preferable whenever possible. If direct repair without tension is possible, this is performed. Otherwise, a cable graft may be inserted to produce a tensionless coaptation of the proximal nerve stump to the distal branch or branches. Nerve crossover techniques are used when the proximal nerve stump is inadequate or inaccessible, preventing its use for grafting.
Another simple rule of thumb is that the sooner one can repair an injured facial nerve, the better the long-term result. This has in the past been somewhat controversial, but it is now believed to be true for most cases. In cases of trauma, in which the continuity of the nerve is in question, exploring within the first 3 days after injury is extremely desirable. This is because of the ability of the surgeon within this timeframe to use a nerve stimulator intraoperatively to identify the branches of the facial nerve. Once degeneration has occurred, stimulation of the nerve is not possible, and identifying the branches in an inflamed field can be extremely difficult.
Fibrosis of the nerve, fibrosis of the motor endplate, and atrophy of the muscle all ensue after injury. The surgeon is in a race against this inevitable process. Thus, the likelihood of success in a repair performed 18 months after the onset of paralysis is sure to be compromised, in comparison with the result obtained with repair in the first month after injury.
Waiting may be appropriate in specific instances, depending on the health of the patient, oncologic surveillance issues, and other concerns. Nonetheless, when possible, maximizing the patients' chance of a satisfactory outcome is desirable. Consider alternatives to repair, such as facial reanimation procedures, in such a case. In addition, patient-specific factors influence the clinical decision-making. In an elderly patient, slower nerve regeneration is expected, with a likely poorer result than in a younger patient. If the patient's life expectancy is short, for example, one may choose an adjunctive procedure to produce an immediate improvement, such as a dynamic muscle sling, rather than a nerve repair that takes quite some time to accomplish in the best of circumstances.
Relevant Anatomy
The facial nerve may be divided into intracranial, intratemporal, and extratemporal components. The intracranial portion of the facial nerve may be considered to include the supranuclear component (ie, voluntary motor cortex, internal capsule, extrapyramidal system, midbrain, pons) and the facial nerve nucleus and intracranial facial nerve. The intratemporal portion begins as the nerve enters the internal acoustic meatus and includes the well-described meatal, labyrinthine, tympanic, and vertical segments. The nerve then exits the stylomastoid foramen and soon divides at the pes anserinus. The subsequent branching to the temporal, zygomatic, buccal, marginal mandibular, and cervical branches shows some variability from person to person.
The blood supply to the facial nerve begins with the middle cerebral artery supplying the motor cortex. The facial nucleus in the pons is supplied by the anterior inferior cerebellar artery and the short and long circumferential arteries. The facial nerve proper is then supplied by the anterior inferior cerebellar artery, the middle meningeal artery, and the stylomastoid branch of the postauricular artery. These tend to overlap; however, the region just proximal to the geniculate ganglion is thought to be somewhat susceptible to vascular compromise secondary to the poorer redundancy present there compared with other areas.
Some discussion of the microanatomy is warranted for the purposes of this topic. Approximately 7000 neuron cell bodies make up the facial nerve, each of which innervates approximately 25 muscle fibers. The axons are surrounded by myelin, produced by the Schwann cells surrounding the axons. Three membranes comprise the nerve sheath. The epineurium is the outer covering, composed of loose areolar tissue, which separates the fascicles and holds them together. The perineurium is the next more inner layer. This is a dense layer of cells that are metabolically active and function as a diffusion barrier. The perineurium provides considerable strength to the nerve sheath. The individual nerve fibers are then each surrounded by endoneurium.
The spatial orientation of the nerve has traditionally been a matter of some debate. In the cortex and brainstem, the nerve is spatially oriented. If it continued in an organized spatial orientation through its extra-axial course, this would have implications for the facial nerve surgeon's technique of repair and ability to help to some degree to prevent synkinesis. It would also allow some identification of the area of injury of the nerve based on clinical findings. Although such clinical observations have been made by several authors, the evidence suggests that the spatial orientation is not present in the extra-axial facial nerve.1
For further information, please see the eMedicine article Facial Nerve Anatomy.
Contraindications
Repair of the facial nerve is contraindicated when the motor endplate muscle unit is no longer functional. This occurs after long-standing paralysis in which fibrosis occurs along with atrophy of the facial musculature. In such instances, reinnervation is not successful. The motor endplate muscle unit may fuse in cases of long-standing paralysis (ie, >1-1.5 y). Electrophysiologic testing can help to determine this.
