HEAD AND NECK
CHAPTER 36 FACIAL PARALYSIS
JULIA K. TERZIS AND KATERINA ANESTI
Injury to the facial nerve results in facial paralysis, a devastating condition, as it deprives the afflicted patients of their ability to communicate and express their emotion and negatively affects all aspects of the patient’s life. The subsequent loss of voluntary action of the muscles of facial expression results in facial laxity and a mask-like expression, especially in bilateral cases.
In addition to the aesthetic deformity, there are functional problems related to competence of the eye and oral sphincters causing difficulties with eating, drinking, swallowing, articulation, and speech. Ocular problems include inability to close the eyelids, decreased tear production, loss of blink, and ectropion of the lower eyelid. Speech is variably affected with a degree of dysarthria, as the facial nerve innervates many of the muscles for articulation.
The aim of reconstructive surgery in established facial palsy is to restore symmetry and coordinated animation.
This overview on the most effective reconstructive techniques for reanimation of the unilaterally or bilaterally paralyzed face includes dynamic procedures of neuromuscular rehabilitation, along with supplementary static procedures, which contribute significantly to the overall functional and aesthetic result.
Factors that influence surgical strategies and prognosis in facial reanimation include the patient’s age, denervation time, availability of the proximal facial nerve, whether the paralysis is partial or complete, and availability of motor donors that can be used for reinnervation. Procedures that attempt to restore neural input to a neuromuscular junction give the best results.
The choice of surgical procedures is based on the duration of the facial paralysis, the age of the patient, the cause of the lesion, and the compliance of the patient for a long-lasting and complex rehabilitation program.
Function can be restored by nerve repair or nerve grafting of the facial nerve, or by using the contralateral healthy facial nerve via cross-facial nerve grafts (CFNGs) as long as the time since onset of the palsy is short enough that the paralyzed muscles can still be reinnervated (up to 6 months). Longer denervation times (6 to 24 months) demand the use of a powerful ipsilateral “babysitter” motor donor (for example, partial hypoglossal) that will maintain the musculature, until the CFNGs take over in 9 to 12 months.
For unilateral, irreversible, complete palsy, a three-stage concept is described including CFNGs, free functional muscle transplantation, and several ancillary/revisional procedures.
The role of local muscle transpositions, such as temporalis muscle transfer, and the value of static procedures are also presented.
ANATOMY OF THE FACIAL NERVE
The facial nerve arises from the brain stem nuclei.1 The motor fibers loop dorsally around the abducens nerve nucleus and exit at the cerebellopontine angle (CPA). The parasympathetic and sensory fibers form the nervus intermedius, which join the motor component of the facial nerve as it exits the brain stem.
The course of the facial nerve is divided into six segments: the cisternal segment in the CPA, the intracanalicular segment, the labyrinthine segment, the tympanic segment (separated by the anterior genu where the geniculate ganglion is located), the mastoid segment (separated by the posterior genu), and the extracranial segment. Several branches are given off during the intracranial course.
The geniculate ganglion is the location of the first three branches and mediates parasympathetic functions: the greater petrosal nerve (to the lacrimal gland), the external petrosal nerve, and the lesser petrosal nerve (to the parotid gland).
The next three branches of the facial nerve occur in the mastoid segment: the nerve to the stapedius muscle, a sensory auricular branch, and the chorda tympani, which supplies taste sensation to the anterior two-thirds of the tongue and parasympathetic innervation to the submandibular and sublingual glands. As the facial nerve exits the stylomastoid foramen, it passes anteriorly to the posterior belly of the digastric muscle and lateral to the styloid process of the temporal bone.
The extracranial segment gives off branches to the posterior digastric, stylohyoid, and postauricular muscles, before the nerve splits into the upper (frontozygomatic) and lower (cervicofacial) divisions at the posterior edge of the parotid gland.
The facial nerve further divides in the parotid gland into several branches. Most commonly, the upper division gives off the frontal, zygomatic, and buccal branches, and the lower division gives off the mandibular and cervical branches. These five terminal branches form a rich plexus that supplies the facial musculature (Figure 36.1).
The facial nerve innervates 23 paired muscles and the orbicularis oris muscle. Seventeen of the paired muscles responsible for facial expression are derived from the mesenchyme of the second branchial arch and are arranged in four layers. The muscles in the three most superficial layers are innervated on their deep surfaces, while the fourth layer muscles (mentalis, levator anguli oris, and buccinator) are innervated through their superficial surface.
ETIOLOGY OF FACIAL PARALYSIS
Facial paralysis is a sign or symptom of many disorders, the differential diagnosis of which has been reviewed by May.2 The etiologies can be classified into three major categories: intracranial, intratemporal, and extracranial, depending on the location of the facial nerve lesion. The intracranial causes include vascular abnormalities, brain tumors (CPA tumors being the commonest) (Figure 36.2), developmental abnormalities or agenesis of the facial nerve nuclei, trauma, and/or degenerative disease of the central nervous system. Intratemporally, the causes can be developmental, infectious (bacterial or viral), cholesteatoma, tumors of the middle ear or mastoid area (acoustic neuroma being the commonest), trauma involving fractures of the temporal bone and skull base, or surgery in the region. Extratemporal causes include trauma, malignant tumors of the parotid gland and skin, and iatrogenic.
FIGURE 36.1. Anatomy of the extratemporal facial nerve and the corresponding facial musculature.
FIGURE 36.2. Complete facial paralysis after extirpation of a brain tumor.
Idiopathic (Bell’s) palsy is the most common cause of facial palsy, followed by trauma, infections, and tumors. Bell’s palsy resolves in the majority of cases (85%), leaving occasionally some residual weakness in 10% to 15% of patients.
