TITLE: Reanimation of the Paralyzed Face
SOURCE: UTMB Dept. of Otolaryngology Grand Rounds
DATE:
November 11, 1998
Resident Physician: Stephanie Cordes, MD
Faculty Physician: Christopher Rassekh, M.D.
Series Editor: Francis B. Quinn, M.D.

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"This material was prepared by physicians in partial fulfillment of educational requirements established for Continuing Postgraduate Medical Education activities and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a interactive computer mediated conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of subscribers or other professionals and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."


Facial nerve paralysis is devastating both cosmetically and functionally. Not only does society place great emphasis on facial expression, but also facial paralysis severely hinders mastication, speech production, and eye protection. This has led to the development of numerous reanimation techniques.(1) The ability to restore symmetry and motion to patients afflicted with facial paralysis is one of the most rewarding skills of the reconstructive surgeon.

The facial nerve, once injured by transection, rarely attains full recovery of normal function. The slightest injury to one branch, even if the nerve is not divided, may produce permanent weakness or other dysfunction, such as spasm or weakness. It is important that the surgeon ensures that a patient who has a facial nerve injury or may be contemplating surgery that has any chance of sustaining facial nerve injury understands that their face will never regain normal movements.(2) Regardless of the rehabilitative strategy chosen, spontaneous facial function will not be returned with any amount of practice or training. However, the hope of facial symmetry in repose, protection of the cornea, and a smile with conscious effort can be confidently offered to patients.(3)

Anatomy

To perform reanimation procedures, the surgeon must have a thorough knowledge of the anatomy of the facial nerve. The motor nucleus of the facial nerve lies deep within the reticular formation of the pons where it receives input from the precentral gyrus of the motor cortex, which innervates the ipsilateral and contralateral forehead. The cerebral cortical tracts also innervate the contralateral portion of the remaining face. The facial nerve and nervus intermedius exit the brainstem at the pontomedullary junction and travel laterally 12 – 14 mm with the eighth cranial nerve to enter the internal acoustic meatus. The meatal segment of the nerve then travels 8 – 10 mm within the anterosuperior quadrant of the internal auditory canal to the meatal foramen where the canal narrows from 1.2mm to 0.68mm in diameter. The labyrinthine segment then runs 2 – 4 mm to the geniculate ganglion. Here the greater superficial petrosal nerve exits to carry parasympathetic secretomotor fibers to the lacrimal gland. Just distal to this branch, the lesser superficial petrosal nerve exits to supply parasympathetic secretomotor fibers to the parotid. The tympanic segment begins just distal to the geniculate ganglion where the nerve turns 40 – 80 degrees and runs posteroinferiorly 11 mm across the tympanic cavity to the second genu. A branch leaves the segment near the pyramidal eminence to supply the stapedius muscle. The nerve then turns about 90 degrees at the second genu inferiorly where the mastoid segment travels for 12 – 14 mm inferiorly in the anterior mastoid to exit the stylomastoid foramen. The extratympanic segment is composed entirely of motor fibers and enters the parotid gland after giving off the posterior auricular branch and a branch to the posterior belly of the digastric muscle. The pes anserus forms 20 mm from the stylomastoid foramen and further divides the nerve into the upper (temporal and zygomatic) and lower (buccal, mandibular, and cervical) branches.(4) The terminal ramifications of these branches to the temporal, zygomatic, buccal, mandibular, and cervical regions are variable.


The type of injury will greatly influence the reanimation procedure utilized. Sunderland describes five degrees of nerve injury. They are:

Factors Determining Rehabilitation

The pathogenesis and eventual course of facial paralysis varies, depending on the causative injury or disease. This presentation will focus on the clinical situations requiring facial reanimation. There is no one modality universally appropriate for all afflictions of facial nerve function. As a general rule, however, the order of preference is as follows:

 A wide array of facial reanimation procedures is available to the surgeon. Any single protocol is ill advised for the management of facial paralysis because patients’ needs vary. All the factors determining the outcome of rehabilitation should be considered before any facial reanimation procedure is undertaken.(2)

Factors influencing the timing and performance of facial reanimation procedures include: presence of partial regeneration, donor consequences, proximal and distal nerve integrity, viability of facial muscles, status of donor nerves, time elapse since injury, age, radiation injury, other metabolic or vascular disorders, and nutrition. Partial regeneration is often overlooked, and yet is extremely important in understanding which operation should be performed. Partial regeneration of the facial muscles by a few axons may preserve the facial muscles for many years. This situation optimizes nerve transfer type procedures.

