11 Facial paralysis
Facial paralysis is a complex multifaceted condition with profound functional deficiencies, devastating aesthetic effects, and tragic psychological consequences. It may be congenital or acquired, affect the old and the young, and vary from mild to severe. In this chapter we will focus on the clinical problem and the surgical solutions available today.
Surgical correction of facial paralyses continues to evolve and improve. Early attempts were directed at static repositioning to address functional problems around the eye and mouth. Muscle transplants were initially nonvascularized grafts but function was impaired shortly thereafter with the muscle being revascularized and reinnervated. At first this was via ipsilateral nerves and later using contralateral nerves. For facial musculature that has the potential for reinnervation, nerve transfers were introduced as a very effective method of maintaining nerve function and muscle activation. Recent combinations of nerve transfers and muscle transplantation have been developed.
At present surgical methods to recover facial nerve function range from nerve repair, nerve grafting, and nerve transfer to static slings and muscle transfers and finally functioning muscle transplantation. A variety of combinations have also been introduced as this complex field continues to develop with newer and more effective treatment options.
The extratemporal portion of the seventh cranial nerve begins at the stylomastoid foramen. It is in a deep position below the earlobe but becomes more superficial before it passes between the superficial and deep portions of the parotid gland. Here it divides into two main trunks which then further divide within the substance of the gland. In a series of anatomic dissections, Davis et al.1 demonstrated several branching patterns of the facial nerve. Traditionally, it is taught that this results in five divisions of the facial nerve: frontotemporal, zygomatic, buccal, marginal mandibular, and cervical. In practice, however, there is no distinct separation between the zygomatic and buccal branches either in their location or in the muscles they innervate.
On leaving the parotid, the facial nerve may have 8–15 branches making up the five divisions. Distally, there is further arborization and interconnection of these branches (Fig. 11.1). The net effect is a great deal of functional overlap between the branches. For example, a single zygomaticobuccal branch may supply innervation to the orbicularis oculi as well as to the orbicularis oris.
Fig. 11.1 A typical pattern of facial nerve branching. The main branch is divided into two components, each of which then branches in a random manner to all parts of the face. The extensive distal arborization and interconnections are apparent.
(Reprinted with permission from www.netterimages.com ©Elsevier Inc. All rights reserved.)
The temporal division consists of three or four branches2 that run obliquely along the undersurface of the temporoparietal fascia after crossing the zygomatriarch in a location 3–5 cm from the lateral orbital margin. The lower branches run along the undersurface of the superior portion of the orbicularis oculi for 3–4 mm before entering the muscle to innervate it.3 According to Ishikawa,2 the upper two branches entering the frontalis muscle at the level of the supraorbital ridge are usually located up to 3 cm above the lateral canthus. The nerves usually lie approximately 1.6 cm inferior to the frontal branch of the superficial temporal artery. Because there is relatively little adipose tissue at the lateral border of the frontalis, those nerves are virtually subcutaneous and susceptible to injury.
The zygomaticobuccal division consists of five to eight branches with significant overlap of muscle innervations such that one or more branches may be divided without causing weakness. These nerves supply innervations to the lip elevators as well as to the lower orbicularis oculi, orbicularis oris, and buccinators. Functional facial nerve mapping and cross-facial nerve grafting require the precise identification and stimulation of these zygomaticobuccal branches to isolate the exact branches responsible for smiling. These nerves lie deep near the parotid-masseteric fascia in the same plane as the parotid duct. There are sometimes connections between the lower branches and the marginal mandibular division.
The marginal mandibular division consists of one to three branches4 whose course begins up to 2 cm below the ramus of the mandible and arcs upward to cross the mandible halfway between the angle and mental protuberance. It has been well documented2,3,5 that these branches lie on the deep surface of the platysma and cross superficial to the facial vessels approximately 3.5 cm from the parotid edge. Nelson and Gingrass5 described separate branches to the depressor angularis, depressor labii inferioris, and mentalis, and a variable superior ramus supplying the upper platysma and lower orbicularis oris.
The cervical division consists of one branch that leaves the parotid well below the angle of the mandible and runs on the deep surface of the platysma, which it innervates by entering the muscle at the junction of its cranial and middle thirds. This point of entry is 2 or 3 cm caudal to the platysma muscle branch of the facial vessel.6
Facial musculature consists of 17 paired muscles and one unpaired sphincter muscle, the orbicularis oris (Fig. 11.2). The subtle movements that convey facial expression require coordination between all of these muscles.