In the pediatric population, facial palsy present at birth should be investigated thoroughly, as the early recognition of developmental facial palsy will lead to appropriate treatment and eliminate long-term sequelae. Congenital facial paralysis refers to conditions that are acquired during or at birth (e.g., from trauma or infection), while developmental facial paralysis (DFP) is the result of anomalies of fetal development. DFP can present in isolation or as part of a recognized syndrome, such as Möbius (Figure 36.3), Goldenhar, and CHARGE.
Paul of Aegina (626 to 696 AD) was the first to describe repair of divided nerves, while Avicenna introduced epineurial coaptation in the 10th century. Facial nerve surgery developed as a result of research in nerve injuries during the 18th century.
The history of facial nerve surgery can be viewed as five overlapping periods.3 In the first period (1829), Sir Charles Bell demonstrated that the facial nerve innervates the muscles of facial expression and in 1829 described cases of facial paralysis due to trauma. The second period, 1873 to 1960, was the era of facial nerve repair. The focus of facial nerve surgery in the third period, 1908 to 1969, was decompression of the facial nerve.
FIGURE 36.3. Two-year-old boy with Möbius syndrome. Möbius syndrome is classically characterized by bilateral facial nerve and abducens nerve paralysis leading to the typical mask-like face. In addition to the sixth and seventh cranial nerves, the fifth, ninth, tenth, and twelfth cranial nerves may be involved.
The fourth period, 1970 to 2000, has been characterized as the “bottleneck” period in honor of the contributions by Ugo Fisch and other surgeons who sought ways to operate on the proximal intraosseous portion of the facial nerve. Scaramella and Smith independently introduced the concept of CFNG, while Anderl popularized its use. The concept brought about new possibilities in restoration of facial expression. In 1976, Harii et al.4 transferred the first gracilis muscle to the face by microneurovascular technique using the deep temporal nerve as the motor donor. O’Brien and Morrison5recommended the combination of CFNG with microneurovascular muscle transfer, but their use of the extensor digitorum brevis muscle lacked the bulk and power to yield an adequate smile. In 1979, Terzis introduced the pectoralis minor transfer, which subsequently was followed by other authors.6
In the fifth period, 2000 to the present day, further refinements have been made with the introduction of new techniques.
Vascularized nerve grafts are indicated when unfavorable perioperative factors inhibit regeneration (e.g., scarring of recipient bed or radiotherapy). Direct muscle neurotization introduced at the beginning of the 19th century has received recent attention. The use of nerve transfers has also received a following recently (such as the use of the masseteric nerve) for “quick fix” reconstruction. Improvements in surgical outcomes are anticipated especially with microsurgical techniques. The need for comparison of functional results among different centers in a more standardized fashion is generally expressed.
AIMS OF RECONSTRUCTION
The aim of reconstructive surgery is to restore symmetry and coordinated dynamic animation with normal appearance at repose, and symmetry during voluntary and involuntary expression, competent ocular and oral sphincters, preservation of existing facial function, and minimal loss of function in other donor motor nerves should be the goal.
The history and physical examination are imperative for establishing a management plan. The physical examination includes a complete cranial nerve examination and a careful evaluation of the facial musculature, parotid gland, and neck.
The optimal assessment of the neonate born with unilateral facial paralysis is performed as soon after birth as possible, with the goal to distinguish between a congenital and developmental etiology. It is also important to identify dysmorphic features and multisystem syndromal pathology. May in 19817 provided a list of factors that can aid in differentiating the two forms. The presence of other anomalies and/or bilateral facial paralysis suggests developmental paralysis, while the absence of these signs and the presence of a history of prolonged labor, forceps delivery, hematotympanum, or marks over the ear/mastoid suggest birth trauma.
DFP does not improve, whereas traumatic palsy often does. With recovery following trauma, there may be faulty regeneration, yielding synkinesis, spasm, or mass action (Figure 36.4).
FIGURE 36.4. Posttraumatic synkinesis. Forty-three-year-old male patient who presented with a 24-year history of left facial paralysis secondary to cranial bone fracture and subdural hematoma. Note synkinesis between the eye and oral sphincter and paresis of the commissure and upper lip elevators along with paresis of the left depressor complex.
A variety of topographic tests exist because of the complex anatomy of the nerve in the CPA and petrosal bone and the fact that the facial nerve is a mixed nerve with motor, sensory, and secretory fibers. To detect the anatomical site of the lesion, tests such as the Schirmer test, stapedius reflex, taste examination, and salivary flow test can be used to assess the severity of nerve degeneration and its evolution over time.7 Electroneurography provides an objective record of evoked compound muscle action potentials and can quantify nerve fiber degeneration. Other studies include needle electromyography (EMG), nerve conduction, blink reflex, and nerve excitability testing. In addition, the high spatial resolution of multisliced spiral computed tomography and magnetic resonance imaging has yielded a more coherent picture of facial nerve disorders. The integrity and dimensions of the osseous facial canal can be delineated along with other central nervous lesions. This is particularly important in the differential diagnosis of neonatal facial palsy.
When possible, primary neurorrhaphy is performed. Immediate reconstruction of sharp transections of the facial nerve by primary, direct end-to-end coaptation produces the best results. However, this is only possible in a small percentage of patients. Injuries resulting in long nerve gaps or presence following a significant delay requires alternative techniques, such as nerve grafts, nerve transfers, regional muscle transfers, free tissue transfers, or static procedures.
Epineurial repair is the preferred method for monofascicular nerve stumps, but when dealing with multiple neural segments, perineurial repair is advocated in order to obtain optimal alignment of the severed bundles.
The most common way to overcome a wide neural gap is by the use of autologous nerve grafts (mainly the sural nerve). The average rate of nerve regeneration is 1 to 1.5 mm/d and can be monitored by an advancing Tinel’s sign. Although autologous nerve grafts produce good results, the disadvantages include numbness at the donor site, leg scars, inadequate size match of donor and recipient nerves, and nerve suture sites. In addition, if executed in the intraosseous part of the facial nerve, aberrant motor activities (synkinesis) in selected mimetic muscle groups are frequent occurrences.
