Facial palsy is a devastating condition with profound functional, aesthetic, and psychosocial implications. Although the complexity of facial expression and intricate synergy of facial mimetic muscles are difficult to restore, the goal of management is to reestablish facial symmetry and movement. Facial reanimation surgery requires an individualized treatment approach based on the cause, pattern, and duration of facial palsy while considering patient age, comorbidities, motivation, and goals. Contemporary reconstructive options include a spectrum of static and dynamic procedures. Controversies in the evaluation of patients with facial palsy, timing of intervention, and management decisions for dynamic smile reanimation are discussed.
Key points
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Determining the cause, pattern, and duration of facial palsy is critical. Timely intervention is perhaps the most important factor that influences outcome after facial reanimation.
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Smile reanimation options include regional muscle transfer, neurotization, and free muscle transfer. The selection of a donor nerve for the last two is highly individualized.
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Dual innervation by the masseteric nerve and cross-facial nerve graft may optimize both strength and spontaneity of movement when free muscle transfer is used.
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Analysis of clinical outcomes in facial nerve reconstruction remains limited because of the lack of universal evaluation methods and standardized outcome measures.
Video content accompanies this article at http://www.facialplastic.theclinics.com
Introduction
Facial palsy (FP) is a devastating condition with profound functional, aesthetic, and psychosocial implications. Injury to the facial nerve disrupts the complex association between facial expression and emotion, thereby compromising social interactions and adversely affecting quality of life. FP can result in a myriad of aesthetic and functional sequelae, including facial asymmetry, paralytic lagophthalmos and subsequent exposure keratopathy, eyelid retraction and ectropion, nasal obstruction secondary to nasal valve collapse, impaired oral competence, and articulation deficits. Ultimate outcomes following facial nerve insult are widely heterogeneous, ranging from full return of normal function to complete flaccid facial paralysis, with varying degrees of static and kinetic hypoactivity, hyperactivity, and synkinesis in between. There are numerous causes of FP. The most common cause is Bell palsy, followed by benign or malignant tumors, iatrogenic injury, Varicella-zoster virus–associated FP, trauma, and congenital palsy. The treatment of FP is equally as diverse and requires a thoughtful, highly individualized approach based on the cause, pattern, and time course of FP.
Introduction
Facial palsy (FP) is a devastating condition with profound functional, aesthetic, and psychosocial implications. Injury to the facial nerve disrupts the complex association between facial expression and emotion, thereby compromising social interactions and adversely affecting quality of life. FP can result in a myriad of aesthetic and functional sequelae, including facial asymmetry, paralytic lagophthalmos and subsequent exposure keratopathy, eyelid retraction and ectropion, nasal obstruction secondary to nasal valve collapse, impaired oral competence, and articulation deficits. Ultimate outcomes following facial nerve insult are widely heterogeneous, ranging from full return of normal function to complete flaccid facial paralysis, with varying degrees of static and kinetic hypoactivity, hyperactivity, and synkinesis in between. There are numerous causes of FP. The most common cause is Bell palsy, followed by benign or malignant tumors, iatrogenic injury, Varicella-zoster virus–associated FP, trauma, and congenital palsy. The treatment of FP is equally as diverse and requires a thoughtful, highly individualized approach based on the cause, pattern, and time course of FP.
Overview of facial reanimation
Although the complexity of facial expression and intricate synergy of facial mimetic muscles are difficult to fully restore, the ultimate goal of FP treatment is to reestablish facial symmetry and movement. Static techniques and nonsurgical procedures lack true reanimation, although they are a useful adjunct in many patients to improve facial resting appearance. In order to identify the appropriate techniques for dynamic reanimation, it is essential to have a thorough understanding of the mechanism and extent of facial nerve injury, the duration of palsy, and viability of facial musculature. Equally as important are patient factors, such as age, overall health, motivation, and goals for rehabilitation. A holistic approach with attention to both the paralyzed and nonparalyzed sides of the face tends to yield more effective results.
Classification of Facial Palsy
Outcomes following facial nerve insult are widely heterogeneous, ranging from full return of normal function to complete flaccid facial paralysis, with varying degrees of static and kinetic hypoactivity, hyperactivity, and synkinesis in between. Complete flaccid FP results in loss of symmetry at rest, paralytic lagophthalmos, nasal obstruction, oral incompetence, and loss of dynamic facial movement. In nonflaccid FP , symptoms are dictated by the specific pattern of dysfunction with varying degrees of mass movement and synkinesis occurring on the affected side and compensatory hyperactivity on the healthy side. Lack of a meaningful smile can also occur in severe nonflaccid palsy. It is important to identify the type of facial paralysis as it intimately affects management.
