Assessment of the Deformity

Physical examination includes complete head and neck examination with attention to cranial nerve function and the presence of functional masseter and temporalis muscles. The degree of facial nerve function is recorded using the House-Brackmann Facial Grading System² (Table 172-1). A number of facial nerve grading scales have been developed, but the House-Brackmann scale was adopted by the Facial Nerve Disorders Committee of the American Academy of Otolaryngology–Head and Neck Surgery in 1985 because of its reproducibility and ease of use.² This scale is useful for evaluation of overall function, but it is insufficient for precise assessment of defects affecting one or more branches of the facial nerve, and it does not allow precise measurement of effectiveness of treatments isolated to one region of the face. Therefore, the examination should assess deformity of the upper, middle, and lower thirds of the face independently. This approach allows more precise characterization of defects, aids the decision-making process for rehabilitation, and allows more precise assessment of treatment results. Facial tone also is noted, as is the presence of any reinnervation. Thorough assessment of the eye also is performed. Visual acuity, corneal integrity, eyelid closure, tearing, Bell’s phenomenon, lagophthalmos, lower lid laxity, position of the lacrimal puncta, and eyebrow position are noted. Nasal examination focuses on the position of the ala and nasal septum and the presence or absence of nasal obstruction. Oral competence and height and position of the lower lip are carefully reviewed. In long-term paralysis (of more than 1 year’s duration), electromyography (EMG) of the facial muscles is performed before reinnervation procedures. Occasionally, muscle biopsy provides additional information about the presence of viable muscle for innervation. If nerve fibrosis is suspected, nerve biopsy occasionally is indicated.

Table 172-1 House-Brackmann Grading System

Time since Transection

A chronic, long-standing paralysis with complete muscle degeneration poses several problems with regard to eventual reinnervation surgery. The facial muscles may undergo denervation atrophy. Severe atrophy renders the reasonably normal muscles incapable of reinnervation and contraction. Such severe atrophy may occur after 18 months of complete denervation, although in some clinical situations, muscles have been known to persist inexplicably for many years without incurring such atrophy.⁴ EMG is the most helpful method for assessing facial muscle atrophy and is therefore a preoperative prerequisite for all reanimation candidates if the paralysis is of more than 12 months’ duration. The presence of nascent, polyphasic, or normal voluntary action potentials in a patient with facial paralysis indicates the occurrence of reinnervation. If more than 12 months have passed since the facial nerve injury, the situation can be assumed to be stable, and an attempt at surgical reanimation may be warranted. Within the first 12 months, however, the presence of potentials may mean that reinnervation is occurring and that facial movements may return in the next few months. Reanimation surgery should therefore be postponed. Fibrillation or denervation potentials mean that the EMG electrode is positioned in denervated muscle. This is an optimal situation for cable nerve grafting or, when no viable proximal facial nerve is available, for hypoglossal-facial anastomosis.

One of the most significant EMG findings is electrical silence, reflecting denervation atrophy of the facial muscles. The surgical implication is that nerve grafting or transfer is futile and therefore contraindicated. If the facial muscles are absent or atrophied, muscle transfers are indicated.

Another effect of time includes endoneural scarring within distal nerve segments. It is not known whether endoneural scarring acts as an impediment to nerve regeneration, but when associated with muscular atrophy, it probably further precludes nerve grafting or transfer.

Presence of Partial Regeneration

Partial regeneration often is overlooked but is extremely important in determining which operation to perform. If the facial nerve has undergone enough regeneration to permit a few axons to reach the facial muscles, this partial innervation may be sufficient to preserve the muscles for many years, even though they may be totally paralyzed. In these clinical circumstances, results with hypoglossal-facial anastomosis, which generally is preferable to muscle transfer, will be optimized.

