Elliott H. Rose
INTRODUCTION
Clinical characteristics of the totally or partially paralyzed face can be directly attributed to absence or weakness of the mimetic muscles of facial expression. The arborizing cranial nerve VII acts as the “electrical wiring” of the face (Fig. 43.1). Injury to the facial nerve, whether infectious, developmental, traumatic, or of tumor origin impacts the “targeted” facial muscles (Fig. 43.2) and creates very predictable functional and structural deficits based on specific innervation of the VII nerve branches as follows:
FIGURE 43.1 The arborizing VII cranial nerve acts as the “electrical wiring” of the face.
FIGURE 43.2 A facial nerve deficit creates generalized facial laxity related to atonicity of the deep foundation of the face, upper lip immobility, related to weakness of the lip elevators, zygomaticus major and minor muscles, and an inadequate smile “spread” related to weakness of the risorius muscle. Additionally, oral incompetence (pursing, blowing, whistling, intraoral seal) related to weakness of the orbicularis oris sphincter, lower lip flaccidity related to paralysis of the depressor labii muscle, and inspiratory collapse of nasal vestibule related to weakness of the levator labii superioris alaeque nasi muscle can occur. The upper face suffers from paralytic ectropion of the eyelids related to weakness of orbicularis oculi muscle and ptosis of the brow related to paralysis of the frontalis muscle.
1. Generalized facial laxity related to atonicity of the deep foundation of the face (mimetic muscles and superficial aponeurotic system)—VII nerve trunk
2. Upper lip immobility (asymmetric smile with “shadowing” of the upper teeth) related to weakness of the lip elevators and zygomaticus major and minor muscles—buccal branch of the facial nerve
3. Inadequate smile “spread” (asymmetric smile) related to weakness of the risorius muscle—buccal branch of facial nerve
4. Oral incompetence (pursing, blowing, whistling, intraoral seal) related to weakness of the orbicularis oris sphincter—buccal branch of facial nerve
5. Lower lip flaccidity (drooling, speech impairment, chewing) related to paralysis of the depressor labii muscle—marginal mandibular branch of facial nerve
6. Inspiratory collapse of nasal vestibule (decreased nasal air flow, congestion) related to weakness of the levator labii superioris alaeque nasi muscle—buccal branch of the facial nerve
7. Paralytic ectropion of the eyelids (tearing, corneal exposure, lagophthalmos) related to weakness of orbicularis oculi muscle—zygomatic (orbital) branch of facial nerve
8. Ptosis of the brow (impaired upward gaze) related to paralysis of the frontalis muscle—frontalis branch of facial nerve
In view of the myriad of functional and structural deficits, successful reanimation of the paralyzed face is a lofty challenge to the reconstructive facial surgeon. The two defining objectives of any successful reanimation surgery are to achieve (1) static facial balance at rest and (2) symmetric, dynamic movement (preferably voluntary and spontaneous) by supplementation or substitution of the paralyzed muscles.
I have delineated methods of static rebalancing in my description of multiple applications of autogenous fascia lata slings in providing deep structural support of the facial foundation and correction of droopiness of the lips, eyelids, and nostrils.
Given the “symphony of motion” of the multiple mimetic muscles of facial expression, no single procedure can supplant the intricacies of motion/vectors needed for “natural” facial movement. The ideal situation, of course, is direct and/or interpositional nerve grafting of a recent facial nerve injury. Frequently, however, those repairs are neither feasible nor temporally suitable, and secondary reconstructive options need to be considered. In cases of partial paralysis or in older adults, regional muscle transfers (temporalis, masseter, platysma, frontalis) are the procedures of choice. These procedures, although very effective, require lengthy neuromuscular retraining and may lack involuntary spontaneity. In younger patients, however, the preference is for facial nerve “specificity” by reinnervation from the contralateral facial nerve (via cross-facial nerve graft) into the distal branches of the injured facial nerve. Or, in long-standing facial paralyses where the target muscles have undergone “denervation atrophy,” a substitute muscle is necessary to reanimate the paralyzed face (free gracilis muscle transfer). The focus of this chapter is on the use of cross-facial nerve grafts and microvascular free gracilis muscle flaps in achieving such dynamic motion.