Age of the patient is considered by some to be a relative contraindication. Anecdotal evidence demonstrates poorer results of reinnervation techniques in elderly patients. The nerve regenerates more slowly, and results are ultimately poorer than in procedures performed on younger patients.
Planned radiation therapy is not a contraindication to facial nerve repair. Regeneration of nerve function has been demonstrated despite subsequent ablative doses of radiation.
Facial nerve repair may be contraindicated in other situations. These would include instances when the general health status of the patient prevents elective surgery.
Workup
Imaging Studies
- In selected cases in which either the location or site of injury is unknown, both CT scanning and MRI may be helpful.
- High-resolution CT scanning of the temporal bone provides the best imaging of the bony confines of the facial nerve and may reveal the pathologic site at any point along its course.
- MRI is superior in delineating the details of the soft tissues, including the nerve itself. Thus it is the study of choice to diagnose acoustic neuromas and facial nerve schwannomas, for example.
Other Tests
- Several electrodiagnostic tests are used to evaluate the status of the facial nerve. These may be helpful in instances when the continuity of the nerve is unknown, such as after penetrating trauma in which the function of the nerve immediately after injury is not documented. More often, nerve testing is helpful in cases in which transection is not a concern, but the viability of the nerve is questionable. Examples in which testing would be helpful include patients with complete paralysis after acoustic neuroma surgery in which the nerve was maintained or in cases of idiopathic facial nerve paralysis. These tests are useful of course for cases of complete facial nerve paralysis.
- The nerve excitability test (NET), maximal stimulation testing (MST), electromyography (EMG), and electroneurography (ENoG) are available to evaluate the status of facial nerve function. Today, the two most helpful are the ENoG and EMG.
- ENoG is an objective quantitative measurement of nerve function. The test measures the summation potential of the response on the normal side of the face upon stimulation and compares the amplitude of the response to the paralyzed side. It is thought to correspond to remaining functional nerve fibers. This provides data that are predictive of the likelihood of spontaneous recovery. For example, in Bell palsy, patients who demonstrate greater than 90% degeneration within 14 days of onset have a decreased chance of recovery. Note that the ENoG (in addition to the MST and NET) is not useful in the first 3 days following injury because Wallerian degeneration has not yet occurred to a significant enough extent. Function is overestimated from tests performed during this timeframe.
- EMG is often complimentary to ENoG. EMG can be used to determine if a nerve in question is in fact in continuity (volitional activity recorded), shows evidence of Wallerian degeneration (fibrillation potentials), or has signs of reinnervation (polyphasic innervation potentials). Fibrillation potentials typically arise 2-3 weeks following injury, and polyphasic reinnervation potentials may precede clinical signs of recovery by 6-12 weeks.
Treatment
Medical Therapy
Currently, no medical treatment exists for facial nerve repair. Systemic corticosteroids are advocated by some to minimize swelling of the nerve in certain cases, such as facial paralysis following acoustic neuroma surgery when the nerve is known to be intact. In animal models, the use of electrical stimulation therapy appears to be beneficial in initiating and accelerating facial nerve recovery.2 A number of metabolic factors, such as neurotrophic factors, growth factors, stem cells, and others, show promise in the laboratory in aiding nerve repair, although these remain in the investigational phase.
The use of these agents has shown mixed results. For example, in animal experiments, glial cell line – derived neurotrophic factors were found to promote facial nerve regeneration in delayed grafting but were found to inhibit immediate nerve grafting.3 Similar animal experiments using stem cell therapy, such as bone marrow – derived mesenchymal stem cells in collagen, have shown that the stem cells in fact promote excessive growth support for axon regeneration and, in turn, excessive collateral nerve branching of the facial motor endplates. The unorganized branching pattern is not improved by manual stimulation, and, in its current form, stem cell therapy will need additional studies for it to be clinically useful for facial nerve repair.4
Surgical Therapy
Presently, 3 options exist for repair of the facial nerve. They are direct repair, cable nerve grafting, and nerve substitution techniques. Primary end-to-end nerve anastomosis and cable graft interposition have shown to produce superior functional outcome compared with nerve substitution techniques.5
Primary facial nerve repair
Direct repair of the facial nerve is the best method to rehabilitate the paralyzed face. This provides a chance of restoring spontaneous emotional expression to the face. Restoring continuity of the nerve by coaptation of the 2 nerve ends is indicated whenever the length of nerve is adequate to do so without undue tension. This may be performed virtually anywhere along the course of the nerve. An exception is the most proximal nerve in the cerebellopontine angle if the length is inadequate for grafting. In addition, if a transection of the nerve is present distal to the lateral canthus, repair is usually unnecessary because the nerve generally regenerates spontaneously in the more medial areas of the face.