Status of the Proximal and Distal Facial Nerve

The optimal source for rejuvenation of the paralyzed face is the ipsilateral facial nerve. Anastomosis or grafting to the ipsilateral nerve has no donor consequence (other than the minor hypesthesia or anesthesia from the harvesting of a nerve graft) and facilitates natural voluntary and involuntary control. Exceptions to this general rule are those cases in which the patient needs prompt relief from corneal exposure or drooling, and a tissue transfer or sling technique may be preferred because its effects are immediate.

Accordingly, the integrity of the proximal facial nerve is critical. As with other motor nerves, no reliable electrical tests exist to confirm the viability of the proximal nerve when it is discontinuous with its distal portion. Factors that affect proximal nerve viability and are therefore important considerations in the clinical evaluation include (1) nature of the nerve injury (e.g., clean transection versus crush), (2) location of injury (proximal versus distal), (3) age (younger nerves tend to regenerate more quickly and fully), (4) nutritional status (which directly affects nerve regeneration), and (5) history of irradiation (which may impede neural regeneration).

The facial nerve distal to the injury site serves as a conduit for neural regeneration to the facial muscles after neurorrhaphy, grafting, or hypoglossal-facial anastomosis. With acute injuries (incurred less than 72 hours previous), the electrical stimulator may be used to identify the distal nerve and the muscular innervation of distal branches. After this “golden period,” however, the surgeon must rely on visual identification of the divisions and branches of the distal nerve, because the capability of being stimulated electrically generally is lost after approximately 72 hours. For this reason, transected nerve branches in trauma or tumor cases should be tagged for identification by placing a small colored suture around or adjacent to each nerve branch. Any anatomic or surgical landmarks should be precisely dictated in the operative note. If no suture markers are available, and the golden period has elapsed, careful surgical searching (preferably with use of loupes or an operating microscope) may reveal each of the divisions or branches of the facial nerve. A topographic map is essential in guiding the dissection. A review by Bernstein and Nelson⁵ describes the variability with which these branches are placed. The following landmarks are helpful (Fig. 172-1).

Figure 172-1. Topographic map of distal facial nerve anatomy, useful as a guide in finding nonstimulatable nerve branches for grafting. Pes anserinus is 2 cm inferior to a point 1 cm anterior to tragus. Marginal mandibular branch courses from the pes anserinus to the angle of the mandible: buccal branch parallels the zygomatic arch 1 cm below its inferior border. Superior division arcs from pes anserinus toward lateral end of the eyebrow, under a line that is convex superiorly.

(From House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93:146.)

As an example of selective routing, when a parotid tumor operation results in excision of the pes anserinus and the proximal facial branches, a branched nerve graft may be placed to reinnervate the zygomatic and the buccal branches, excluding unimportant branches. Fisch⁶ advises clipping branches of cervical branches in order to route innervation to the more important portions of the face. Data confirming the efficacy of this technique, however, are very limited.

If no nerve branches are found, and EMG shows that denervated facial muscles are present, the nerve graft may be sutured directly to the muscles targeted for reinnervation (muscular neurotization). In these instances, the most important muscles are those of the midface (zygomaticus major and minor, levator labii superioris) and orbicularis oculi muscles. Reinnervation will not be as complete as in routine nerve grafting because the regenerating axons must form new connections to the old motor endplates, or they must create their own.⁷

Viability of Facial Muscles

Four types of EMG responses are observed⁸:

Donor Consequences

Many surgical procedures designed for facial reanimation borrow neural elements or signals from other systems (i.e., the hypoglossal and trigeminal systems). The consequences of sacrificing the donor nerve (known as donor deficit) are most important in planning for the overall needs of the patient. Certainly, the surgeon must assess the donor nerve preoperatively in all cases. The hypoglossal nerve must be tested for strength and vitality before it is transected and anastomosed to the distal facial nerve. Similarly, the trigeminal nerve must be intact and functional when its muscles, either masseter or temporalis, are considered for transposition into the facial muscle system.