The contemporary era of dynamic correction of facial palsy emerged with the introduction of the microvascular free transfer of the gracilis muscle by Harii in 1976 based on Tamai’s earlier experimental (1970) and clinical work in the transfer of muscle as a vascularized unit. The initial gracilis transfer was neurotized by the ipsilateral V cranial nerve but, of course, required “triggering” by smiling or clenching the teeth (that concept is now being “recycled” by Manktelow and Klebuc’s work using the branch to the masseter as the motor nerve). Usage of the contralateral normal facial nerve as a source of innervation was conceived by Scaramella (1970) and further refined by Smith and Anderl (1979). Gordon and Buncke showed in rhesus monkeys that heterotopic muscles could function adequately when motored by long interpositional nerve grafts. O’Brien in 1980 synthesized these concepts into an algorithm defining the clinical indications for cross-facial nerve grafting and free microvascular gracilis muscle transfers in long-standing facial paralysis. Other muscles, such as pectoralis minor, serratus anterior, extensor brevis, latissimus dorsi, and palmaris longus, have also been used as recipient muscles in facial reanimation. The gracilis muscle, however, is the most commonly used and, in my opinion, the easiest to work with and most predictable in outcome. The advantage of this approach is the ability to obtain synchronous and spontaneous bilateral facial expression and a more “natural” smile.
HISTORY
A careful history is elicited from the patient (or parents) confirming mode of onset, duration, and improvement (if any) since onset. In infants or toddlers with congenital facial paralysis, parents are questioned regarding problems during the pregnancy (infection, drug exposure, smoking, and eclampsia), positioning of the fetus, family history, and birth trauma (forceps delivery, small pelvic canal). If a hereditary etiology (i.e., CHARGE syndrome) is suspected, a geneticist should evaluate the family or siblings. A description of the timing of the onset (immediate or delayed), early treatment, and neurophysiologic testing should be obtained from the family.
In teens or adult patients, the etiology is usually more clear (intracranial or facial nerve trauma, developmental, acoustic neuroma, brain stem tumor, parotid tumor, Bell palsy, lymphangioma or hemangioma, or iatrogenic). Timing of the onset, early treatment, response to physical therapy or acupuncture, staging of return of facial function (timing of initiation of return and “plateau” of facial movement), prior testing (EMG/NCS or CAT scan), and neurologic, ophthalmologic, and speech evaluations should be elicited from the patient. Prior photos from family events are very helpful in assessing smile and facial expression. Work history and impact on social and professional interactions are helpful in understanding self-esteem issues and coping skills related to the functional disabilities. The final question in the assessment should be “Are you motivated to have your facial paralysis corrected?”
Functional problems associated with an established facial paralysis are fairly predictable (see clinical characteristics above). History related to periocular problems should include queries regarding visual impairment, corneal exposure, immobile brow, excessive tearing, impaired upward gaze, incomplete eye closure, and blepharospasm (synkinesis). Does the patient require taping, eye drops, or night time lubrication? Midface subjective findings include facial atonicity and flaccidity (while puffing cheeks); biting of the inside of the mouth, tongue, and lips; droopiness of the nostrils, cheek, and corner of the lip; difficulty with bolus management (oftentimes needing tongue to sweep food to healthy side); impaired chewing; inadequate oral seal while whistling, blowing, or sucking; and dribbling from the corner of the mouth while cup feeding or drinking through straw. Speech patterns affected are primarily the bilabial sounds—plosives (p’s and b’s) and phonemes (f’s, w’s, v’s, and m’s). Patients may complain of late-day lack of articulation, lower volume, or speech fatigability.