If the nerve repair is to be successful, functional motor units must be available to receive reinnervation. That is, the facial musculature must not have atrophied excessively, and the motor endplates must be functional without significant fibrosis preventing reinnervation. Some controversy exists regarding the time course after injury in which these conditions may still be met. Most authors consider reinnervation by direct repair possible 1 year following the injury. Some argue that less than or more than a year is reasonable. EMG may be helpful in selected cases to determine if the nerve and muscle can be stimulated distal to the site of injury. If it can be stimulated, this implies a functioning motor endplate muscle unit.
Optimal timing of repair has been discussed extensively in the literature. The commonly accepted belief today is that the best time to repair an injured nerve is as soon as possible, not in a delayed fashion. This was promoted by some in the 1970s because of experimental data that suggested that repair was ideally performed 3 weeks after injury. More recent data, however, demonstrate that the best long-term results occur when the repair is performed as soon as possible.
Cable nerve grafting
When the length of facial nerve available is insufficient to graft primarily, the best option is cable grafting. In cases requiring cable grafting, the same general principles of microsurgery apply. Preoperative considerations must include a discussion with the patient regarding the options for donor nerves for repair. Commonly used nerves include the great auricular nerve and the sural nerve. The great auricular nerve has the advantages of proximity to the operative field and ease of harvest. The diameter is usually an appropriately sized match for the facial nerve. Up to 10 cm may be harvested, making this a good choice for most cable nerve grafts.
Downsides include the numbness of the ear that inevitably results. Also, in cases of malignant disease, use of the great auricular nerve has been discouraged because of the possibility of microscopic involvement of the nerve. Those who caution against this suggest using an alternative donor out of the field of involvement in cases resulting from facial nerve sacrifice secondary to malignancy, particularly when the tail of the parotid is involved or metastases to the neck are present.
The sural nerve is another option. It has the advantage over the great auricular nerve of having greater length (up to 40 cm) as well as a greater number of neural fascicles. Lateral foot numbness results. Another nerve available is the medial antebrachial cutaneous nerve of the upper arm. This can provide 15 cm of length and has a branching pattern that can be used to graft to multiple facial nerve branches.
Nerve substitution techniques
Cranial nerve substitution techniques include hypoglossal-facial (XII-VII) anastomosis and cross-face grafting. The spinal accessory–facial anastomosis is another well-described procedure, but it is largely relegated to historical status or situations in which other options are not available.
Hypoglossal-facial anastomosis
XII-VII anastomosis is considered the criterion standard for reanimating the face when the proximal end of the facial nerve is not available and the peripheral system is still viable. This may occur after surgery of the skull base, as in resection of acoustic neuroma. If sacrifice of the facial nerve is known at the time of the tumor removal, hypoglossal-facial anastomosis is best performed at that time. In cases in which paralysis becomes evident postoperatively, the same principles of timing apply. If no return of function becomes obvious, then performing the cranial nerve substitution procedure is appropriate. A successful result is possible many months later, but the likelihood of such an outcome is small after 12-18 months.
Essentially, 2 options exist for this procedure. Either the hypoglossal nerve is completely transected and connected to the facial nerve or a partial transection of the hypoglossal nerve is attached to facial nerve. The latter case may be accomplished with an interposition cable graft. An alternative is to mobilize the facial nerve via a mastoidectomy and nerve dissection, allowing the facial nerve to be transected more proximally. Then, the facial nerve can be brought to the partially transected hypoglossal nerve for repair.
Classic end-to-end anastomosis involves sectioning of the hypoglossal nerve distal to the takeoff of the descendens hypoglossi. This produces reliably improved facial tone and symmetry in over 90% of patients. The improvement is largely observed in the mid face, is less noticeable in the lower face, and is even less significant in the upper face, and improvement occurs over 4-6 months. On the other hand, the hemitongue mobility is impaired. This loss of function must be weighed against the expected gain in facial tone, symmetry, and movement. Spontaneous mimetic function is not expected to return, and some training is necessary to learn to smile by stimulating the hypoglossal nerve. Despite these factors, this procedure is generally well tolerated and fairly successful.