The donor effects of facial reanimation surgery may be quite detrimental to the patient’s welfare. For example, a patient with previous hypoglossal nerve injury on the opposite side could become an “oral cripple” if the remaining hypoglossal nerve were to be transected for use in a XII-VII anastomosis.

The ideal reanimation procedure is one that yields the following results: (1) no donor deficit; (2) immediate restitution of facial movement; (3) appropriate involuntary emotional response; (4) normal voluntary motion; and (5) facial symmetry. No currently available operative procedure satisfies all of these parameters. In fact, even with a bacteriologically sterile and precise surgical transection and immediate microsurgical repair of the facial nerve, completely normal neurologic function cannot be restored. Therefore, the surgeon must have a clear understanding of all operations available, including potential outcomes and sequelae.

Status of Donor Nerves

The hypoglossal nerve is the most frequently used nerve source for transfer. Reflex and physiologic similarities between the hypoglossal and facial nerves have been described.⁹ The integrity of the hypoglossal nerve must be determined before it is transferred for reinnervation. Irradiation of the brainstem, lesions of the skull base and hypoglossal canal, and surgical procedures of the upper neck may affect the integrity and function of this nerve.

The trigeminal nerve has been used for facial reanimation in many ways. The methods currently used most often involve masseter or temporalis muscle transfer (necessitating that the motor portions of the trigeminal nerves be intact). Palpation of the muscle during jaw clenching confirms whether the muscle is functional.

The cross-face nerve graft procedure (faciofacial anastomosis) initially was thought to be the most appropriate and ingenious facial reanimation procedure.^10,11 The procedure is unique in that it borrows appropriate neural input from the contralateral normal side and routes it to the paralyzed side. Such a procedure requires a fully intact (contralateral) facial nerve.

Age

The proximal neuron’s ability to regenerate declines with time because of denervation and aging-related changes. The etiologic mechanism probably involves diminishing regenerative vitality of the perikaryon (cell body), although peripheral scarring may play a role. The clinical implication is that facial reanimation surgery should always be performed as soon as possible, provided that the operative procedure does not interfere with or injure existing innervation or ongoing reinnervation.¹²

Health Status

Among patients with diabetes, regeneration of injured nerves is notoriously poor. Microangiopathy is an additional factor that may affect the grafted segment. These factors do not preclude a nerve graft procedure in a diabetic patient, but when combined with radiation, advancing age, and other factors, they may cause the surgeon to consider muscle transfer or a suspensory operation, rather than a neural anastomosis.

Prior Radiotherapy

Radiotherapy, a necessary component of treatment for certain salivary gland malignancies, appears to have a deleterious effect on reinnervation through facial nerve grafts. McCabe¹³ demonstrated satisfactory muscle reinnervation from grafting despite irradiation in animals. These investigators subsequently have documented return of facial function in nine patients who received post-grafting radiotherapy. McGuirt and McCabe¹³ and Conley and Miehlke¹⁴ have published reports indicating that facial nerve grafts function well even though irradiated, and that nerves are among the most radioresistant tissues of the human body. Pillsbury and Fisch¹⁵ found that radiotherapy reduced the average outcome from 75% to 25% of nerve function recovery in a review of 42 grafted patients. Irradiation probably affects the neovascularization of the nerve graft by decreasing vascularity of the tissue bed and probably injures the proximal and distal segments of the nerve as well. The most radiosensitive portion of the nerve—the pontine nucleus—should be assessed to determine whether it was present in the field of irradiation.

Congenital Paralysis

In a series of 95 infants with neonatal paralysis, Smith and associates⁸ found 74 of the cases to be secondary to intrauterine injury or birth trauma, whereas 21 were thought to be congenital. These infants should be studied with nerve excitability and EMG testing early in life to ascertain the status of nerves and muscles. Most patients with injury-related neonatal paralysis recover rapidly, whereas the paralysis associated with other congenital anomalies (such as Möbius syndrome) is permanent. Nerve exploration or transfer generally is futile in the latter cases.