PHYSICAL EXAMINATION
Specific findings on physical examination are dependent on the level and extent of the lesion. In total or near total paralyses, the perioral, midface, and periocular regions are most affected. In milder cases, the patient may appear normal at rest; in more severe cases, droopiness and loss of muscle tone may be apparent (flatness of the nasolabial fold, loss of the nasolabial crease, elongation of the upper lip, sagging of the brow and corner of the eye, “open” eye). With animation, however, the discrepancies are much more visible. While smiling, there is asymmetry between the void and active side with an overpull by the healthy muscles. “Shadowing” of the upper teeth is noted (tooth exposure on the palsied vs. the healthy side is an easy measure of upper lip mobility). “Smile spread” is diminished on the affected side (measured by the distance between the midline tubercle and lateral commissure). The paralyzed lower lip is invaginated/inverted causing “shadowing” of the lower teeth. On inspiration, there is downward displacement of the affected nostril with snarling causing obstruction of the vestibular airway. Puckering and pursing of the lips are impaired, compromising the ability to create an intraoral seal. With attempted lip approximation or puckering, there is usually a gap between the upper and lower lip allowing escape of air or fluids.
In the periocular region, the affected eyebrow is “flattened” having lost is arch and paralleling the supraorbital rim. With upward gaze, there is a 1.0 to 1.5 cm discrepancy between the affected and healthy side. In residual Bell palsy or neuropraxic injuries within the intratemporal canal, intensive blepharospasm (synkinesis) may be “triggered” by the yawning, chewing, or clenching teeth. Extensive tearing (epiphora) may be noted in the affected “tear trough” (particularly when tilting the head) due to inadequate seal of the lower lid to the eyeball. In severe cases, lagophthalmos (gap) is noted between upper and lower lip with voluntary closure. The cornea is usually protected by automatic upward deviation of the globe with incomplete closure (Bell phenomenon). The blink reflex is often absent in lesions at the brain stem level.
INDICATIONS
Facial reanimation by cross-facial nerve grafting and gracilis muscle transfer is primarily an operation for younger patients. Axonal regeneration across an interpositional nerve graft tends to diminish with age and may be inadequate to neurotize the transferred muscle from a distant source. In my opinion, age 35 to 40 is the “cutoff” for cross-facial nerve grafting. Very excellent regional muscle transfers (temporalis and platysma) offer a “one-stage” facial reanimation with evidence of facial movement at 4 to 6 weeks postoperatively (albeit extensive neuromuscular retraining is necessary to “trigger” the transferred muscle). Most adults are not willing to wait the 1½ to 2 years necessary to experience spontaneous facial movement after microsurgical reconstruction utilizing the two-stage procedure. Regional muscle transfers (temporalis and platysma) are also the procedures of choice in the partialparalyses following Bell palsy, acoustic neuroma resection and trauma. In these patients, the risk of jeopardizing existing motion by splicing into intact facial nerve branches on the palsied side does not justify the more extensive microsurgical reconstruction.
CONTRAINDICATIONS
Elderly patients, particularly those with medical comorbidities, may not tolerate the lengthy operative times of the respective two stages and should be considered as candidates for static and/or regional muscle transfers.
PREOPERATIVE PLANNING
Initial evaluation should include CT imaging to rule out an intracranial lesion (acoustic neuroma, tumor, or vascular abnormality), skull fracture, or stenosis of the facial canal within the petrous portion of the temporal bone (in developmental facial paralysis). EMG/NCS studies determine the degree or localization of facial nerve neuropathy as well as strength of muscle motor action potentials. In longer-standing facial paralyses, the presence of fibrillations indicates potential viability of mimetic muscle (after neurotization) whereas “flat line” indicates denervation atrophy of the target muscles has occurred (not amenable to reinnervation). Photographs and videotapes in repose and while emoting (smiling, speaking, smirking, snarling, grimacing, puckering, sucking, blowing, closing eyes, looking upward) document facial asymmetry and aberrant speech patterns. Evaluation by a speech pathologist using the Frenchay Dysarthria Assessment delineates functional impairment of activities of daily living (chewing, swallowing, fluid management, lip seal, and bolus management) and critically analyzes alterations in speech articulation and clarity. Examination by a board-certified ophthalmologist inspects for conditions of paralytic ectropion, epiphora, brow ptosis, lagophthalmos, blepharospasm (synkinesis), and contralateral hyperactive frontalis, associated with facial palsy. All muscle activities are recorded on a 0–5 scale based on the Sunnybrook Facial Grading Scale. Asymmetric smile patterns are digitized and analyzed by facial recognition software comparing movement of fixed perioral landmarks on the palsied versus the healthy side.