Cross-Facial Nerve Graft
Alternative methods of reconstruction of neural defects are required in two occasions: when there is loss of the proximal nerve stump and loss of the distal nerve stump and/or muscles of facial expression.
When the proximal nerve stump is unavailable, the contralateral unaffected facial nerve can be utilized to serve as donor nerve, by borrowing axons from selected branches. These are then connected with nerve grafts that cross the face to reach the affected side, thereby providing motor axons from the normal to the affected side. With this method, coordinated facial motion can be achieved, with the fibers from the intact facial nerve functioning as “pacemakers” for the affected side (Figure 36.5). In a second stage, 9 to 12 months later, the axons in the CFNGs are connected to branches of the affected facial nerve or reach the facial muscle targets directly (direct neurotizations) if the distal nerve stumps were unavailable. The latter requires that the preoperative needle EMGs indicate that some muscle fibers are still present (fibrillations or occasional potentials). If needle EMGs are totally silent, direct neurotization cannot be performed and muscle substitution is recommended, with the CFNG fibers innervating the new muscle unit.
FIGURE 36.5. Cross-facial nerve graft (CFNG) procedure. The number of grafts placed is determined by the number of contralateral paretic muscle targets that will require surgical rehabilitation. Note that the upper graft always carries motor facial nerve fibers that innervate the normal eye sphincter. Secondary coaptations 9 to 12 months later of the distal end of the CFNG to similar branches on the affected side will allow synchronous, coordinated, and physiological eye closure and blink. In a similar fashion, the middle CFNG carrying “smile” fibers is destined for corresponding distal facial nerve branches on the paretic side or is “banked” for future neurotization of a free muscle for smile restoration. Finally, the lower graft is for depressor restoration.
Requirements for nerve transfers8 include a) unavailability of the proximal facial nerve stump, b) intact distal nerve, c) viable facial muscles, and d) inability to use the contralateral facial nerve as a motor donor (e.g., in Möbius syndrome). The ideal time window is determined by the availability of facial musculature. The major disadvantage is loss of function of the donor cranial nerve unless end-to-side coaptation is used. Extensive preoperative electrophysiological testing of all possible motor donors is necessary prior to nerve transfer surgery.
The Principle of “Babysitters”
Although the concept of CFNG is ingenious, it necessitates a prolonged denervation period of the affected facial muscles while regeneration and elongation of the contralateral axons take place. This could lead to irreversible muscle atrophy, unless the CFNG procedure is undertaken soon after the facial nerve injury (within the first 6 months).
For later cases (over 6 months to 2½ years), Terzis in 1984 introduced the “babysitter” procedure.9 This is a two-stage procedure (Figure 36.6): the first stage involves the use of 40% of the ipsilateral hypoglossal nerve, which provides powerful motor fibers to the affected facial nerve, reaching target connectivity quickly, and therefore preserving the facial muscle bulk. At the same time, several CFNGs are placed, which are connected to selected branches of the unaffected facial nerve. The second stage, usually 9 to 12 months later, involves secondary microcoaptations between the CFNGs and selected distal branches of the affected facial nerve. Variations of the “babysitter procedure” have been reported,10 including techniques such as end-to-side grafting11 and concomitant CFNG and hypoglossal facial grafting using a single sural nerve graft.12
FIGURE 36.6. Example of the “babysitter” procedure. A. Twenty-seven-year-old female 19 months after a closed head injury with skull fractures and complete left facial paralysis. She had mini-hypoglossal to the left facial nerve transfer and placement of four cross-facial nerve grafts (CFNGs) followed a year later by microcoaptations of the CFNGs to selected branches of the left facial nerve. B. Patient is shown 2 years after completion of the two-stage “babysitter” procedure.
When there is no peripheral stump, direct neurotizations to the muscle target13,14 can take place, provided that the period elapsed is no more than 2 years and preoperative EMG yields fibrillations. In direct muscle neurotization, the contralateral facial nerve or other ipsilateral motor donors (such as part of the hypoglossal or masseteric, or ipsilateral C7 root, or part of the accessory nerve) can be used.15
In long-standing facial paralysis, introduction of a new muscle is required. For older less demanding patients or those who are not candidates for lengthy surgery and prefer a one-stage procedure, a regional muscle such as the temporalis can be used.16
The transferred muscles are innervated by cranial nerves other than the facial nerve. Thus, coordinated movements are not produced and require the patient’s conscious efforts to activate the muscle. Extensive re-training and biofeedback in motivated patients can lead to some degree of coordinated movement.
Free Muscle Transfer
These procedures are ideal for patients with long-standing paralysis and pediatric patients with DFP. Free microneurovascular muscle transfers may include muscles such as the gracilis,4 pectoralis minor,6 latissimus dorsi,17 serratus anterior, split rectus abdominis, coracobrachialis, oblique internal abdominis, and extensor digitorum brevis.5 However, many of these have been aborted because of poor excursion or contraction such as the extensor digitorum brevis.
The free muscles are neurotized usually with the contralateral facial nerve via CFNGs or from an ipsilateral motor donor such as the hypoglossal or the masseteric nerve. In the latter case, the produced muscle contractions may be stronger, but in adults there is no possibility of coordinated animation with the normal side of the face, which necessitates intensive muscle retraining by the patient. In contrast, use of CFNGs produces harmonious, coordinated, and synchronous animation with the normal side.