Many surgical procedures borrow neural elements or signals from other systems, like the hypoglossal or trigeminal systems. There are consequences of sacrificing the donor nerve that are important to consider in planning for the overall needs of the patient. The donor nerves must be tested preoperatively for adequacy of function and vitality. The donor effects of facial reanimation surgery must be assessed for each patient prior to reconstructive surgery.

As a general rule, the most desired neural tissue source for rejuvenation of the paralyzed face is direct reanastomosis or interpositional grafting. Therefore, the integrity of the proximal facial nerve is very important. Anastomosis or grafting of the proximal facial nerve has relatively no donor deficits except for hypesthesia for nerve graft harvest. It also allows for some degree of voluntary and involuntary control of facial movement. There is no reliable electrical test to evaluate the function of the proximal nerve when it is not in continuity with the distal facial nerve. Other factors like nature of the injury, location of the injury, age of the patient, and nutritional status of the patient should be assessed as these all affect proximal nerve viability.

The facial nerve distal to the injury is the conduit for neural regeneration to the facial muscle following neurorrhaphy or grafting. Therefore, the distal nerve must be anatomically and functionally intact. The distal facial nerve can be electrically stimulated and identified in the first 72 hours after injury or resection. After this time, the surgeon must rely on visual identification of the branches of the facial nerve. There are some general landmarks to aid in the identification of the distal facial nerve branches. These include:

Several anatomic variations of the facial nerve may exist. If all facial nerve branches cannot be reinnervated, an order of priority for selective routing of reinnervation of facial nerve branches calls for the buccal and zygomatic branches to be addressed first. Then the marginal mandibular, frontal, then cervical can be reinnervated.

Several variables affect the facial muscles and the results of nerve grafting and transfer procedures. The viability of the facial muscles can be tested with electromyography (EMG). This is the single most important test in determining the type of operative procedure to be performed. Four types of information are generally available for the EMG. Normal voluntary action potentials mean that functioning motor axons have connections with and are stimulating motor units of facial muscles. Polyphasic potentials are seen during reinnervation and may precede visible evidence of reinnervation. Denervation or fibrillation potentials indicate that otherwise normal denervated muscle exists. Electrical silence, with no potentials seen, indicates atrophy or congenital absence of muscle. Preexisting innervation prevents reinnervation by another neural source. Denervation atrophy of the facial muscles can occur after 18 months of complete denervation. EMG is the most helpful method for assessing facial muscle atrophy and is a preoperative prerequisite for all candidates for reanimation if the paralysis is more than12 months’ duration. The presence of polyphasic or normal action potentials seen in a patient with facial paralysis indicates that reinnervation is present but incapable of producing facial movement. If over 12 months have elapsed since the facial nerve injury, the situation can be assumed to be stable and an operative procedure may be warranted. However, in the first 12 months, these potentials may mean that reinnervation is occurring and that facial movements may return in the next few months. In this case reanimation surgery should be postponed. Fibrillation or denervation potentials mean that the electrode is positioned in denervated muscle, which is optimal for nerve grafting procedures. If the EMG shows electrical silence, this means that the muscles have undergone denervation atrophy and nerve grafting or transfer is futile.

The age of the patient affects the ability of the proximal neuron to regenerate. Its regeneration potential declines with increasing time since injury and increasing age of the patient. The clinical implication is that facial reanimation surgery should be performed as soon as possible.