SURGICAL TECHNIQUE
Two-stage cross-facial nerve grafting (with or without free gracilis transfer) is generally indicated in younger patients with complete palsy of the entire side of the face or an isolated sector of the face (i.e., perioral, periocular, midface, lower face, etc.). If the duration of the injury to the facial nerve is less than 2 years, the “target muscles” are still receptive to reinnervation (should be confirmed by EMG/NCS). That “window” may be extended to 2½ years in infants or children before denervation atrophy becomes permanent. Additional time can also be obtained by DC stimulation of the denervated muscles during the reconstructive period or incorporation of a “baby sitter” partial hypoglossal transfer as an interim step (Terzis). Time for axonal regeneration across the face (generally, 1 inch per month) must be accounted for in assessing total “denervation time.” Multiple cross-facial nerve grafts may be employed to restore eye closure, midface movement, oral competence, and smile symmetry. In my experience, fine mimetic muscle movement (eye closure, nostril elevation, and lower lip eversion) can be achieved with direct cross-facial nerve grafting. Upper lip elevation (for creation of smile symmetry) usually requires the addition of a mini-gracilis muscle transfer to overcome the effects of gravity. In those cases, two buccal cross-facial nerve grafts are used—one for distal neurorrhaphy to the buccal branch on the injured side and the other to motor the gracilis transfer (Fig. 43.3). In long-standing facial paralyses, a single cross-facial nerve graft from the buccal branch is used to motor the gracilis transfer.
FIGURE 43.3 A. In select cases, one to four buccal cross-facial nerve grafts are utilized. B. Clinical photo outlining the gracilis position and the cross-facial nerve graft orientation.
Cross-Facial Nerve Graft (Figs. 43.3 and 43.4)
FIGURE 43.4 A. A nasotracheal tube is passed through the nostril on the nonaffected side and anchored with a silk horizontal mattress suture to the nasal septum. The grafts are oriented to ensure the appropriate length. B. Rubber vessel loupes are passed around the individually identified nerve branches. For ease of mapping identification, microhemoclips are placed on the vessel loupes to correspond with the specific facial nerve branch—1 for frontal, 2 for zygomatic (orbital), 3 for buccal, and 4 for marginal mandibular. C. The proximal neurorrhaphy is carried out under 40 to 50× magnification with 10-0 nylon on a 100-μm needle. Fascicles from the fresh end of the identified duplicate facial nerve branch are aligned with the proximal cut end of the sural nerve graft. Repair is by perineural placement of the sutures in a “watertight” closure around the nerve to preclude protruding of fascicles at the repair site.
A nasotracheal tube is passed through the nostril on the nonaffected side and anchored with a silk horizontal mattress suture to the nasal septum (Fig. 43.4A). Covering with a sterile drape allows the tube to be manipulated out of the way during the operative procedure. Short-acting paralyzing agents are used for induction. The anesthesiologist should check for muscle contractibility before mapping of the facial nerve. The surgical approach is through a face-lift incision on the healthy side with horizontal extension beneath the angle of the mandible (Ridson type neck extension) to gain greater exposure. Soft tissue should be injected with a fresh epinephrine mixture of 1:100,000 concentration prior to dissection (Xylocaine or Marcaine should be avoided during mapping). The buccal flap is retracted and hemostasis obtained with the bipolar cautery. The superficial musculoaponeurotic system (SMAS) fascia is gently teased apart at the anterior margin of the parotid gland. The individual branches of the facial nerve are identified by microdissection in the periparotid region and stimulated with the handheld nerve stimulator (2 mV). Observation is made by the assistant for brow elevation, eye twitching, upper lip/nostril movement, and lower lip eversion. Rubber vessel loupes are passed around the individually identified nerve branches (Fig. 43.4B). For ease of mapping identification, microhemoclips are placed on the vessel loupes to correspond with the specific facial nerve branch—1 for frontal, 2 for zygomatic (orbital), 3 for buccal, and 4 for marginal mandibular. The largest branches are the ones selected as recipients for the sural nerve grafts. Duplicates of the individual nerve branches are confirmed prior to proximal nerve repair.