Reversible Versus Irreversible Facial Palsy
One of the most critical assessments in FP management is determining whether the FP is reversible or irreversible. Although reanimation (via regional or free muscle transfer) is possible even in cases of irreversible paralysis, reinnervation is not. Thus, the clock starts ticking from the day of onset of facial paralysis. Facial nerve biopsies from patients with long-term FP show that the size and number of nerve axons decline even during the first 3 months. Facial muscles with reversible palsy have viable muscle fibers with intact motor units that will respond to ingrowing axons. When the time from injury to reinnervation exceeds more than 18 to 24 months, facial paralysis becomes irreversible; denervated muscles develop nonfunctional motor end plates and irreversible atrophy, eliminating any chance of successful reinnervation.
Key Principles in Dynamic Facial Reanimation
The facial nucleus and nerve provide tone, volitional movement, and emotional animation that cannot be adequately replaced. Where feasible, primary facial nerve repair provides the best outcomes. When tension-free primary repair is not possible but the proximal facial nerve remains intact and available, a nerve interposition graft (most commonly with the greater auricular or sural nerve) is the next best choice. However, when the proximal facial nerve stump is not available because of damage of its intracranial and/or intratemporal segments, neurotization or nerve transfer using a new motor nerve is an option. Neurotization procedures seek to repurpose an alternative neural source to restore existing facial mimetic muscles and are indicated when the native muscles remain amenable to reinnervation. The most commonly used nerve substitutes are the contralateral facial nerve, motor nerve to the masseter muscle, and the hypoglossal nerve.
Methods that reinnervate native facial muscles in a timely matter are preferred if possible, as no other skeletal muscle can adequately simulate the complex morphology and organization of facial mimetic muscles. However, when native muscles are congenitally absent or are irreversibly paralyzed because of prolonged denervation, regional muscle transfer (ie, temporalis tendon transfer) or free muscle transfer (ie, microvascular gracilis muscle transfer) can be used to replace muscle function in dynamic reanimation. Static suspension techniques, nonsurgical procedures such as chemodenervation, and physical therapy are useful adjuvant and, sometimes, primary treatment options for some patients.
The duration of facial muscle denervation and timeliness of intervention are perhaps the most important factors that determine the ultimate success of any reinnervation procedure. Patient age has also been shown to be an important factor influencing outcomes, with elderly age associated with poorer results. The age-related decline in neural regeneration is well established and thought to be multifactorial, secondary to myelin sheath deterioration, axonal atrophy, decline in nerve conduction, and slower rate of axonal regeneration.
Controversies in contemporary facial reanimation
The management of FP is challenging because of the wide variability in cause and presentation and the diversity of available treatment options. Contemporary facial reanimation is particularly charged with debate in the following areas (summary in Table 1 ):
Patient evaluation
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How should FP be graded and outcomes assessed?
Timing of intervention
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At what point in the time course of FP is reanimation surgery appropriate, particularly in cases of complete facial paralysis whereby the facial nerve is anatomically intact?
Smile reanimation
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What is the optimal approach for smile reanimation? What is the best donor nerve for neurotization or free muscle transfer procedures and why? When is regional muscle transfer a better choice than free muscle transfer? What is the role for reanimation surgery in incomplete, nonflaccid FP?
| Controversial Topics | Summary Points |
|---|---|
| Patient evaluation : Evaluating patients with FP is challenging because of the wide variability in cause, presentation, and treatment options. | |
| FP grading scales |
|
| Timing of dynamic reanimation: When the facial nerve is interrupted, there is no question that immediate or early nerve repair is recommended. Timing is not so clear in cases of complete facial paralysis whereby the facial nerve is thought to be anatomically intact, such as after vestibular schwannoma extirpation. | |
| Timing of intervention |
|
| Smile reanimation: Dynamic smile reanimation may be achieved through reinnervation of native facial musculature (in reversible paralysis) via nerve transfer procedures or replacement of facial mimetic muscles (in irreversible paralysis) with regional or free muscle transfers. | |
| Nerve transfers: selection of a donor nerve |
|
| Regional muscle transfer vs free muscle transfer |
|
| Free muscle transfers: selection of a donor nerve |
|
| Reanimation in incomplete palsy |
|
An evidence-based discussion regarding these controversial questions is presented.