Radiotherapy, a necessary component of treatment of certain salivary malignancies, appears to have a deleterious effect on reinnervation via facial nerve grafts. Pillsbury and Fisch (1979) found that radiotherapy reduced the average outcome from 75% to 25% in a review of 42 grafted patients. Others have found minimal effects on nerve grafts from radiation. It is thought that irradiation probably affects the neovascularization of the nerve graft by decreasing vascularity of the tissue bed. However, radiation is not a contraindication to reanimation procedures that require nerve grafting. Diabetes and nutritional factors can also have a deleterious effect on the regeneration of nerve fibers after injury especially if combined with increasing age and radiation.(2)

Surgical Reanimation

Before attempting any surgical repair, it is extremely important to understand the etiology and duration of the facial paralysis. The duration of facial paralysis determines the choices of techniques, since the neural techniques depend heavily on the survival of the motor end plates. If there is any doubt whether the integrity of the facial nerve is disrupted, a waiting period of at least 12 months should lapse before attempting a surgical interruption that may result in irreversible damage to the facial nerve.(1)

Preoperative assessment should include a complete history and physical examination. The types of injury as well as time since injury are important details. The surgeon should look for prior incisions or scars and evaluate the integrity of the hypoglossal and trigeminal nerves. The degree of facial motion should be assessed and graded, as well as, the status of the eye. An ophthomology consult should be obtained on every patient. All patients who have had facial paralysis for more than one year should undergo EMG. Preoperative photos should be taken and some surgeons use video recording to document to patient’s deficits. Further imaging will be dictated by the etiology of the facial paresis (trauma, idiopathic, parotid tumor, other tumor, or congenital.

In the evaluation of the patient with unilateral facial paralysis, the physician should first focus on the associated ocular complications. These complications include exposure keratitis, epiphora, and exopthamus. Facial paralysis results in the inability to close the upper lid because the upper lid levator muscle is unopposed by the denervated orbicularis muscle. Paralytic lagophthalmos may lead to corneal dryness, punctate keratopathy, corneal ulceration, and, ultimately, decreased vision.(3) Traditional medical therapy has included ocular lubrication with ointment and drops and corneal protection with moisture chambers, taping, and pressure patches. These methods are often used when facial nerve recovery is anticipated.(5) These techniques have led to failures and poor patient compliance especially when the facial function does not return for a long time.

Traditional surgical therapy with tarsorrhaphy has proven highly effective in eye protection. A temporary lateral tarsorrhaphy is performed with a horizontal mattress suture of 5-0 nylon. Approximately 3 mm medial to the lateral canthus, the first suture is placed through a partial thickness of the upper eyelid, 6 mm from the lid margin. The suture exits through the upper eyelid grayline. It then enters the lower eyelid grayline, passes through a partial thickness of the lower lid, and exits the skin about 5 mm below the lid margin. The suture is then passed through a 3 mm long, 4 french red rubber catheter, which acts as a bolster for the lower lid. The suture is then passed 3 mm medially through the grayline of the lower lid. The suture then enters the upper lid grayline and exits the upper lid 3 mm nasally from the previous entrance site. Another bolster is made with red rubber catheter and the suture is tied and pulled tight. To make a permanent tarsorrhaphy a 1 to 2 cm superficial layer of the upper and lower eyelid margins along the graylines from just lateral to the limbus to the lateral canthal area is removed.(6) The results of the tarsorrhaphy are cosmetically unappealing and visual defects are often noted by the patient.

Such complications lead to the development of a number of techniques for the rehabilitation of the paralyzed eyelid. These include lid loading techniques and lid shortening techniques. In the past decade, upper eyelid gold weight implants have become popular and widely used as a technique for lid closure in patients with paralytic lagophthalmos. The levator momentarily relaxes when the opposite eye blinks or closes, thus allowing one to take advantage of gravity by weighting the paralytic lid and producing closure of the fissure. Gold is the preferred material because of its inert nature, high specific gravity, and good color match to skin.(3)