Harvesting of the sural nerve grafts is accomplished by a second team of surgeons. The length of the graft is determined by the number of cross-facial nerves needed (15 to 18 cm per graft). Generally, two grafts can be obtained per calf (maximum length 30 to 35 cm). A hockey-shaped incision is made 1 cm posterior to the lateral malleolus of the ankle. The retinaculum is released, and the sural nerve is dissected within the groove. Additional length can be obtained by extending the incision over the lateral foot to dissect the lateral dorsal cutaneous nerve. The nerve is traced proximally beneath the investing fascia of the calf. Serial transverse incisions are made on the posterior calf, and the nerve is delivered beneath the subcutaneous tunnel.
The sural nerves are “reversed,” transposed to the recipient site, and “preset” within the face prior to microneural repair. A periauricular face lift incision is made on the palsied side and the cheek flap retracted to allow for placement of the fascia lata sling and SMAS tightening. A Kleinert tendon passer is used to deliver the respective nerves across the face (supraorbital, transnasal, and submental) from the healthy to the palsied side. Stab incisions are made in the frown lines, midline nose, and chin cleft and submentally to assist in passage of the nerve grafts. The distal end of each cross-facial nerve graft is delivered to the palsied side and attached to the deep SMAS with microclips, the number corresponding with the mapping of the nerve—1 for frontal, 2 for zygomatic (orbital), 3 for buccal, and 4 for marginal mandibular. A blue Prolene suture is used as a “tracer” interconnecting the fresh end of the distal nerve to an appropriate site on the cauda helix, tragus, or lobe of the ear.
One (buccal) to four cross-facial nerve (orbital, buccal × 2, marginal mandibular) grafts are inset and tagged. The operating microscope is brought into the field. Proximal neurorrhaphy is carried out under 40 to 50× magnification with 10-0 nylon on a 100-μm needle (Fig. 43.4C). Fascicles from the fresh end of the identified duplicate facial nerve branch are aligned with the proximal cut end of the sural nerve graft. Repair is by perineural placement of the sutures in a “watertight” closure around the nerve to preclude protruding of fascicles at the repair site. Felt-tip external skin markings are made of the position of the individual grafts on the face and documented photographically and numerically.
Axonal regeneration is monitored by advancing Tinel sign at monthly intervals postoperatively. The course of the nerve is tapped with fingertip or eraser tip to elicit a “shock.” Distances of advancing Tinel are documented and dated on facial drawings contained within the chart. Regeneration across the face usually takes 6 to 9 months (1 inch per month). In toddlers in whom Tinel monitoring is not feasible, 6 to 7 months is the arbitrary time for secondary exploration. External DC stimulation may be used to stimulate the denervated facial muscles in the interval between the first and second stages.
At the second stage, the periauricular face lift incision on the palsied side is reopened and extended horizontally beneath the angle of the mandible (Ridson type neck extension). The blue “tracer” sutures are followed to the distal end of the cross-facial nerve. Corroboration of the specific nerve branch is confirmed by counting the microclips at the distal end of each nerve graft. The neuromata are resected, and frozen section biopsies are sent from the distal cut end of each graft to confirm axonal regeneration. Microdissection of the facial nerve branches on the palsied side is comparable to the opposite side by gently teasing away the SMAS fascia at the anterior parotid border. Distal neurorrhaphy is similar to the contralateral side as the distal end of the crossfacial nerve graft is microneurally repaired to the cut end of the distal branch of the facial nerve (or obturator nerve of the free gracilis transfer).
Moderately compressive dressings are applied circumferentially around the face. Patients are generally kept in the hospital 2 to 3 days after each stage. Diet is advanced from liquid to soft, and excessive facial expression is avoided for 10 to 14 days.
