History

The possibility of facial nerve surgery was initially conceived by Sir Charles Bell in 1821 when he established that the facial nerve innervates the muscles of facial expression.1 Historically, facial nerve paralysis was treated medically with topical ointment, medicine, and electrotherapy.2 The first nerve transfer was performed by Drobnick in 1879 when he anastomosed the spinal accessory nerve to a dysfunctional facial nerve.3 Manasse and Korte, in the early 1900s, performed hypoglossal to facial nerve substitution in addition to the spinal accessory nerve.4,5 In that same time period, Stacke resected a portion of the facial nerve and juxtaposed the cut ends.6

The first facial nerve graft within the temporal bone was performed by Bunnell in 1927.7 In addition to Bunnell′s work, Lathrop and Myers demonstrated that the facial nerve could regenerate and that facial movement could be improved with facial nerve reconstruction.8,9 Sir Charles Balance, the founder and first president of the Society of British Neurological Surgeons, showed that nerve grafts for the facial nerve had more favorable results than those obtained by anastomosis of the facial nerve to the hypoglossal and glossopharyngeal nerves.10,11 Lexer and Eden in 1911 described temporalis and masseter regional muscle transposition techniques.12 These dynamic techniques were also later reported by Erlacher in 1915 and Owens in 1947.13,17

The modem era of free tissue transfer introduced novel treatment modalities that have subsequently revolutionized facial reanimation outcomes. Scaramella described cross-face nerve grafts in 1970.14–16 Thompson proposed free muscle transplantation to reanimate the paralyzed face, which was subsequently supported by Ruben and Harii et al.17–20 Cross-facial nerve grafts followed by vascularized muscle free flaps paved the way for modern facial reanimation surgery.20

Facial paralysis can result from a variety of factors including congenital, iatrogenic, idiopathic, infectious, metabolic, neoplastic, neurologic, toxic, and trauma ( Table 24.1 ). Paralysis of the facial musculature results in aesthetic, functional, and psychosocial morbidity.4 Unilateral cases cause facial asymmetry at rest and/or during animation. Although individuals with bilateral facial paralysis can have a more symmetrical appearance, the psychological effect of not being able to effectively express one′s emotions can be significant.

While facial paralysis leads to aesthetic deformity and psychosocial issues, the functional consequences can lead to even more significant morbidity and deteriorating quality of life.4 Patients with facial palsy often do not communicate effectively, experience oral incompetence, and may have significant tension from synkinesis. Lagophthalmos and lower lid malposition can lead to corneal dessication, ulceration, and eventual blindness.

Patient Evaluation

Chapter 4 of this book discusses the details of facial paralysis evaluation and will serve as an excellent reference. In terms of individuals seeking lower facial reanimation, there are a few key issues that need to be determined. Most patients have likely been examined by a clinician and given a diagnosis for the etiology of their facial paralysis. While the physical manifestations of facial nerve paralysis are distressing for all patients, it is important to take a detailed history and perform a thorough physical examination to determine the underlying etiology. It is extremely important not to be sidetracked by an established diagnosis at the time of evaluation, which may or may not be accurate. A significant amount of time needs to be spent on confirming the correct diagnosis in this patient population. Many patients diagnosed with Bell palsy may harbor serious malignancies.

Other key issues that need to be clarified during the patient evaluation include severity of the facial paralysis and synkinesis, duration of palsy, patient age, functional deficits, and long-term goals. Individuals with partial paralysis who have synkinesis will often require a different treatment protocol than those with complete flaccid paralysis. Duration of facial palsy is also critical, as most surgical interventions are typically performed only after the regenerative functions of the nerve have been clearly established (typically 1 year). The etiology of the paralysis will help guide the surgeon as to what is the appropriate time frame to wait before initiating treatment. Finally, the patient′s long-term goals need to be clearly understood. The main complaint from patients with facial paralysis is oral incompetence, facial asymmetry, and inability to generate a smile. Some individuals just desire to improve symmetry at rest and reduce functional deficits, whereas others desire spontaneous dynamic facial movements.

During the physical examination, the eyes are inspected for narrowing or widening of the aperture, degree of lagophthalmos, Bell phenomenon, lower eyelid position, and laxity (snap test). The facial movements corresponding to each of the facial nerve branches must be evaluated carefully by asking the patient to raise the eyebrows, shut the eyes, wrinkle the nose, smile, show the teeth, and pucker. The key factor is to determine whether the patient has complete flaccid paralysis or partial paralysis with muscle tone. Patients with partial paralysis need to be further evaluated for any evidence of synkinesis, which typically involves simultaneous and uncoordinated oculo-facial muscle contractions (such as orbicularis oculi contraction while trying to smile). Synkinesis often leads to “auto- paralysis,” where simultaneous activation of the orbicularis oris, buccinators, oral commissure elevators, and depressors result in a frozen smile and prevent the patient from having a true smile mechanism.