The gold implant is a very simple procedure and offers consistently satisfactory results, even when performed by a surgeon with little operative experience. Preoperative assessment determines the amount of weight to be used by taping weights to the upper eyelid until the distance between the eyelids is 1 mm or less. An additional 0.2 grams is added to the gold weight to counteract the strengthened levator muscle function that usually develops.(2) Under local anesthesia, the midpupillary line is marked and an incision is made 1 cm above the lash line and below the supratarsal fold. Tenotomy scissors are used to dissect down through the orbicularis muscle fibers to expose the tarsal plate. The weight should be positioned such that approximately two thirds if the weight is medial to the midpupillary line and one third is lateral. The gold weight rests fully on the tarsal plate. The inferior border of the gold weight should rest 2 – 3 mm above the upper lash line, however, in order to improve cosmesis some surgeons place it on the inferior most border of the lash line. The weight should be placed so that there are two holes inferior and one hole superior. The weight is sutured to the orbicularis muscle and tarsal plate with 6-0 clear prolene. The two lower sutures should be placed first, followed by the upper suture. There needs to be enough orbicularis muscle to completely cover the gold weight without shortening the upper lid. The muscle and skin are then closed.(7) Because gold weight placement is so successful in reducing the supportive care needed to protect the eye and is easily reversible, the procedure should be done in any patients whose paralysis is expected to be incomplete, delayed, or permanent.

An alternative to the gold weight implant is the less frequently used upper lid spring. This approach uses a custom-made stainless steel spring, which is surgically implanted in the upper lid. When the levator muscle relaxes as the opposite eye closes, the spring actively pushes the lid down. The spring, being an active implant rather than a passive implant like the gold weight, allows for more rapid eyelid excursion and is more effective in the supine position. Unfortunately, the spring’s disadvantages may outweigh its benefits because it is more prone to exposure and extrusion, is technically difficult, and often requires multiple surgical adjustments.(3)

Patients with great laxity of the lower eyelid with resulting ectropion may benefit from a lower lid tightening procedure. Resuspension of the lateral canthal tendon protects the lower edge of the cornea, improves epiphora, and gives some lateral facial support. A modified lateral canthoplasty is generally successful in resuspending the lower lid in patients with mild or moderate lateral laxity. It is recommended that the repair of paralytic ectropion be delayed at least 3 months following the onset of paralysis to allow complete muscle atrophy and loss of facial tone. A lateral canthotomy incision is placed precisely in the lateral canthus and extended for 5 – 6 mm. Complete lower lateral cantholysis is preformed submuscularly to fully mobilize the lower lid. The anterior and posterior lamellae are then separated by incising along the grayline for a distance determined by the amount of skin laxity present. The inner surface of the canthal-tarsal complex is denuded of mucosa and trimmed as needed. A pocket is dissected through the soft tissue overlying the periosteum of the lateral orbital rim just above the level of Whitnall’s tubercle. The canthal-tarsal complex is then sutured to the periosteum of the inner surface of the lateral orbital rim. Once the lid has been reattached in this fashion, conservative trimming of any redundant skin can be done and the skin and muscle layers are sutured. It is important to realign the graylines of the upper and lower eyelids at the new lateral canthus to avoid any rounding of the canthus.(3)

Other methods used to address the lower lid include medial canthoplasties and implantation of material to provide rigid support. Medial canthoplasty is an effective procedure but may cause injury to the lacrimal canaliculi or lacrimal dysfunction caused by postoperative scarring. Others have advocated the use of rigid support to the lower eyelid with implantation of autogenous cartilage or chondrodermal grafts. These methods have been used with reportedly high rates of success but often result in excessive bulk, poor cosmesis, donor-site morbidity, and potential graft failure.(5,8)

Restoration of the continuity of the facial nerve is the only means of reestablishing some approximation of normal facial balance. Bunnell performed the first successful repair of the facial nerve within the temporal bone and in fact noted that transposition of the nerve out of the canal gained sufficient length that the neuroma could be resected and still permit direct anastomosis.(9) When the facial nerve has been disrupted it is important to reapproximate the nerve without tension. The best time for direct reanastomosis is within the first few days (3 days or 72 hours), if feasible, since the degeneration has not yet occurred and the surgeon can still stimulate the distal ends of the nerve for assistance in identification. If this is impossible, then repair within 30 days is acceptable. During this time, there is maximal axoplasmic flow, particularly within the 3 to 4 week period, so that the nerve has the best physiologic opportunity to regenerate.