Free Gracilis Muscle Transfer (Figs. 43.5 and 43.6)
FIGURE 43.5 A. Harvest of the gracilis muscle (usually on the contralateral side) is performed through a vertical incision in the upper one-third of the inner thigh along the course of a line interconnecting the pubic tubercle to the medial malleolus of the knee. B. The arterial and venous leashes are traced laterally in the deep thigh to their origin from the profundus femoris vessels. C. The resting length of the muscle is marked by placement of silk sutures at 5-cm intervals on the surface of the muscle prior to detachment.
FIGURE 43.6 A. The muscle is transposed to the recipient cheek and anchored proximally to the lateral zygomatic arch and deep temporal fascia with heavy Prolene suture. Orientation of the muscle is predetermined by the anatomy of the smile on the contralateral healthy side. B.This photo demonstrates the orientation of the muscle. The attachments from the zygoma to the modiolus of the orbicularis.
In long-standing paralyses where facial muscles have undergone permanent denervation atrophy, reinnervation by direct neurotization is not a viable option. In those cases, replacement of the target muscle is mandatory. A variety of options have been described by various authors—gracilis, pectoralis minor, latissimus dorsi, extensor digitorum brevis, serratus anterior, and palmaris longus. In my hands, the gracilis has proven to be the most reliable and predictable and has an excursion similar to the zygomaticus muscles to be replaced. Motor input is via the buccal cross-facial nerve graft from the contralateral side passed submentally or by an ipsilateral branch of the trigeminal nerve to the masseter (I prefer the former because of the specificity of motor nerve input and preclusion of neuromuscular retraining postsurgically; the latter is indicated in bilateral Mobius cases).
Anesthesia is once again delivered through a nasotracheal tube on the nonaffected side. The access to the cheek is via a face lift incision with Ridson neck extension on the palsied side. A large cheek flap is elevated at the level of the SMAS over the buccal cheek and premaxillary area. A counter incision is made just beneath the mucocutaneous border of the lateral third of the upper lip and slightly around the lateral commissure. The upper lip skin is teased away from the orbicularis oris with fine tenotomy scissors and undermined to the nasolabial crease. A tunnel is created interconnecting the lip and cheek flaps (through which the gracilis muscle will pass). The course of the facial artery and vein (or external jugular vein) is auscultated by a Doppler probe at the inferior border of the body of the mandible (junction of middle and posterior thirds). An incision is made transversely through the platysma muscle. The artery and vein are isolated and tagged with colored vessel loupes.
A separate surgical team harvests the gracilis muscle (usually on the contralateral side) through a vertical incision in the upper one-third of the inner thigh along the course of a line interconnecting the pubic tubercle to the medial malleolus of the knee. The investing fascia is split and the gracilis muscle dissected. The obturator nerve is dissected proximally for 7 to 8 cm. The arterial and venous leashes are traced laterally in the deep thigh to their origin from the profundus femoris vessels. The gracilis is debulked longitudinally in situ following stimulation of the fascicles of the obturator nerve to identify maximum locus of contraction (usually the lateral two-thirds). The resting length of the muscle is marked by placement of silk sutures at 5-cm intervals on the surface of the muscle prior to detachment. Perfusion of the muscle is verified and the muscle is stimulated again in situ to assure contractility.