The House-Brackmann and Sunnybrook Facial Grading System are useful tools to evaluate facial palsy and synkinesis (see Tables 5.2 and 5.5 in Chapter 5). The House-Brackmann grading system is a six-point scale, and the Sunnybrook Facial Grading System evaluates synkinesis at rest, during movement, and with voluntary movement.6 The scale is continuous from 0 through 100, where 0 indicates complete paralysis and 100 is normal.10

In clinical practice, the senior author categorizes facial palsy patients into five categories:

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  Type A: Normal facial function

  
  
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  Type B: Partial paralysis with mild synkinesis

  
  
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  Type C: Partial paralysis with moderate to severe synkinesis

  
  
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  Type D: Partial paralysis without synkinesis

  
  
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  Type E: Complete facial paralysis

To complete the physical exam, the remaining cranial nerves should be evaluated and radiographic imaging (computed tomography or magnetic resonance imaging) may be required. Electromyographic studies can be useful in determining viability of the muscle fibers; however, in patients with long-standing facial paralysis, physical examination will provide enough information about the muscle tone and function. Preoperative photography and video assessment at rest and during animation is recommended. A multidisciplinary approach with a physical therapist that is knowledgeable and skilled in working with patients with facial paralysis is strongly recommended for optimizing outcomes.

Etiology

Prior to any intervention, appropriate evaluation of the patient in an effort to determine the underlying etiology is critical. Facial paralysis can be congenital or acquired (see Table 24.1 ). The most common etiology of unilateral facial paralysis is idiopathic, also referred to as Bell palsy.11 Approximately 85% of patients with Bell palsy start to have spontaneous recovery within a few weeks after onset. The remaining 15% may not experience facial movement for up to 6 months; however, most of these patients will have some level of recovery. The duration of time is directly correlated to higher incidence of synkinesis, loss of mimetic function, and contracture. The likelihood of recovery is best for younger age groups.7

If the facial paralysis is caused by a traumatic event and the nerve ends can be identified and stimulated, repair within the first 3 days of the injury yields the highest likelihood of recovery.21 Generally, if damage is to the buccal or zygomaticus branches medial to the lateral canthus, the nerve is able to recover on its own and no repair is indicated. Proximal injuries to these branches will require surgical repair. The buccal and zygomaticus branches have extensive arborization, and therefore the likelihood of permanent paralysis is less common than trauma to frontal and marginal mandibular branches, which are terminal branches. In acoustic neuroma resection and parotid neoplasms, the facial nerve may be intentionally sacrificed for tumor resection. In temporal bone fractures, the facial nerve may be transected, crushed, or impinged, leading to facial palsy.

Nonsurgical Intervention

The main nonsurgical treatment options for lower facial reanimation are the use of neuromodulators, injectable fillers, and neuromuscular rehabilitation. The authors emphasize that neuromodulators such as botulinum toxin-A (BTX-A) play a crucial role in creating facial symmetry, improving synkinesis, increasing oral commissure excursion, and reducing functional deficits.8,22 Patients with Type B and C partial paralysis with synkinesis and congenital unilateral lower lip palsy are typically the best candidates. Patients with synkinesis typically have simultaneous activation of oral commissure elevators, orbicularis oris, buccinator, and lower lip depressor activity. They therefore can have improvement in their dynamic smile function by reducing the downward force of depressors such as the depressor labii inferioris, risorius, and depressor anguli oris.

In the senior author′s practice (Azizzadeh), neuromuscular rehabilitation and BTX-A are the primary treatment strategies for younger patients with limited facial palsy and minimal to moderate amount of synkinesis (Type B and C patients). In patients who are older and/or have a more dense paralysis, BTX-A and neuromuscular retraining are used to complement other surgical reanimation techniques. Facial fillers such as hyaluronic acids, calcium hydroxyapatite, and injectable poly-L-lactic acid are also used to improve facial volume asymmetry, which is commonly seen in patients with facial paralysis.

Surgical Intervention

Surgical intervention for facial paralysis can be divided into static and dynamic reanimation. Dynamic reanimation can be further subdivided into “volitional” and “spontaneous” reanimation. Volitional dynamic reanimation requires the patient to be conscious about moving the face, whereas spontaneous reanimation does not. Static surgical procedures only improve the patient′s symmetry at rest and technically do not reanimate the face.