Controversies in patient evaluation
A thorough history should elicit the cause of FP, onset and duration, clinical symptoms, patient concerns, and goals of care. Comprehensive physical examination should then be performed in a zonal fashion to systematically assess facial function. Photographs and video recordings are essential for documenting facial appearance at rest and during a full range of volitional movements (repetitive blink, brow elevation, light-effort and full-effort eye closure, lip pucker, light-effort and full-effort smile, and lower lip depression). These photographs and video recordings should be obtained on presentation and at every follow-up visit.
Facial Palsy Grading Scales
The measurement of facial nerve function through a robust grading system is essential for evaluating and communicating the course of FP and outcomes after intervention. However, the development of a universal grading system is challenged by the complexity of facial nerve dysfunction and the inherent subjectivity of describing facial expression. Consensus among facial nerve specialists regarding appropriate clinician-graded and patient-reported scales is lacking.
The ideal facial nerve grading system should be relatively quick and convenient, reproducible with low interobserver variability, include measures of both static and dynamic components of facial muscle function, and incorporate secondary defects of facial nerve dysfunction, such as synkinesis. Introduced in 1983 and officially endorsed by the American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS), the Facial Nerve Grading System 1.0 or more commonly known as the House-Brackmann (HB) scale ( Table 2 ) has been the standard for facial nerve disorders. It is a 6-point grading scale originally intended solely for reporting the degree of FP following vestibular schwannoma resection. As it has been applied to a variety of other conditions that result in FP, the major criticisms of the HB scale have been its lack of sensitivity in tracking zonal changes and in distinguishing subtle differences in facial nerve recovery as well as poor interobserver reliability.
| Grade | Gross | Resting Tone | Forehead | Eye Closure | Mouth |
|---|---|---|---|---|---|
| I | |||||
| Normal function | Normal | Normal | Normal | Normal | Normal |
| II | |||||
| Mild dysfunction | Slight weakness | Normal | Moderate to good movement | Complete with minimal effort | Slight asymmetry |
| III | |||||
| Moderate dysfunction | Obvious difference, noticeable synkinesis | Normal | Slight to moderate movement | Complete with full effort | Slightly weak with maximal effort |
| IV | |||||
| Moderately severe dysfunction | Disfiguring asymmetry | Normal | None | Incomplete | Asymmetric with maximal effort |
| V | |||||
| Severe dysfunction | Barely perceptible motion | Asymmetric | None | Incomplete | Slight movement |
| VI | |||||
| Total paralysis | No movement | Asymmetric | None | Incomplete | No movement |
Newer scales have been developed as a result; the most commonly used one is the Sunnybrook scale ( Table 3 ). Published in 1996, it is a weighted system that provides a composite score based on the evaluation of resting symmetry, degree of voluntary excursion, as well as synkinesis. Although it is susceptible to the same interobserver variability as the HB scale, the Sunnybrook system provides a continuous scale that is more sensitive to finer differences in facial nerve function. In 2009, the Facial Nerve Disorders Committee of the AAO-HNS published a revised version of the HB scale called the Facial Nerve Grading System 2.0 ( Table 4 ), with the goal of preserving the simplicity of the original while incorporating the valuable features of the newer grading scales. This new system includes regional scoring of facial movements and accounts for synkinesis but maintains agreement comparable with the original scale.