The muscle is transposed to the recipient cheek and anchored proximally to the lateral zygomatic arch and deep temporal fascia with heavy Prolene suture. Orientation of the muscle is predetermined by the anatomy of the smile on the contralateral healthy side. The resting length of the muscle is preserved at the inset. Distal neurorrhaphy between the buccal cross-facial nerve graft and obturator nerve usually lies deep to the muscle and is performed prior to the final inset. The distal end of the muscle is brought through the lip incision and tapered with the electrocautery. Muscle fibers are imbricated with vertical mattress Prolene sutures to the orbicularis oris muscle of the lateral third of the lip. Fibers of the lateral edge of the gracilis are sewn to the insertion of the fascia lata sling at the modiolus. If shortening of the upper lip element is necessary, it is trimmed on its inferior margin before closure of the incision at the mucocutaneous border. The nasolabial crease is recreated by placement of dermal sutures on the undersurface of the premarked crease and attached to the deep muscle. Standard vascular repairs are completed under the microscope prior to releasing the clamps. Anoxia time from muscle detachment to revascularization should be limited to less than 2 hours. Hemostasis is achieved and the cheek flap redraped and inset on the hemiface. A Jackson-Pratt drain parallels the muscle mass, and a small Penrose drain is placed along the inferior gutter. The nasotracheal tube is left overnight, and the patient is deeply sedated to prevent violent head motions during the first 24 hours postoperatively. Patency of the anastomoses is confirmed by hourly Doppler checks for the first 72 hours. Liquid diet is progressed to a soft diet by the 3rd or 4th day. Jaw activity and facial expressions are discouraged during the first couple of weeks.
POSTOPERATIVE MANAGEMENT
Rehabilitation is critical to the successful outcome of patients who have undergone facial reanimation. Toward that end, a comprehensive physical therapy protocol has been designed by the author and a PhD physical rehabilitation specialist. In the early stages post–muscle transfer (at 4 to 6 weeks), low-dose continuous phase E-stim is initiated to increase circulation and introduce E-stim to the patient. Electrodes are placed at the nasolabial fold and temporomandibular joint. Involuntary quivering (fasciculations) are usually observed at 2 to 3 months progressing to voluntary movements over the next 6 to 12 weeks. Increased interrupted pulse surface E-stim at increasing amplitudes is used during the active phase of muscle activity to boost strength of contraction. E-stim is supplemented by a home exercise program. As voluntary muscle activity reaches a plateau, E-stim should be tapered to prevent hypercontractibility. Patients are actively engaged in Biofeedback exercises in front of the mirror to “train” a symmetrical smile. The maximum spontaneous smile is usually achieved by 9 to 12 months. Most patients are able to achieve unilateral “specificity” over time. Frequent correspondence between the physical therapist and the surgeon is essential to monitor progress and adjust treatment modalities accordingly.
COMPLICATIONS
Patients are generally young and healthy and tolerate well the extensive anesthesia times (often 8 to 10 hours) of each operation. Postsurgical hematomas or take-backs for reexploration of thrombotic anastomoses are relatively rare (3% to 5%). Asymmetry due to excessive muscle fullness can be addressed by debulking of the gracilis by reelevating the skin flap of the cheek and recontouring the muscle mass (that is less of a problem now that the gracilis muscle is more aggressively debulked in situ prior to transfer). Corrections of overpull or underpull should be deferred for at least a year postsurgically until final muscle activity is determined. Underpull can be corrected by distal plication of the muscle or shortening of the fascia lata sling. In a few instances, a minitemporalis turnover flap (regional muscle transfer) has been used to supplement the elevation of the upper lip. Overpull creates a more difficult challenge, particularly in children during rapid growth phases of the head/face. If release of the fascia lata sling at the modiolus fails to ameliorate the problem, reexploration and “slide” of the proximal gracilis muscle attachment may reduce tension and produce a more symmetric smile. Botox chemodenervation of the gracilis or contralateral lip depressor can effectively assuage minor imbalances. Secondary “refinements” are often necessary to address cosmetic concerns such as increased fleshiness of the lips, sharpness of the corner of the mouth, hypertrophic postsurgical scars, poor definition of the nasolabial crease, or droopiness of the corner of the mouth.
An area of approximately 5 to 6 cm of sensory loss on the lateral foot is to be expected in the donor site. This diminishes with time as the neurotization occurs from adjacent areas. Twenty-five percent to thirty percent of the patients report cold intolerance, scar tenderness, and minimal levels of discomfort, most of which resolves after a year. Minimal morbidity is experienced in the donor thigh.