The surgeon should use magnification in this repair. The nerve endings are freshened and then sutures of 8-0 nylon or smaller are applied to the epineurium. A nerve injury involving one of the major branches should be repaired in a similar fashion. As a general rule, however, if a line is dropped from the lateral canthus and the injury is distal to this line, it is usually unnecessary to repair the injury. Spontaneous recovery will usually occur.(1)

The cable or interposition nerve grafts are frequently the desired approach to facial muscle reinnervation. Any situation in which viable proximal nerve can be sutured and distal elements of facial nerve can be identified can undergo nerve grafting. In the event that nerve grafting is not undertaken at the time of nerve sacrifice, it should be completed within 72 hours thereafter so that the facial nerve stimulator can be used to identify the distal facial nerve branches.(2) The choice of nerve graft material depends on the size and nature of the defect. The greater auricular nerve is frequently used for defects up to 6 – 8 cm.(9) It can be located by drawing an imaginary line between the mastoid tip and the angle of the mandible. The nerve usually bisects this distance perpendicular to the line, lying on the superficial surface of the sternocleidomastoid muscle. Other cervical nerves in this area can also be used for interpositional grafts.(1) Baker has used the cervical plexus to give multiple branches for reconstruction of more distal portions of the facial nerve and states that grafts up to 12 cm can be obtained. Grafts longer than 10 - 12 cm can be obtained from the sural nerve, requiring a separate surgical site in the posterior calf.(9) It is harvested by making an incision on the lateral aspect of the leg. The nerve lies 1 – 2 cm lateral to the saphenous vein, medial and posterior to the lateral malleous of the ankle.(1) Once the donor nerve has been harvested it should be placed in lactated Ringer’s solution. For neurorrhaphy, simple interrupted sutures of 9-0 or 10-0 monofilament nylon on an atraumatic, taper needle are preferred. Both ends of the nerve graft and the proximal and distal stumps should be transected cleanly with a fresh sterile blade. For nerve trunk anastomosis, four simple epineural sutures will align the nerve ends accurately. The surgeon should use some type of magnification, such as the operating microscope or loupes, for the anastomosis. The nerve graft should lie in the healthiest possible bed of tissue with 8 – 10 mm of extra length for each anastomosis, so there is a tension free anastomosis.(2) These techniques offer the best results for reanimation of the face, the results are never completely normal, with some weakness and some synkinesis noted in most patients.(9)

It is only when a proximal facial nerve stump is not viable or available that attention should be turned to other systems, for example, muscle or nerve transfer. There are basically three crossover techniques: hypoglossal to facial, spinal accessory to facial, and facial to facial. The first is by far the most popular and commonly used technique. All of these techniques require irreversible facial nerve injury, intact mimetic function, intact motor end-plate function, intact proximal donor nerve, and intact distal facial nerve.(1)

The cross facial grafting is the only procedure that has the theoretic ability of specific divisional control of facial muscle groups. Originally described by Scaramella and Smith in independent reports in 1971, the technique has not proven as advantageous as it was first thought to be. The operative technique consists of transection of several fascicles on the nonparalyzed side through a nasolabial fold incision. Sural nerve grafts are sutured to these fascicles and passed through subcutaneous tunnels to the paralyzed side. The anastomosis with the paralyzed facial nerve branches is done by most surgeons at a second stage, 6 –12 months after the first. Currently the technique is only used in conjunction with free muscle transfers. Reinnervation of the paralyzed facial muscles is not sufficient to justify the procedure without muscle transfer.(2) This procedure is technically demanding, generally requires two procedures, and also invades both the normal side of the face and the leg.(9) The results from the cross-facial nerve grafting with neuromuscular transfer has not proven superior to the hypoglossal to facial crossover graft.(3)