Augmentation of Residual Function. Treatment of the patient with facial paresis, due to either a partial nerve injury or suboptimal recovery after reconstruction, is a challenging problem. Direct muscle neurotization can be a useful procedure for augmenting muscle contraction and promoting facial expression.13
REANIMATION OF THE UPPER, MIDDLE, AND LOWER FACE
Reanimation of the Eye
One area often neglected in the restoration of the chronically paralyzed face is the eye. Lagophthalmos, or inability to close the eyelids, is a significant functional deficit and exposure keratitis and tearing are common sequelae. The primary aim is to limit ocular exposure, protect the eye, restore eye closure and blink, and improve appearance.18 Temporary measures such as eye protection with tapes or other occlusive measures during sleep, protective glasses, and routine eye lubrication may be adequate for the recovery period. However, patients that will not have return of function require more permanent solutions. Static maneuvers include insertion of a gold weight or eye spring for patients with partial blink.19 The lower eyelid position can be improved with canthoplasty, tendon graft for suspension,20 or lid shortening (wedge excision).
For restoration of a natural, reflexive blink, dynamic eyelid reanimation is required. Primary repair of the injured upper zygomatic branch of the facial nerve and direct neurotizations via implantation of motor donor nerves via nerve graft in the orbicularis oculi muscle are both applicable when there are still viable muscle fibers in the eye sphincter (Figure 36.7).
For natural reflexive blink, if there is no orbicularis oculi muscle available, importation of a new neuromuscular unit either as a regional or as a free muscle transfer is appropriate.18,21 The neurovascular muscle units that were introduced by Terzis in the early 1980s for orbicularis oculi muscle substitution are the contralateral platysma and the frontalis muscle, which have shown promise in reestablishing a dynamic and reflexive blink,18 as long as the transferred muscles are neurotized by the contralateral facial nerve “eye” fibers (Figure 36.8). Mini-temporalis transposition can also be used for eye sphincter substitution but unfortunately does not restore synchronous blink.
While muscle and nerve transfers may be used to reanimate the paralyzed face, static procedures, such as eyelid weighting and/or sling procedures, also enhance both functional and aesthetic results.19,20 The use of gold weights has been the standard technique to correct this problem.19 The palpebral eye spring is an option for patients with a partial blink.19
FIGURE 36.7. Example of direct muscle neurotization (DMN) to the right eye sphincter. A. Four-year-old boy with right developmental facial paralysis. Note inability to close right eye sphincter. Patient was treated with four cross-facial nerve grafts (CFNGs) and a free gracilis muscle for smile (the left pectoralis minor was explored but was found not to be transferrable due to the absence of dominant vessels). B. The upper CFNG was used for orbicularis oculi muscle direct neurotization. The patient’s eye closure is seen here 10 years after the DMN of the upper and lower eye sphincter.
FIGURE 36.8. Contralateral pedicle frontalis transfer for restoration of eye closure and blink. A. Twenty-three-year-old male with left facial paralysis and left hemifacial microsomia noted at birth. Note inability to close left eye. He was treated with cross-facial nerve grafts (CFNGs) × 4, followed a year later by a pedicle transfer of the right frontalis to substitute for the atrophic left orbicularis oculi sphincter. The nerve to the frontalis was neurotized by the first CFNG carrying “eye” motor fibers from the right facial nerve to achieve coordinated eye closure and blink. B. Patient is shown 4 years after the pedicle frontalis transfer to the left eye sphincter.
Reanimation of the Smile
Use of Regional Muscles. Partial or total transfer of the masseter muscle, originally described by Lexer, has been described, but the direction of pull was suboptimal and the results were substandard.
The utilization of the temporalis muscle initially proposed by Gillies is more popular for provision of static symmetry and dynamic voluntary motion. Segmental rather than full transfer is currently the preferred method of the majority of surgeons. Although inferior to free muscle transfer, the advantages of a short procedure, early results, and low complication rate make the temporalis transposition a favorable option in selected cases. Commitment to motor re-education is essential to achieve adequate outcomes.16
Free Microneurovascular Muscle Transfer. These procedures involve one or two stages. The two-stage operation by CFNGs and later free microneurovascular muscle transfer has been established as the gold standard of management for the long-standing paralysis or DFP. The two most frequent muscles used are the gracilis muscle (Figure 36.9)22 and the pectoralis minor (Figures 36.10 and 36.11).6
One-Stage Free Tissue Transfers. Over the last two decades, a number of reports advocated one-stage free muscle transfer for facial reanimation.23,24 These groups report muscle recovery as early as 6 months after one-stage procedures and successfully treated children with hemifacial microsomia.25 Harii et al.26 give two explanations for the rapid muscle reinnervation. First, the retrograde blood flow from the muscle converts the supplying nerve into a vascularized nerve and second, the single neurorrhaphy needed for one-stage transfer versus the two coaptations required in CFNGs.
Although long-term follow-up of one-stage transfers is warranted, this technique is gaining favor for its shorter recovery period. However, so far the published results have not been comparable to the time-tested two-stage strategy.
For patients with long-standing palsy who are not candidates for multiple lengthy procedures, due to age, medical comorbidities, or patient preference, static correction of facial asymmetry has been attempted using fascial slings,27 alloplastic materials such as expanded polytetrafluoroethylene (Gore-Tex; WL Gore, Flagstaff, AZ),28 acellular dermal matrix (AlloDerm; LifeCell, Branchburg, NJ), or a multivectored suture suspension technique that has been recently reported as an alternative to the traditional fascial sling.
Reanimation of Lip Depressors. Lower lip paralysis has been traditionally managed with selective myectomy or neurectomy on the normal side. Similar effects on a temporary basis can be produced by botulinum toxin type A injection. This can produce a lower lip with good symmetry, but which becomes incontinent.
By contrast, dynamic restoration of the depressor complex by neural manipulation and muscle substitution are surgical interventions that have been used successfully by the senior author.29 Mini-hypoglossal nerve transfer to cervicofacial division of the ipsilateral facial nerve or use of CFNGs can produce satisfactory results if remaining muscle is present. Direct muscle neurotization can take place when the distal nerve stumps are not available. In long-standing facial palsy or unilateral lower lip developmental palsy, regional muscles such as the anterior belly of the digastric or the lateral platysma muscle if available can be transferred as pedicled muscles with remarkable results (Figures 36.12–36.15).29
Finally, soft tissue rejuvenative techniques such as the superficial musculoaponeurotic system cervicofacial rhytidectomy, blepharoplasty, browlift, and lower lid tightening can augment aesthetic restoration. Furthermore, nasal valve dysfunction can be addressed with functional rhinoplasty, static slings, or dynamic reanimation procedures.