Two options are commonly used for the anastomosis. The classic technique is an end-to-end anastomosis. Recently, jump grafts have been performed, in which the hypoglossal nerve is just partially transected and a graft such as the great auricular nerve is used to connect the transected portion of the hypoglossal nerve to the end of the facial nerve. Advantages of this technique include minimizing tongue weakness and a purported decrease in synkinesis. The disadvantage is the need for 2 anastomoses, as well as fewer nerve cells used to "drive" the face.6
Cross-face grafting
The facial nerve cross-face anastomosis attempts to connect branches of the facial nerve of the normal side with corresponding branches of the paralyzed side. This procedure may be chosen for cases in which the proximal facial nerve of the involved side is unavailable for repair. This is possible because of the redundancy of the facial nerve innervation that is often present to many areas of the face, particularly the mid face. Alternatively, a donor nerve with less associated morbidity, such as the marginal mandibular nerve, may be sacrificed for the sake of the other side. Some iatrogenic weakness of the donor side is expected, and the patient must be well informed of this prior to consenting to undergo the procedure.
Some facial nerve surgeons think that donor side weakness can contribute to the success of the procedure, pointing out that many patients are happier with a more symmetric-appearing face, even at the cost of some function. This is a matter of some debate. As in all of the reinnervation procedures, the patient must have functioning motor end plates in the paralyzed side for this procedure to be successful. Thus, for cases of paralysis longer than 1 year's duration, the likelihood of success may be compromised. The cross-face technique has had variable success in different reports and remains somewhat controversial.
Intraoperative Details
Primary facial nerve repair
The facial nerve is exposed to a length sufficient to allow enough exposure and mobility to perform the grafting procedure. A parotidectomy incision is performed, followed by identification of the facial nerve as it exits the stylomastoid foramen using the traditional landmarks (ie, tragal pointer, sternocleidomastoid, posterior belly of digastric, stylomastoid suture). Once identified, the nerve is followed distally as necessary, using meticulous gentle technique as in a parotidectomy. If the intratemporal portion of the nerve is involved or requires exposure, this is performed via a mastoidectomy.
The key to successful nerve grafting is the careful coaptation of the nerve ends without tension. Several principles apply regardless of which specific type of procedure is chosen. The nerve tissue must be handled atraumatically with microinstruments. Magnification with an operating microscope is essential to allow meticulously precise alignment of the nerve ends. A colored background is helpful in clearly visualizing the anatomy. Typically, 2-3 sutures are carefully placed through the epineurium. Fine monofilament permanent suture is used, size 8-0 to 10-0. This minimizes tissue reactivity. Newer proposed methods of holding the edges together are discussed later in the article.
Although the criterion standard of repair is the epineural suture technique, this is somewhat controversial. Perineural and endoneurial or intrafascicular repairs have been advocated, but the data are unclear regarding the advantages of these techniques. The important relationship is the size match of the endoneurial surfaces. This must be inspected with magnification, and if a mismatch is evident, then one end may be trimmed in a beveled fashion to obtain a better surface area match of the ends to be approximated.
Instances may occur in which a segment of nerve is unavailable for reapproximation, either from resection due to malignancy or destruction by trauma. This prevents primary grafting without tension. This problem may be addressed in a number of ways. If the site of injury is intracranial or intratemporal, then the facial nerve must be rerouted, repaired with a cable graft, or both. In this instance, one may mobilize the facial nerve from the fallopian canal by decorticating the nerve via a transmastoid approach. If hearing preservation is not a concern, a translabyrinthine approach allows exposure of the nerve the entire length to the internal auditory canal. The mastoid tip may be removed to allow greater mobility of the nerve. Furthermore, the entire nerve can be rerouted by combining the mastoidectomy with a middle fossa approach, allowing grafting of the proximal portion of the nerve.
Peripheral injuries, likewise, may require mobilization of the nerve from one of the above-mentioned techniques in order to allow primary repair. Repairing the nerve with primary grafting is always preferable when feasible. If not, then a cable graft may be used.
Cable nerve grafting
The great auricular nerve is found by drawing a line between the angle of the jaw and the mastoid tip. This line is bisected at a right angle by the great auricular nerve as it passes around the posterior border of the sternocleidomastoid muscle just behind the external jugular vein. The nerve is the largest of the ascending branches of the superficial cervical plexus and arises from C2-3. Extra branches can be found by following the nerve toward its origin behind the sternocleidomastoid muscle.