The use of nerve crossovers dates to the turn of the century, when anastomosis to both the spinal accessory and hypoglossal nerves was described. Both the phrenic and the spinal accessory nerves have been used as motor donor nerves for crossover to the distal facial nerve. The phrenic may give rise to twitching with breathing, and the eleventh cranial nerve seems less capable of reeducation. These nerves should be considered for transfers only if the hypoglossal is not available.(9) Because the VII-XII anastomosis leads to paralysis of the ipsilateral tongue muscles, the procedure is contraindicated in patients who have, or who have the potential for, any other lower cranial nerve deficits. Although the classic VII-XII anastomosis is generally well tolerated, select patients can have significant speech, mastication, and swallowing difficulties.(3) An alternative to the classic procedure is a partial hypoglossal to facial anastomosis, which provides innervation to the mimetic facial muscles with reduced denervation of the donor hypoglossal nerve. The procedure involves an end to side nerve graft from the distal hypoglossal nerve and an end to end anastomosis of the graft to the distal facial nerve. This is also known as a "jump graft".(10)

A modified parotidectomy incision is made in the preauricular skin crease and then extended two fingerbreadths below the mandible. The facial nerve is identified at the stylomastoid foramen. The nerve is dissected to the pes anserinus, and then transected at the stylomastoid foramen. The digastric muscle is retracted superiorly and the hypoglossal nerve is identified. The nerve is followed anteriorly and medially as it travels deep to the mylohyoid muscle and enters the tongue muscles. It is divided at its most distal portion to gain the most length. The two cut ends are freshened and then sutured using atraumatic technique with an 8-0 monofilament suture. The wound is closed in layers. Return of facial function begins in approximately 4 to 6 months. With a successful result, tone in the muscles and resting symmetry, as well as volitional movement, will be seen. The region of initial reanimation activity is often noted around the lips and oral commissure. All patients will experience some degree of synkinesis. Some undesirable movement of the face with chewing, swallowing, or speaking is universal, but generally well tolerated.(3)

Muscle transposition techniques are used when neural techniques are unsuitable because there is no longer an intact facial neuromuscular system, there is loss of motor end-plates from long standing facial nerve interruption for at least 3 years, or other cranial nerves are sacrificed so they cannot tolerate a crossover technique. The fifth nerve innervation to the temporalis and masseter muscle must remain intact, however.(1) Temporalis muscle transfer was described by Gillies in 1934, with the use of fascia lata grafts to lengthen the muscle down to the upper lip.(9) The temporalis is a fan shaped muscle radiating from the narrow coronoid process of the mandible to the broad temporal fossa of the temporal bone. Because of its large area it can be used for multiple areas of the face. The temporalis should be used mostly for reanimation of the corner of the mouth and can be used for the eye, whereas the masseter muscle cannot.(1)

The temporalis transfer is begun through a vertical incision in the scalp above the ear or an extended facelift incision. Dissection is carried out through the superficial layers of the scalp and the temporalparietal fascia, until the superficial layer of the deep temporal fascia is identified. An appropriate segment of the central one third of the muscle is outlined and incised. The muscle is dissected off of the underlying bone down to the level of the zygomatic arch. The temporal branches of the mandibular nerve enter the muscle from its medial surface at the level of the arch. A subcutaneous tunnel is made from the corner of the mouth to the level of muscle dissection. An incision is made within the melolabial crease and the lateral fibers of the orbicularis are identified. The muscle strip is passed through the subcutaneous tunnel to the lip incision. An assistant elevates the corner of the mouth and the temporalis strip is sutured to the orbicularis muscle. It is essential to overcorrect the corner of the mouth as the muscle flap will stretch and elongate the first couple of weeks. Most patients who undergo temporalis transposition will have excellent correction of the drooping corner of the mouth and jowls. The suspension will also help restore symmetry to the melolabial folds and alar base. Greater than 90 % of patients will learn to control the contraction of the temporalis muscle in such a way that they will have significant mouth motion with smiling.(3)

Masseter muscle transfer was first reported in 1911.(9) This technique is used when the temporalis muscle is unavailable. The disadvantage of this muscle is that it is smaller and the vector force of the muscle is in a more horizontal plane, thus providing less superior angulation to the corner of the mouth. The muscle is exposed by making a large incision in the gingival mucosa along the sulcus of the mandible. A plane is created between the mucosa and the muscle to isolate the masseter muscle. The muscle is freed by raising the muscle off of the mandible using periosteal elevators. Once the muscle is freed medially and laterally, it is detached from its insertion at the inferolateral edge of the mandible with a curved right-angled scissors. The vertical incision must not be extended too far superiorly or posteriorly or the nerve supply to the muscle could be damaged. The anterior half is split into two slits of muscle. This is then sutured to the orbicularis muscle through subcutaneous tunnels to the corner of the mouth (lips and commissure). The masseter muscle may also be exposed through an external incision if used in conjunction with other reanimation techniques.(1)