Eye Protection: Evaluation and Treatment of Eyelid Paralysis

Paralysis of the orbicularis oculi results in exposure and drying of the cornea. Patients at increased risk for exposure keratitis may be identified by applying the acronym BAD—absence of Bell’s phenomenon, corneal anesthesia, and history of dry eye. An inability to protect the cornea is the result of incomplete eye closure, preventing effective distribution of the tear film across the surface of the eye, and ectropion occurs because the atonic lower lid and lacrimal punctum fail to appose the globe and bulbar conjunctiva. This causes faulty eyelid closure and improper distribution of tears across the cornea.

Epiphora may result from failure of tears to enter the lacrimal punctum, secondary to pooling of tears due to ectropion and the loss of the orbicularis oculi tear-pumping mechanism. The response to abnormal corneal sensation may be reflex tear hypersecretion, which will further increase the epiphora.

Any patient with facial paralysis who demonstrates a poor Bell’s phenomenon is at risk for the development of exposure keratitis. Eye pain may herald the onset of keratitis. In patients with diminished corneal sensation, however, exposure keratitis may asymptomatically progress to corneal ulceration. Accordingly, all patients with diminished orbicularis oculi function require ophthalmologic consultation.

Initial eye care is directed toward moisturizing the dry eye and preventing exposure. It is important to communicate to the patient the potential consequences of failure to protect the eye, in hopes of improved compliance. If the eyelid paralysis is temporary or partial, these local measures may be all that are necessary to adequately protect the eye. Regular use of artificial tears commonly is the first-line method used to keep the eye moist. Ointments also may be used, but they are less practical in the daytime because they tend to blur vision.

Lacriserts, contact lenses, and occlusive bubbles commonly are used, although patient compliance may be problematic¹⁶ (Fig. 172-2). The eyelids frequently are patched or taped, but if incorrectly used, these methods may result in corneal injuries. Tape should not be placed vertically across the eyelashes, but applied horizontally above the eyelashes on the upper eyelid, or supporting the lateral canthal portions of the lower eyelid.¹⁷ When an eye patch is used, care must be taken to ensure that the eye cannot open, because this would allow contact between the patch and the cornea.

Figure 172-2. Occlusive bubble worn by a patient after acoustic neuroma surgery. The appliance has a foam rubber skin contact surface that is firmly attached to a thin Plexiglas lens. In our experience, patient compliance is relatively high with this type of device.

(Courtesy of Moisture Chamber, Pro-optics, Palatine, Illinois.)

Procedures to Treat Paralysis of the Lower Lid (Ectropion)

Tarsorrhaphy

The temporary lateral tarsorrhaphy is an expeditious and effective method for protecting the eye in patients with mild lagophthalmos and mild corneal exposure. A horizontal mattress suture of 7-0 silk or nylon is placed laterally to approximate the gray line (mucocutaneous junction) of the upper and lower lids. Tarsorrhaphy sutures will remain effective longer if they are placed through bolsters made of rubber (Robinson) catheters.

For longer-lasting protection, the lid adhesion tarsorrhaphy is preferred. The lid margin (gray line) of each lid is denuded 4 to 6 mm from the lateral canthus, and a similar suture technique is used to approximate the denuded mucocutaneous junctions of upper and lower lids (Fig. 172-3). Like the temporary lateral tarsorrhaphy, this procedure can be reversed if function returns. The cosmetic deformity of tarsorrhaphy and the availability of improved, alternative techniques to rehabilitate the eyelids have reduced the use of tarsorrhaphies.

Figure 172-3. A, Tiny single skin hook being used to evert the lower lid for denuding of “gray line” (mucocutaneous junction). Note that a gray line of upper lid has been denuded. B, Healed tarsorrhaphy at 4 months. Increased eye closure may be achieved by extending the denudation and sutures medially.

Procedures to Treat Paralysis of the Upper Lid (Lagophthalmos)