| Score | Region | |||
|---|---|---|---|---|
| Brow | Eye | NLF | Oral | |
| 1 | Normal | Normal | Normal | Normal |
| 2 | Slight weakness >75% of normal | Slight weakness >75% of normal Complete closure with mild effort | Slight weakness >75% of normal | Slight weakness >75% of normal |
| 3 | Obvious weakness >50% of normal | Obvious weakness >50% of normal Complete closure with maximal effort | Obvious weakness >50% of normal Resting symmetry | Obvious weakness >50% of normal Resting symmetry |
| 4 | Asymmetry at rest <50% of normal | Asymmetry at rest <50% of normal Cannot close completely | Asymmetry at rest <50% of normal | Asymmetry at rest <50% of normal |
| 5 | Trace movement | Trace movement | Trace movement | Trace movement |
| 6 | No movement | No movement | No movement | No movement |
| Score | Degree of Secondary Movement |
|---|---|
| 0 | None |
| 1 | Slight synkinesis; minimal contracture |
| 2 | Obvious synkinesis; mild to moderate contracture |
| 3 | Disfiguring synkinesis; severe contracture |
| Grade | Total Score (Sum for Each Region and Secondary Movement) |
|---|---|
| I | 4 |
| II | 5–9 |
| III | 10–14 |
| IV | 15–19 |
| V | 20–23 |
| VI | 24 |
A recently validated electronic facial paralysis assessment tool (eFACE) is a 16-item clinician-graded digital instrument that allows for the assessment of static, dynamic, and synkinesis parameters on continuous scales. It consists of a database-linked graphical user interface designed for rapid administration using a touch-screen device. In this smart-phone and tablet-dominated age, the eFACE software is a promising new tool, still being studied to define its ease, reproducibility, and application in clinical practice. A digital and database-amenable format, if globally accepted, would be tremendous in permitting easy communication among providers and patients and in allowing comparison of different treatments across studies.
In addition to clinician-graded scales for facial function, standardized patient-graded assessments of symptom severity and quality of life are necessary to track the burden of disease as well as response to interventions. The Facial Disability Index and the Facial Clinimetric Evaluation are validated for use in FP and are highly recommended for tracking patient experience and response to interventions over time.
Controversies in timing of dynamic reanimation
When the facial nerve is interrupted, there is no question that immediate or early nerve repair is recommended, ideally with tension-free primary repair or interposition grafting. The timing is not so clear in cases of complete facial paralysis whereby the facial nerve is thought to be anatomically in continuity, a scenario that is unfortunately not uncommon after cerebellopontine angle (CPA) tumor extirpation. If there is a potential for recovery, a period of observation of 1 year has been traditionally recommended. However, this approach delays the timely intervention in the subset of patients who ultimately do not recover spontaneously or satisfactorily. Identifying patients who will ultimately benefit from early intervention is desirable but challenging as no patient, tumor, or intraoperative factors have yet been found to be reliably prognostic of a poor outcome.
In a review of 281 patients with an anatomically intact facial nerve following vestibular schwannoma resection, Rivas and colleagues found that the rate of recovery during the first year could be used to predict long-term facial nerve recovery. Their predictive model using rate of functional improvement as the sole independent variable was found to anticipate poor outcomes in patients with initial HB grades V to VI as soon as 7 months after surgery, with 97% sensitivity and 97% specificity. Therefore, they suggest that after resection of a vestibular schwannoma, if a patient with an anatomically intact facial nerve and an HB grade V to VI shows no improvement of at least one HB grade after 6 months of observation, early reinnervation should be considered to limit the degenerative effects of muscle denervation. Rivas and colleagues also observed that lack of intraoperative electromyographic facial nerve stimulation at the brainstem after tumor resection had a strong correlation with poor functional outcome. However, when present, the nerve stimulation response threshold failed to correlate with facial nerve function.
In a follow-up study using the rate of recovery during the first 6 months after CPA tumor resection as the sole predictor of outcome, patients with postoperative FP (with an anatomically intact facial nerve) were prospectively stratified into an observation group and an intervention group. The observation group was composed of patients who were expected to spontaneously regain satisfactory facial function. The intervention group consisted of patients who showed no clinical signs of recovery by 6 months postoperatively and were offered nerve transfer using the masseteric or hypoglossal nerve. Overall, early facial reanimation surgery decreased the total duration of paralysis. Masseteric nerve grafting resulted in earlier recovery compared with hypoglossal nerve grafting (5.6 vs 10.8 months). In patients who underwent nerve grafting, there was a 0% risk of premature intervention; direct facial nerve stimulation at the time of surgery yielded no electromyographic response and facial muscle contraction in all of these patients. Of note, 8 patients who demonstrated no signs of recovery by 6 months postoperatively but declined surgery demonstrated, at best, an HB grade V recovery after a mean follow-up of 20 months. This finding provides some insight into the natural course of the anatomically intact but injured facial nerve, when early facial nerve function is poor.