THE AUTHORS’ APPROACH
Advances in microsurgery over the past 30 years have led to greater expectations and allowed for the realization of a coordinated dynamic panfacial reanimation.
Our unit stresses panfacial reanimation and follows a multistage approach for long-standing facial paralysis for reanimation of the paralyzed face, with CFNGs on the first stage, free muscle transfer on the second stage, followed by further revisional stages.30 During the first stage, functional motor nerve fibers are introduced to the paralyzed side of the face for direct neurotization or banking for future free muscle transfer. In unilateral facial palsy, a preauricular incision is made on the uninvolved side, and the entire extratemporal facial nerve with its branches are identified with electrophysiologic mapping (Figure 36.1). Bilateral sural nerve grafts are harvested and tunneled across the face. The degree of the paralysis determines the number of CFNGs placed. Microcoaptations are accomplished between selected branches of the facial nerve and the CFNGs. Axonal regeneration across the face is followed by the advancing Tinel’s sign.
FIGURE 36.9. Free gracilis muscle to the right face for smile restoration. A. Thirty-six-year-old male with right facial paralysis since the age of 6 months following a febrile illness. Note absence of a right nasolabial fold. He was treated with cross-facial nerve graft (CFNG) × 3 followed a year later with a free gracilis muscle to the right cheek for smile restoration. The obturator nerve was neurotized by CFNG #2 (the second CFNG) which was carrying “smile” fibers from the left facial nerve. B. The patient is shown 2 years following the free muscle transfer with symmetrical dental show and a coordinated smile.
FIGURE 36.10. Second stage of facial reanimation. Note how the right pectoralis minor fits on her left cheek. The length–width requirements are ideal for pediatric smile restoration; its four slips allow insetting in the lower lip, commissure, upper lip, alar base, and infraorbital rim. Furthermore, no debulking is necessary and the muscle grows in harmony with the facial skeleton of the child. The dual nerve supply allows reinnervation by two separate cross-facial nerve grafts, thus increasing the possibilities of facial expressivity. Note the typical preauricular incision, through which the requisite “pocket” is formed to receive the free muscle. Finally, the muscle will be inserted under its original tension. This was facilitated by placing sutures at measured distances on the muscle surface prior to transfer.
The “babysitter principle” introduced by Terzis in the early 1980s is a technique used to provide neuronal input to the denervated muscles while the contralateral facial nerve fibers are regenerating through CFNGs.
In the second stage, 6 to 9 months later, a similar incision is used on the paralyzed side in order to expose the extratemporal branches of the paretic facial nerve and the distal ends of the sural nerve grafts. Extensive microstimulation of all branches takes place. Branches that respond powerfully to stimulation are left alone, while branches with moderate response are coapted to the previously placed CFNGs. In cases of free muscle transfer, the recipient vessels, usually facial artery and vein, are also identified and isolated. Angiography may be helpful in evaluating the recipient facial vessels. The muscle flap is harvested at the same time by a second team and sculptured (in the case of gracilis) accordingly prior to transfer.
The senior author favors the use of gracilis in adults, due to its reliable vascular supply, ease of harvesting, and the ability to sculpture the muscle unit in situ, prior to transfer. In children, her preferred option is the pectoralis minor muscle, because of excellent length–width characteristics, dual innervation, and no need for debulking in this age group. The insetting of the free muscle is guided by preoperative videos and photographs, and the tension of the individual slips to the lower lip, commissure, upper lips, nasolabial fold, lateral ala, and infraorbital area is adjusted to reproduce pretransfer tension in situ. The origin is anchored to the superior portion of the zygomatic arch and on occasion to the deep temporal fascia.
FIGURE 36.11. Right free pectoralis minor muscle for smile restoration. A. Five-year-old girl presented with left developmental facial paralysis. She was treated with two cross-facial nerve grafts and a year later, the right pectoralis minor was transferred to the left cheek for smile restoration. B. The patient is shown 3 years after the free muscle transfer with a symmetrical coordinated smile. No rehabilitation was necessary due to great cortical plasticity.
Microvascular anastomoses are accomplished with the facial vessels while microneural repairs are carried out very close to the muscle entry zone, with the CFNG carrying smile fibers from the contralateral VII.
FIGURE 36.12. Mini-hypoglossal transfer to right cervicofacial branch of the facial nerve for depressor complex augmentation. A. Twenty- seven-year-old male presented with a right partial facial paralysis that occurred 20 months earlier. He was treated with cross-facial nerve grafts × 3 and mini-hypoglossal transfer to the right cervicofacial branch of the affected facial nerve. B. The patient is shown 3 years after the nerve transfer procedure.
FIGURE 36.13. Direct muscle neurotization for depressor restoration. A. Nine-year-old girl with left developmental facial paralysis. She was treated with cross-facial nerve grafts (CFNGs) × 3, free muscle for smile restoration, and direct neurotization of the depressor complex with the lower graft (CFNG #3) carrying motor fibers that innervated the depressor complex on the unaffected side. B. Patient is shown 3 years later. Note restoration of dynamic and symmetrical depression.
A patient with classic Möbius syndrome has a mask-like face that is immobile because of bilateral facial and abducens nerve paralysis (Figure 36.3). Because of the variety of cranial nerves involved, a standard procedure for dynamic restoration cannot and should not be promoted; instead, a careful preoperative objective and quantitative assessment should guide the reconstructive surgeon to the optimal reconstructive strategy.