The sural nerve can be located between the lateral malleolus and Achilles tendon. It lies just deep or posterior to the saphenous vein. It then runs superiorly up the back of the lower leg in a subcutaneous plane until it descends between the 2 heads of the gastrocnemius toward the popliteal fossa and its origin off the tibial nerve. The nerve may be harvested either by making a single long incision from the ankle to the popliteal fossa (depending on the length of nerve required) or a series of shorter transverse incisions. The nerve may be dissected under direct vision with the single incision or by using a fascia stripper and making the stepwise incisions.
The technique of nerve grafting is the same as for primary repair. In the case of cable grafting, obtaining enough nerve graft length to allow the graft to have some redundancy between the ends of facial nerve may be helpful. This would create a C or S shape and ensure tension-free coaptation.
Hypoglossal-facial anastomosis
A parotidectomy-type incision is made. The facial nerve is identified as it exits the stylomastoid foramen and is followed to just beyond the pes anserinus. It is sharply transected where it exits the stylomastoid foramen. The hypoglossal nerve is then isolated in the neck. It may be identified by following the posterior belly of the digastric toward the hyoid bone. The hypoglossal nerve passes lateral to the carotid artery and medial to the internal jugular vein. The nerve may then be followed distally to gain the maximum length for anastomosis. The descendens hypoglossi is usually transected to aid in mobilization and length. In the case of an end-to-end anastomosis, the hypoglossal nerve is transected distally and brought to meet the facial nerve by passing it either medial or lateral to the digastric muscle. The grafting of the nerve ends proceeds as previously discussed.
If a jump graft is performed, identification and transection of the facial nerve proceeds in the same manner. In this case, an appropriate length of great auricular nerve is then harvested. The hypoglossal nerve is then identified, including the descendens branch. The hypoglossal nerve is partially incised in a beveled fashion, most authors recommending a third to half the way across. The great auricular nerve graft is anastomosed to the proximal portion of the beveled cut. The other end is grafted to the distal end of the facial nerve in a typical fashion.
Another option for preserving tongue function is the split hypoglossal nerve graft. In this case, the hypoglossal nerve is split and dissected back to obtain a length that can be anastomosed to the facial nerve. This would therefore require only a single anastomosis. However, because the hypoglossal nerve also exhibits a lack of spatial orientation, with the nerve fibers interwoven randomly, some think this is a flawed concept because splitting of the nerve any significant distance would result in significant denervation of the tongue.
Cross-facial nerve graft
Several variations of the cross-facial anastomosis have been described. These differ in terms of which donor facial nerve branches are used, how many cross-facial grafts are performed, and the path chosen to pass the graft across the face to the other side. In each, a suitable nerve to graft must be chosen. The sural nerve is most commonly used because the length of nerve required to thread across the entire face, particularly if several branches are to be anastomosed, is quite significant. Alternatively, one may perform a single graft, and the great auricular nerve may be sufficient.
The dissection on the paralyzed side is performed first to ensure that the distal nerve can be identified. If several branches are to be grafted, the branches may be identified by following the nerve beyond the pes anserinus and identifying the branches within or just beyond the parotid gland. The contralateral normal facial nerve is identified in the standard fashion. The branches are individually identified. The donors are taken at the distal border of the parotid gland. A nerve stimulator is used to determine the areas innervated by the individual branches, and for each facial region, an attempt is made to find multiple nerve branches supplying a given area. This allows for the sacrifice of one branch with preservation of an adequate degree of function for a given anatomic region.
The sural nerve is then harvested and the branches tunneled across the face. This may be performed above and below the lip and through the neck. Passing the nerve across the forehead may have a poorer result secondary to a lesser blood supply to the graft lying within a relative lack of soft tissue. The nerve graft is sutured to the normal side. The graft may then be sutured to the chosen branch or branches on the paralyzed side.
Another option is to forego the anastomosis on the paralyzed side. A babysitter hypoglossal nerve anastomosis may be performed instead. This provides innervation to the paralyzed facial musculature and thereby prevents further degradation of the motor end plates and muscle atrophy as regeneration occurs across the considerable distance necessary for the cross-face graft. In this situation, the Tinel sign (ie, paresthesias associated with areas of nerve regeneration) is followed across the face for several months, and the patient is returned to the operating room when this sign indicates that regeneration has completely spanned the gap. The grafts are then anastomosed to the paralyzed branches.
A simpler technique uses only the marginal mandibular branch, which is sacrificed and anastomosed to the main branch of the paralyzed nerve in one setting. Function for each of these cases takes at least 6 months to begin to return. Synkinesis, as with the other procedures, is expected.