Timing of intervention has also been shown to be critical in patients with vestibular schwannoma who present with preoperative FP. Ozmen and colleagues retrospectively reviewed 194 patients who underwent interposition grafting in the internal auditory canal at the time of vestibular schwannoma resection and found that duration of preoperative facial nerve deficit was the only significant predictor of prognosis; the most critical time for recovery to HB grades III and IV function was preoperative deficit of 6 months or less. When suboptimal recovery of the repaired facial nerve is expected, such as in the setting of prolonged preoperative FP, a masseteric nerve or hypoglossal nerve interposition graft can be coapted to a distal buccal branch for signal upgrading, leaving the facial nerve intact.
The specific timing considerations for neural transfer techniques are discussed in a later section.
Controversies in dynamic smile reanimation
Dynamic facial reanimation seeks to restore 2 critical functions: eyelid reanimation and smile reconstruction. Although treatment options for periocular reanimation are complex, they are less fraught with controversy and the goals are simple: to maximize corneal protection and improve periocular symmetry. The authors, therefore, focus on dynamic smile reanimation in the remainder of this article.
Depending on the time course and pattern of FP, dynamic smile reanimation may be achieved through reinnervation of native facial musculature (in reversible paralysis) via nerve transfer procedures or replacement of facial mimetic muscles (in irreversible paralysis) with regional or free muscle transfers.
Selection of a Donor Nerve for Direct Reinnervation
When the ipsilateral facial nucleus and proximal facial nerve are not available, neurotization procedures are used to repurpose an alternative neural source to restore facial mimetic muscles that remain amenable to reinnervation. The most commonly used donor nerves in facial reanimation are the contralateral facial nerve, masseteric nerve, and hypoglossal nerve. The accessory, phrenic, and C4 and C7 root nerves have also been used. Each donor nerve varies with respect to its donor deficit and morbidity, axonal density and motor power, and synergy with facial expression to allow for cortical readaptation in function.
Contralateral facial nerve (cross-facial nerve graft)
Originally developed by Scaramella and Smith working independently in the early 1970s, the cross-facial nerve graft (CFNG) has long been considered the criterion standard donor nerve source ( Box 1 , Fig. 1 ). By synchronizing the transmission of neural impulses from the contralateral, intact facial nerve to similar branches of the affected facial nerve through the use of an interposition nerve graft (most commonly, the sural nerve or greater auricular nerve), the CFNG is the only procedure that is capable of producing a truly spontaneous/emotional smile in addition to improving resting tone.
Nerve selection
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The most commonly used donor nerve is the sural nerve because of its ease of access, modest donor site morbidity, and favorable length (25–35 cm).
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The medial antebrachial cutaneous nerve has a branching pattern that should be considered for immediate reconstruction of the main facial nerve trunk and pes anserinus after their resection (ie, in radical parotidectomy).
Sural nerve harvest
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The authors find stair-step incisions to be efficient and favorable. A single incision is possible with endoscopic assistance.
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Use of a tendon stripper and long thin malleables are very helpful in the dissection.
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Mark the inferior end for orientation; this end should be coapted to the donor facial nerve on the nonparalyzed side.
Identification of the donor facial nerve
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The donor branches of interest are generally at the midpoint of a line between the tragus and the oral commissure, approximately 2 cm below the zygoma.
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The ideal nerve activates the zygomatic muscle complex, elevating the oral commissure and defining the nasolabial fold. As long as 1 to 2 additional branches that also innervate the zygomatic complex are identified, use the largest branch for the donor (number of axons predicts outcome).
Subcutaneous tunnel
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A subcutaneous tunnel is extended from the selected buccal branch on the intact side to the pretragal region on the contralateral paralyzed side (see Fig. 1 ). A small gingivolabial incision helps connect the two sides.
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If the CFNG is being used to innervate a free muscle transfer, it can be banked within a gingivolabial incision for later coaptation to the obturator nerve. A polypropylene (Prolene) stitch can facilitate its later identification.
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The use of a tendon stripper or a plastic drain with a trocar (where the sural nerve is sutured to the end) is very helpful for creating the subcutaneous tunnel.
Neurorrhaphy
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Two to 3 epineural 9-0 nylon sutures are used to perform a meticulous microneural anastomosis. Some surgeons wrap the coaptation in a dural regeneration matrix (Durepair) and secure it with a fibrin sealant (Evicel) to thwart loss of axons into surrounding tissues. Others prefer sutures alone, as the data on benefit are inconclusive.
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If only one dominant buccal branch on the nonparalyzed side is identified, neurorrhaphy can be performed end-to-side after partial axotomy in the donor nerve.
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