In general, a multistaged approach to reconstruction is followed. If the contralateral facial nerve is minimally involved, it is preferred as a motor donor nerve even if it is not completely normal. In contrast to other authors, the hypoglossal nerve is never used as a motor donor because speech and swallowing are severely impaired in the vast majority of Möbius patients. The fifth cranial nerve, mostly the masseter branch, is a tempting source because free muscle transplants can be connected directly. Further, it is a good idea to coapt the obturator nerve to the masseter nerve in an end-to-side fashion, thus avoiding paralysis of this important masticator muscle. If the accessory nerve is not involved, reinnervation can be achieved with nerve grafts using an end-to-side coaptation. In rare cases with multicranial nerve involvement, the ipsilateral C7 root of the brachial plexus can be used.15 The use of ipsilateral C7 as motor donor allows the neurotization of multiple targets and also provides motor fibers for future free muscle transfers.
Muscles used for facial reanimation are the gracilis and the pectoralis minor. However, because there is an association of absence of the pectoralis minor if Poland syndrome is present, alternative targets should be identified. The gracilis muscle is a safe source for muscle transplantation but it needs to be sculpted to adjust to the hollow cheeks of the Möbius patient.
It is our opinion that the reconstructive surgeon should be comfortable with the full armamentarium of facial reanimation procedures before embarking on the surgical treatment of the Möbius patient.
FIGURE 36.14. Pedicled digastric transfer for depressor restoration. A. Sixteen-year-old girl who developed left facial paralysis at the age of 10 years, of unknown etiology. Note complete paralysis of left depressor. She was treated with cross-facial nerve grafts (CFNGs) × 3 and the pedicle digastric transferred for left depressor substitution. The lower CFNG, carrying fibers from the contralateral marginal mandibular nerve, was used to neurotize the anterior digastric muscle for coordinated lower lip depression. B. Post-op function.
FIGURE 36.15. Pedicle platysma transfer for depressor restoration. A. Seventeen-year-old girl with a 9-year history of left facial paralysis secondary to revision of stapedectomy surgery, during which there was a transection of the facial nerve. This was repaired a few weeks later by end-to-end coaptation, leading to paresis of the levators, the left depressor, and synkinesis. She was treated with cross-facial nerve grafts × 2 and a year later a transfer of the right pectoralis minor for smile restoration. During the revisional stage of her facial reanimation, the left lateral platysma was transferred to the left lower lip for depressor restoration. B. Patient is shown a year after the pedicle transfer of the left platysma demonstrating synchronous, coordinated, and symmetrical depression.
Treatment of facial nerve lesions requires a detailed understanding of anatomy, accurate clinical examination, and timely and appropriate diagnostic studies. Reconstruction depends upon the extent of injury, the availability of the proximal stump, and the time elapsed since injury.
Early timely reconstruction can protect the eye, prevent drooling, restore the smile, and improve facial symmetry. Every management option is specifically tailored to the individual patient’s needs.The goal is physiological coordinated reanimation of all three regions of the face (eye–smile–depressor). Given the complexity of expression restoration, a reconstructive approach based on two-stage or one-stage dynamic reconstruction followed by revisional/ancillary procedures is necessary for panfacial reanimation.
New techniques and methods of preserving the neuromuscular junction will undoubtedly manifest themselves as further refinements of established surgical techniques. Progress continues to be made in all aspects of the treatment of facial rehabilitation. Technical advances in nerve repair such as end-to-side neurorrhaphy and DMN are gaining popularity and microsurgical techniques of cross-nerve transfer are being developed that diminish the damage to the donor nerve. Improved methods of augmenting neural input to paretic muscles have also been reported, giving us therapeutic options for one of the more challenging problems in the field. The next generation of reconstructive surgeons should aim at panfacial reanimation without neglecting targets such as the eye sphincter and depressor complex, as a “smile” is truly a “smile” only when the entire face is reanimated.
1. Agur AMR, Dalley AF. Grant’s Atlas of Anatomy. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009:830.
2. May M. Facial paralysis: differential diagnosis and indications for surgical therapy. Clin Plast Surg. 1979;6:275.
3. May M, Schaitkin BM. History of facial nerve surgery. Facial Plast Surg. 2000;16:301-307.
4. Harii K, Ohmori K, Torii S. Free gracilis muscle transplantation, with microneurovascular anastomoses for the treatment of facial paralysis. Plast Reconstr Surg. 1976;57:133-143.
5. O’Brien BM, Franklin JO, Morrison WA. Cross-facial nerve grafts and microneurovascular free muscle transfer for long established facial palsy. Br J Plast Surg. 1980;33:202-215.
6. Terzis JK. Pectoralis minor: a unique muscle for correction of facial palsy. Plast Reconstr Surg. 1989;83:767-776.
7. May M. Facial paralysis in children: differential diagnosis. Otolaryngol Head Neck Surg. 1981;89:841-848.
8. Terzis JK, Konofaos P. Nerve transfers in facial palsy. Facial Plast Surg. 2008;24(3):177-183.
9. Terzis JK, Tzafetta K. The “babysitter” procedure: minihypoglossal to facial nerve transfer and cross-facial nerve grafting. Plast Reconstr Surg. 2009;123:865-876.
10. Manktelow RT, Zuker RM. Muscle transplantation by fascicular territory. Plast Reconstr Surg. 1984;73:75.
11. Viterbo F, Trindade JC, Hoshino K, et al. Latero-terminal neurorrhaphy without removal of the epineural sheath: experimental study in rats. Rev Paul Med. 1992;110:267-275.
12. Tomita K, Hosokawa K, Yano K. Reanimation of reversible facial paralysis by the double innervation technique using an intraneural-dissected sural nerve graft. J Plast Reconstr Aesthet Surg. 2010;63:e536-e539.
13. Terzis JK, Karypidis D. Outcomes of direct muscle neurotisation in adult facial paralysis. J Plast Reconstr Aesthet Surg. 2011;64:174-184.