Postoperative Details
Postoperative care is similar for each of the above-described procedures. Meticulous hemostasis is important, with drains to prevent hematoma formation. Routine attention to details such as eye protection remains of paramount importance. Return of function takes months to occur.
Follow-up
Early follow-up relates to typical wound care. Long-term follow-up is very important. The results for most procedures are delayed for several months to a year. In some cases results are delayed up to 2 years, particularly with nerve transposition repairs.5 For this reason, adjunctive procedures such as gold weight eyelid implant and brow lift may be considered early. If no improvement is observed 1 year following repair, re-exploring the site of anastomosis is acceptable, and revision is performed if the repair is found to be inadequate. Another option is to consider adjunctive functional and cosmetic procedures or even alternative measures. These may include dynamic or static slings and free tissue transfer techniques.
Complications
Synkinesis is expected for all cases of facial nerve transection regardless of the mode of repair chosen, and the best result one can hope for is a House-Brackman grade III. These results therefore are not complications but expected sequelae. Donor site morbidity is also expected for the hypoglossal crossover technique (tongue weakness), great auricular harvest (ear numbness), and sural nerve harvest (lateral leg numbness). Complications for each of the procedures include hematoma and infection.
Outcome and Prognosis
As mentioned, residual weakness and synkinesis are guaranteed. A House-Brackman grade III is the best possible result. Certain factors, including older age at time of repair, long grafts, and extended delay between time of injury and repair appear to limit the functional outcome of repair. Vast majority of patients have improved symmetry and tone for the primary repair and cable grafting techniques. Hypoglossal facial crossovers improve tone and symmetry in more than 90% of patients. Training is required in these patients to learn to produce a smile by stimulating the hypoglossal nerve.
Future and Controversies
Active research continues to find ways to improve the results of treating facial nerve injuries. These include advances in the molecular biology of nerve regeneration and improved techniques of repair. A variety of neurotrophic and neurotropic factors have been investigated for their effects on the facial nerve. In addition, humoral factors have been identified as having a role in facial nerve regeneration. For example, the facial motor neuron is androgen dependent, and testosterone has been shown to enhance facial nerve regeneration.
Newer proposed techniques as possible alternatives to suture repair include laser neurorrhaphy and tissue adhesive repair. Synthetic and biologic tubules have been created to provide a path for the regenerating axons, even spanning small gaps in the nerve. As yet, these have not clearly shown superiority to the standard nerve grafting techniques. However, they remain important areas of continued investigation.
Controversies persist regarding the type (epineural versus perineural) and the timing of repair, as discussed above. The cross-facial nerve graft has very good results in certain reports but has not been as effective in other hands.
Multimedia
Media file 1: The surgical anatomy and landmarks of the facial nerve.
References
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Keywords
facial nerve repair, facial nerve, facial nerve grafting, nerve grafting, nerve repair, neurorrhaphy, direct facial nerves, cable nerve grafting, nerve crossover techniques
Contributor Information and Disclosures
Author
Tang Ho, MD, MSc, Instructor, Division of Facial Plastic and Reconstructive Surgery, Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine
Tang Ho, MD, MSc is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and Johns Hopkins Medical and Surgical Association
Disclosure: Nothing to disclose.
Coauthor(s)
Patrick Byrne, MD, Associate Professor, Department of Head and Neck Surgery, Division of Facial Plastic and Reconstructive Surgery, Johns Hopkins University School of Medicine
Patrick Byrne, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Cleft Palate/Craniofacial Association, and American College of Surgeons
Disclosure: Nothing to disclose.
John M Hilinski, MD, Clinical Instructor in Surgery, Department of Surgery, Division of Otolaryngology-Head and Neck Surgery, University of California San Diego Medical Center; Private Practice, San Diego Face and Neck Specialties PC
John M Hilinski, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, California Medical Association, and California Society of Plastic Surgeons
Disclosure: Nothing to disclose.
Peter Hilger, MD, Professor, Department of Otolaryngology, University of Minnesota Medical School
Peter Hilger, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, and Minnesota Medical Association
Disclosure: Nothing to disclose.
Medical Editor
Michael E Hoffer, MD, Director, Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center of San Diego
Michael E Hoffer, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery
Disclosure: American biloogical group Royalty Other
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Dominique Dorion, MD, MSc, FRCSC, Program Director and Division Chair, Professor of Surgery, Division of Otolaryngology, University of Sherbrooke, Canada
Disclosure: Nothing to disclose.
CME Editor
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position
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