Static Surgical Reconstruction

Static techniques are the workhorse of facial paralysis reconstruction. Static procedures are indicated for individuals who are not appropriate candidates for dynamic reanimation and/or regions of the face that are not amenable to dynamic reconstruction (e.g., brow ptosis, external nasal valve collapse). Static procedures include repair of brow ptosis, gold/platinum weight reconstruction for lagophthalmos, lower eyelid reconstruction, lower lip shortening, external nasal valve reconstruction, superficial musculoaponeurotic system (SMAS) rhytidectomy, and static sling suspension ( Fig. 24.1 ).

For lower facial paralysis reconstruction, static sling suspension is able to achieve two major goals: improve facial symmetry and reduce functional deficits such as oral incompetence, biting of inner gums, and poor articulation. As static slings do not interfere with nerve regeneration, they can be used to achieve an immediate aesthetic and functional improvement in conjunction with dynamic procedures such as cable nerve grafting, hypoglossal-facial nerve anastomosis, and cross-facial nerve grafts. Static slings can also be used to augment muscle transfer techniques or revise previous dynamic reanimation procedures. As standalone procedures, static slings do not directly address the smile mechanism but do improve a patient′s perception of his or her smile and face.

In the authors’ practice, static slings are offered to individuals who are not candidates for dynamic reanimation such as those who have advanced age, partial paralysis with adequate oral commissure excursion, and major head and neck malignancy. In appropriate candidates, this procedure is considered only after the status of nerve regeneration has been ascertained, typically 1 year after date of onset or if the facial nerve has been deliberately sacrificed. Patients are typically elderly with a history of tumor ablation in the head and neck or cerebellopontine angle region.

Tensor fascia lata (TFL) is the ideal choice for static sling procedures.23 A substantial amount of tissue can be harvested from the lateral thigh, and multiple strips can be created for both oral commissure suspension as well as external nasal valve repositioning. Although TFL does require a separate donor site that can increase patient morbidity, it has the advantage of being an autogenous material with long-term viability.

Commercially available, freeze-dried acellular human dermis (AlloDerm Regenerative Tissue Matrix, LifeCell, Branchburg, NJ) has also been used for facial static slings. The advantage of acellular human dermis is that it precludes a donor site harvest. Acellular human dermis is readily available, integrates into surrounding tissue, and can be customized quickly to create exact facial slings. Although there have been reports of poor long-term outcome with AlloDerm, namely sling failure and infection, the authors’ experience has been satisfactory in both short- and long-term use in a carefully selected patient population who would have significant morbidity from harvesting of TFL.24

Expanded polytetrafluoroethylene (ePTFE, Gore-Tex, Implantech Associates, Santa Barbara, CA) is a synthetic material that can also be considered for use in static sling procedures. Levet and Jost reported on their use of ePTFE for facial suspension in the French literature in 1987 with good results.25 Petroff et al also reported favorable results from facial suspensions with ePTFE soft-tissue patch without infection or extrusion.26 Iwahira and Maruyama, in 1992, reported the use of ePTFE with temporalis transfer as “extensions” when the temporalis muscle fascia was weak and/or short.27 ePTFE circumvents the need to harvest TFL, thus eliminating a second donor site morbidity; however, given its lack of integration with local tissue, its use in our practice has been limited.

Suture suspension techniques that have been popularized in aesthetic midface lifts can also be successfully used for patients requiring minor repositioning of the oral commissure.27,28 Suture suspension techniques are generally less invasive than other static techniques and can be performed percutaneously and under local anesthesia; however, its potential for comprehensive suspension is limited and its long-term outcome has not yet been adequately studied.

The static sling procedure is typically performed simultaneously with a rhytidectomy. Using a rhytidectomy incision, a deep subcutaneous plane is elevated to the level of the oral commissure ( Fig. 24.2a ). A single sheet of 5 × 12 cm sling material (TFL, acellular dermis, ePTFE) is typically used to create an equal amount of tension along the oral commissure and nasolabial fold ( Fig. 24.2b ). The sling is sutured at the modiolus to orbicularis oris or subdermal tissue layer if orbicularis is significantly atrophied. Approximately three to five separate O-Vicryl sutures (Ethicon, Inc., Somerville, NJ) are used to attach the graft to the oral commissure and n asolabial fold ( Fig. 24.2c ). The sling should be slightly overcorrected in a posterolateral vector and secured to the deep temporalis fascia, zygomatic arch, and preauricular SMAS. An additional sheet of sling material (1.5 × 10 cm) is typically used to elevate the nasal alar crease to improve external nasal valve collapse and nasal obstruction.

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