RESULTS
I have performed 46 cross-facial nerve grafts and 25 free gracilis transfers over the last 12 years. Case examples are shown in Figures 43.7, 43.8, and 43.9. Age range is from 18 months to 35 years old. Most common etiologies are congenital (developmental or birth trauma) or following tumor ablation (acoustic neuroma or brain stem). Most patients achieved nearly full symmetry in repose and 75% to 100% of dynamic smile restoration (documented by postoperative photos, videos, and smile recognition software). Development of physiologic activities of daily living (cup feeding, drinking through a straw, chewing, fluid retention) have been restored postsurgically. In toddlers (<4-year-old), feedback from the speech therapists and parents has confirmed that speech patterns have developed at normal landmarks and have not required specialized retraining as is so characteristic of children operated at older ages after poor speech patterns and altered facial expressions have developed.
FIGURE 43.7 A. Six-year-old postresection of medulloblastoma of the posterior fossa. B. One year following cross facial nerve graft/gracilis transfer.
FIGURE 43.8 A. Sixteen-year-old postresection of golf ball size acoustic neuroma. B. Post-op after cross facial nerve grafts × 4 and free gracilis transfer.
FIGURE 43.9 A. Twenty-eight-year-old post resection of a medulloblastoma. B. Postoperative smiling after cross facial nerve grafts × 4 and free gracilis transfer.
PEARLS
• Careful preoperative evaluation is critical in designing the most appropriate approach for facial reanimation.
• Patients should be advised preoperatively of the lengthy rehabilitation and the “time frame” (at least 18 to 24 months) before voluntary muscle activity is observed.
• Patients (or parents) must be “active participants” in the rehabilitation process.
• Nasotracheal intubation places the tube away from the operative site.
• Inset of a primary fascia lata sling at the first stage of reconstruction allows for immediate restoration of facial balance in repose and counteract the “overpull” of the contralateral healthy muscles.
• Fine mimetic muscle movement (eye closure, nostril elevation, lower lip eversion, etc.) can be achieved with direct cross-facial nerve grafting.
• Cross-facial nerve grafts should be “preset” within the face prior to microneural repair. This avoids disruption of the microneural repair during manipulation of the nerve.
• Cross-facial zygomatic (orbital) grafts are passed supraorbitally. Cross-facial buccal (for fine mimetic muscles) grafts are passed transnasally. Cross-facial margin mandibular (for lower lip paralysis) is passed submentally.
• Cross-facial buccal (for motor of gracilis) is passed across the chin.
• Microhemoclips at distal end of nerve grafts and blue “tracer” sutures are critical in identification at the second-stage procedure when scarring has encompassed the nerve graft.
• Biopsy of the fresh end of the distal nerve graft at the second stage confirms axonal regeneration.
• Orientation of the gracilis muscle is best achieved by harvesting from the contralateral side.
• Free gracilis muscle should be placed at normal length at inset (confirmed by sutures at 5-cm intervals on surface).
PITFALLS
• Cross-facial nerve grafting should be avoided in “older” patients since axonal regeneration falls off precipitously by the fourth or fifth decade.
• Cross-facial nerve grafting should be avoided in adult patients with partial paralysis since “splicing” end to end into intact functioning facial nerve on the palsied side may jeopardize existing muscle motion.
• Do not “sell” the more complex microsurgical procedures (cross-facial nerve grafting and free gracilis transfer) to adult patients, since generally, they do not have the tolerance for two major reconstructive procedures and the extensive time (2 years) before facial motion is visualized.
• Always prepare patients of the need for additional “refinement” surgery. Do not fall into the trap of “you told me it would only take two procedures and I would be smiling.”
• Make sure patients have “reasonable expectations” of aesthetic and functional outcome. Avoid young, “narcissistic” patients who expect “perfection.” If necessary, have prospective patients speak with other patients who have undergone similar facial reanimation surgeries.
INSTRUMENTS TO HAVE AVAILABLE
• Facial plastics surgical tray
• Tendon stripper
• Microscope
• Microsurgical instruments
• Kleinert tendon passer
SUGGESTED READING
Chun JK. Facial reanimation and smile reconstruction. In: Rose EH, ed. Aesthetic facial restoration. Philadelphia, PA: Lippincott-Raven, 1998:251–262.
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