14. Terzis JK, Karypidis D. Outcomes of direct muscle neurotization in pediatric patients with facial paralysis. Plast Reconstr Surg. 2009;124:1486-1498.
15. Terzis JK, Konofaos P. Novel use of C7 spinal nerve for Moebius. Plast Reconstr Surg. 2010;126:106-117.
16. Terzis JK, Olivares FS. Mini-temporalis transfer as an adjunct procedure for smile restoration. Plast Reconstr Surg. 2009;123:533-542.
17. Wang W. The neurovascular transfer for the treatment of facial paralysis in one stage. Chin J Microsurg. 1989;12:155.
18. Terzis JK, Bruno W. Outcomes with eye reanimation microsurgery. Facial Plast Surg. 2002;18:101-112.
19. Terzis JK, Kyere S. Our experience with the gold weight and palpebral spring in the management of paralytic lagophthalmos. Plast Reconstr Surg. 2008;121:806-815.
20. Terzis JK, Kyere S. Minitendon transfer for suspension of the paralyzed lower eyelid: our experience. Plast Reconstr Surg. 2008;121:1206-1216.
21. Lee KK, Terzis JK. Microsurgical reanimation of the eye sphincter. In: Terzis JK, ed. Microreconstruction of Nerve Injuries. Philadelphia, PA: W.B. Saunders Co.; 1987:635-650.
22. Terzis JK, Noah ME. Analysis of 100 cases of free-muscle transplantation for facial paralysis. Plast Reconstr Surg. 1997;99:1905-1921.
23. Jiang H, Guo ET, Ji ZL, et al. One-stage microneurovascular free abductor halluces muscle transplantation for reanimation of facial paralysis. Plast Reconstr Surg. 1995;96:78.
24. Koshima I, Moriguchi T, Soeda S, et al. Free rectus femoris muscle transfer for one-stage reconstruction of established facial paralysis. Plast Reconstr Surg. 1994;94:421-430.
25. Takushima A, Harii K, Asato H, et al. Neurovascular free-muscle transfer to treat facial paralysis associated with hemifacial microsomia. Plast Reconstr Surg. 2002;109:1219-1227.
26. Harii K, Asato H, Yoshimura K, et al. One-stage transfer of the latissimus dorsi muscle for reanimation of the paralysed face: a new alternative. Plast Reconstr Surg. 1998;102:941-950.
27. Rose EH. Autogenous fascia lata grafts: clinical applications in reanimation of the totally or partially paralyzed face. Plast Reconstr Surg. 2005; 116:20-32.
28. Singh S, Baker JL. Use of expanded polytetrafluoroethylene in aesthetic surgery of the face. Clin Plast Surg. 2000;27:579-593.
29. Terzis JK, Kalantarian B. Microsurgical strategies in 74 patients for restoration of dynamic depressor muscle mechanism: a neglected target in facial reconstruction. Plast Reconstr Surg. 2000;105:1917-1931.
30. Terzis JK, Olivares FS. Secondary surgery in adult facial paralysis reanimation. Plast Reconstr Surg. 2009;124:1916-1931.
1. Alex JC, Nguyen DB. Multivectoral suture suspension: a minimally invasive technique for reanimation of the paralyzed face. Arch Facial Plast Surg. 2004;6:197-201.
2. Anderl H. Reconstruction of the face through cross-face nerve transplantation. III: facial paralysis. Chir Plast. 1973;2:17.
3. Bance M, Erb J. A reliable radiologic landmark for the facial nerve in axial temporal bone computed tomography scans. Otolaryngol Head Neck Surg. 2003;128:251-256.
4. Bender LF, Maynard FM, Hastings SV. The blink reflex as a diagnostic procedure. Arch Phys Med Rehabil. 1969;50:27-31.
5. Berghaus A, Neumann K, Schrom T. The platinum chain: a new upper-lid implant for facial palsy. Arch Facial Plast Surg. 2003;5:166-170.
6. Brunelli GA, Brunelli GR. Direct muscle neurotization. J Reconstr Microsurg. 1993;9:81-90.
7. Campbell EDR, Hickey PR, Nixon KH, et al. Value of nerve excitability measurements in prognosis of facial palsy. BMJ. 1962;7:7-10.
8. Diels JH. Facial paralysis: is there a role for a therapist? Facial Plast Surg. 2000;16:361-364.
9. Endo T, Hata J, Nakayama Y. Variations on the “baby sitter” procedure for reconstruction of facial paralysis. J Reconstr Microsurg. 2000;16:37-43.
10. Fisher E, Frodel JL. Facial suspension with a cellular human dermal allograft. Arch Facial Plast Surg. 1999;1:195-199.
11. Freilinger G, Gruber H, Happak W, et al. Surgical anatomy of the mimic muscle system and the facial nerve: importance for reconstructive and aesthetic surgery. Plast Reconstr Surg. 1987;80:686-690.
12. Furukawa H, Saito A, Mol W, et al. Double innervation occurs in the facial mimetic muscles after facial-hypoglossal end-to-side neural repair: rat model for neural supercharge concept. J Plast Reconstr Aesthet Surg. 2008;61:257-264.
13. Gillies HD. Plastic surgery of the face. In: Henry F, ed. Based on Selected Cases of War Injuries of the face Including Burns. London: Hodder and Stought Publ; 1920;54-55.
14. Jager L, Reiser M. CT and MR imaging of the normal and pathologic conditions of the facial nerve. Eur J Radiol. 2001;40:133-146.
15. Jobe RP. A technique for lid loading in the management of the lagophthalmos of facial palsy. Plast Reconstr Surg. 1974;53:29-32.
16. Kimata Y, Sakuraba M, Hishinuma S, et al. Free vascularized nerve grafting for immediate facial nerve reconstruction. Laryngoscope. 2005;115:331-336.