Static support in the form of fascia lata slings or Marlex mesh has been advocated for facial reanimation. Fascial or prosthetic slings may provide symmetry at rest as the optimal result. For some patients who refuse or are not good candidates for dynamic reanimation, Gore-Tex is another material that can be used for static suspension of the paralyzed face.(11)

Other ancillary procedures for facial reanimation include rhytidectomy, blepharoplasty, and brow lift, as well as multiple other cosmetic procedures that can be done to help make that patient’s face symmetrical. Another procedure that has been proposed is the selective deanimation of the levator labii superioris alaeque nasi by resection of the muscle. This is postulated to correct the nasal asymmetry in patients with facial paralysis.(12)

In conclusion, the techniques discussed above can provide marked cosmetic improvement and can restore function in patients with facial nerve paralysis. The goal of facial reanimation is to improve the patient’s facial muscle functions. It is important to remember that the highest priority in facial nerve paralysis is to protect the eye. Many times the procedures described above are use in combination to achieve complete results. As these procedures evolve, these patients will be afforded the possibility of leading normal lives without facial disfigurement.


References

  1. Parnes SM: Facial Reanimation. In Bailey BJ, ed.: Head and Neck Surgery –Otolaryngology, second edition, New York, 1998, Lippincott-Raven. 
  2. Crumley RL, Scott TA: Rehabilitation of Facial Paralysis. In Cummings , ed.: Otolaryngology - Head and Neck Surgery, second edition, London, Mosby, 1993 
  3. Julian GG et al.: Surgical Rehabilitation of Facial Nerve Paralysis. In Syms CA and Arriaga MA, eds.: The Otolaryngology Clinics of North America; Rehabilitation of Neurotologic Diseases, London, October 1997, WB Saunders. 
  4. Sweeney KD, Vrabec JT: Facial Nerve Paralysis 1996. In Quinn FB, ed.: Dr. Quinn’s Online Textbook of Otolaryngology, Accessed at: http://www.utmb.edu/oto/Grnds.dir/face961.htm 
  5. Maas CS et al.: Primary surgical management for rehabilitation of the paralyzed eye, Otolaryngology – Head and Neck Surgery 110 (3): 288-295, March 1994. 
  6. Alford EL: Tarsorrhaphy. In Bailey BJ, ed.: Atlas of Head and Neck Surgery – Otolaryngology, New York, 1996, Lippincott-Raven. 
  7. Alford EL: Eyelid Reanimation Procedures. In Bailey BJ, ed.: Atlas of Head and Neck Surgery – Otolaryngology, New York, 1996, Lippincott-Raven. 
  8. May M et al.: Management of the paralyzed lower eyelid by implanting auricular cartilage, Archives of Otolaryngology Head and Neck Surgery 116: 786-788, July 1990. 
  9. Hoffman WY: Reanimation of the Paralyzed Face. In Jackler RK, ed.: The Otolaryngology Clinics of North America; Acoustic Neuroma II, London, June 1992, WB Saunders.
  10. May M: Hypoglossal facial nerve interpositional jump graft for facial reanimation without tongue atrophy, Otolaryngology – Head and Neck Surgery 104 (6): 818-825, June 1991.
  11. Konion RJ: Facial paralysis reconstruction with Gore-Tex soft tissue patch, Archives of Otolaryngology head and Neck Surgery 118: 1188-1194, Nov 1992.
  12. Ressa JE, Cummings CA: The rle of facial muscle resection in reconstruction of the paralyzed face, Annals of Plastic Surgery 30 (6), 537-540, June 1993.
  13. Burgess LPA, Goode RL: Rehabilitation of Facial Nerve Injury. In Weissler MC, Pillsbury HC, eds.: Complications of Head and Neck Surgery, New York, 1995, Thieme Medical Publishers.