17. Koshima J, Umeda N, Handa T, et al. A double-muscle transfer using a divided rectus femoris muscle for facial-paralysis reconstruction. J Reconstr Microsurg. 1997;13:157-162.
18. Kumar PAY. Cross-face reanimation of the paralysed face, with a single stage microneurovascular gracilis transfer without nerve graft: a preliminary report. Br J Plast Surg. 1995;48:83-88.
19. Labbe D, Huault M. Lengthening temporalis myoplasty and lip reanimation. Plast Reconstr Surg. 2000;105:1289-1297.
20. Levine RE, Shapiro JP. Reanimation of the paralyzed eyelid with the enhanced palpebral spring or the gold weight: modern replacements for tarsorrhaphy. Facial Plast Surg. 2000;16:325-336.
21. Lexer E, Eden R. Uber die chirurgische behandlung der peripheren facialisliihmung. Beitr Klin Chir. 1911;73:116.
22. Lifchez SD, Matloub HS, Gosain AK. Cortical adaptation to restoration of smiling after free muscle transfer innervated by the nerve to the masseter. Plast Reconstr Surg. 2005;115:1472-1479.
23. Manktelow RT, Zuker RM. Cross-facial nerve graft—the long and short graft: the first stage for microneurovascular muscle transfer. Oper Tech Plast Reconstr Surg. 1999;6:174-179.
24. May M, Sobol SM, Mester SI. Hypoglossal-facial nerve interpositional-jump graft for facial reanimation without tongue atrophy. Otolaryngol Head Neck Surg. 1991;104:818-825.
25. McLaughlin CR. Surgical support in permanent facial paralysis. Plast Reconstr Surg. 1953;11:302-314.
26. Millesi H. Nerve suture and grafting to restore extratemporal facial nerve. Clin Plast Surg. 1979;6:333-341.
27. Morel-Fatio D, Lalardrie JP. Palliative surgical treatment of facial paralysis: the palpebral spring. Plast Reconstr Surg. 1964;33:446-456.
28. Rauch R, Taber KH, Manoilidis S, et al. A functioning imaging guide to the bony landmarks of the seventh nerve. J Comput Assist Tomogr. 2002;26:657-659.
29. Renault F. Facial electromyography in newborn and young infants with congenital facial weakness. Dev Med Child Neurol. 2001;43:421-427.
30. Rubin LR. The anatomy of a smile: its importance in the treatment of facial paralysis. Plast Reconstr Surg. 1974;53:384-387.
31. Sajjadian A, Song AY, Khorsandi CA, et al. One-stage reanimation of the paralyzed face using the rectus abdominis neurovascular free flap. Plast Reconstr Surg. 2006;117:1553-1559.
32. Salles AG, Toledo PN, Ferreira Me. Botulinum toxin injection in long-standing facial paralysis: improvement of facial symmetry observed up to 6 months. Aesthetic Plast Surg. 2009;33:582-590.
33. Scaramella LF. Preliminary report on facial nerve anastomosis. In: Second International Symposium on Facial Nerve Surgery. Osaka, Japan; Japan Society of Facial Nerve Surgery, Japan Travel Bureau Inc.; 27-30 September 1970.
34. Senders CW, Tollefson TT, Curtiss S, et al. Force requirements for artificial muscle to create an eyelid blink with eyelid sling. Arch Facial Plast Surg. 2010;12:30-36.
35. Shah SB, Jackler RK. Facial nerve surgery in the 19th and 20th centuries: the evolution from crossover anastomosis to direct nerve repair. Am J Otol. 1998;19:236-245.
36. Fisch U. Facial Nerve Surgery. Zurich: Kugler/Aesculopius; 1977.
37. Smith JW. A new technique of facial animation. In: Transactions of Fifth International Congress of Plastic and Reconstructive Surgery. Melbourne: Butterworths Ltd; 1971.
38. Stennert EI. Hypoglossal facial anastomosis: its significance for modern facial surgery, II: combined approach in extratemporal facial nerve reconstruction. Clin Plast Surg. 1979;6:471-486.
39. Taylor IG, Cichowitz A, Ang SG, et al. Comparative anatomical study of the gracilis and coracobrachialis muscles: implications for facial reanimation. Plast Reconstr Surg. 2003;112:20-30.
40. Terzis JK, Manktelow RT. Pectoralis minor: a new concept in facial reanimation. Plast Surg Forum 5; 1982:106-110.
41. Terzis JK. Pectoralis minor: a unique muscle for correction of facial palsy. Plast Reconstr Surg. 1989;83:767-776.
42. Terzis JK, Noah EM. Mobius and Mobius-like patients: etiology, diagnosis and treatment options. Clin Plast Surg. 2002;29:497-514.
43. Terzis JK, Noah EM. Dynamic restoration in Mobius and Mobius-like patients. Plast Reconstr Surg. 2003;111:40-55.
44. Terzis JK, Olivares FS. Use of mini-temporalis transposition to improve free muscle outcomes for smile. Plast Reconstr Surg. 2008;122:1723-1732.
45. Terzis JK, Olivares FS. Secondary surgery in paediatric facial paralysis reanimation. J Plast Reconstr Aesthet Surg. 2010;63:1794-1806.
46. Wang W, Zuoliang Q, Xiaoxi L, et al. Free split and segmental latissimus dorsi muscle transfer in one stage for facial reanimation. Plast Reconstr Surg. 1999;103:473-480.
47. Wang W, Qi Z, Lin X, et al. Neurovascular musculus obliquus internus abdominis flap free transfer for facial reanimation in a single stage. Plast Reconstr Surg. 2002;110:1430-1440.
48. Whitney TM, Buncke HJ, Alpert BS, et al. The serratus anterior free-muscle flap: experience with 100 consecutive cases. Plast Reconstr Surg. 1990;86:481-490; discussion 491.