The major muscles affecting the forehead and eyelids are the frontalis, corrugator, and orbicularis oculi. There are two main groups of muscles controlling the movement of the lips. The lip retractors include the levator labii superioris, levator anguli oris, zygomaticus major and minor for the upper lip, and depressor labii inferioris and depressor anguli oris for the lower lip. The antagonist of these lip-retracting muscles is the orbicularis oris, which is responsible for oral continence and some expressive movements of the lips.
Freilinger et al.3 have demonstrated that the mimetic muscles are arranged in four layers. The depressor anguli oris, part of the zygomaticus minor, and the orbicularis oculi are the most superficial, whereas the buccinators, mentalis, and levator anguli oris make up the deepest layer. Except for the three deep muscles, all other facial muscles receive innervation from nerves entering their deep surfaces.
The muscles that are clinically important or most often require surgical management in patients with facial paralysis are the frontalis, orbicularis oculi, zygomaticus major, levator labii superioris, orbicularis oris, and depressor labii inferioris.
The frontalis muscle is a bilateral broad sheet-like muscle 5–6 cm in width and 1 mm thick.4 The muscle takes origin from the galea aponeurotica at various levels near the coronal suture and inserts on to the superciliary ridge of the frontal bone and into fibers of the orbicularis oculi, procerus, and corrugators supercilii. It is firmly adherent to the skin through multiple fibrous septa but glides over the underlying periosteum. The two muscles fuse in the midline caudally; however, this is often a fibrous junction. Not only is the frontalis essential to elevate the brow, but also its tone at rest keeps the brow from descending. This tone is lost in the patient with facial paralysis, which allows the brow to fall and potentially obscure upward gaze.
The orbicularis oculi muscle acts as a sphincter to close the eyelids. Upper eyelid opening is performed by the levator palpebrae superioris muscle innervated by the third cranial nerve and the Müller muscle, which is a smooth fiber muscle innervated by the sympathetic nervous system. The orbicularis oculi muscle is one continuous muscle but has three subdivisions: pretarsal, covering the tarsal plate; preseptal portions, overlying the orbital septum; and the orbital, forming a ring over the orbital margin. The pretarsal and preseptal portions function together when a patient blinks, whereas the orbital portion is recruited during forceful eye closure and to lower the eyebrows. According to Jelks and Jelks,7 the preseptal portion of the orbicularis oculi is under voluntary control, whereas the pretarsal provides reflex movement.
The pretarsal orbicularis oculi overlies the tarsal plate of the upper and lower eyelids. The tarsal plates are thin, elongated plates of connective tissue that support the eyelids. The superior tarsal plate is 8–10 mm in vertical height at its center but tapers medially and laterally, whereas the inferior tarsal plate is 3.8–4.5 mm in vertical height. The skin overlying the pretarsal orbicularis is the thinnest in the body and is adherent to the muscle over the tarsal plate. The skin is more lax and mobile over the preseptal and orbital regions. The eyelid skin also becomes thicker over the orbital part of the muscle. The preseptal orbicularis provides support to the orbital septa and is more mobile except at the medial and lateral canthi, where the muscle is firmly attached to the skin. The orbital portion of the orbicularis oculi extends in a wide circular fashion around the orbit. It originates medially from the superomedial orbital margin, the maxillary process of the frontal bone, the medial canthal tendon, the frontal process of the maxilla, and the inferomedial margin of the orbit. In the upper eyelid, the fibers sweep upward into the forehead and cover the frontalis and corrugators supercilii muscles; the fibers continue laterally to be superficial to the temporalis fascia.8,9 Because this muscle is one of the superficial group of mimetic muscles,10 in the lower eyelid the orbital portion lies over the origins of the zygomaticus major, levator labii superioris, levator labii superioris alaeque nasi, and part of the origin of the masseter muscle. There are multiple motor nerve branches that supply the upper and lower portions of the orbicularis oculi, and these enter the muscle just medial to its lateral edge.
Freilinger et al.3 extensively studied the three major lip elevators, zygomaticus major, levator labii superioris, and levator anguli oris, and provided data on their length, width, and thickness (Table 11.1).
The zygomaticus major takes origin from the lower lateral portion of the body of the zygoma; the orbicularis oculi and zygomaticus minor cover its upper part. Its course is along a line roughly from the helical root of the ear to the commissure of the mouth, where it leads into the modiolus. The modiolus is the point of common attachment at which the fibers of the zygomaticus major and minor, orbicularis oris, buccinator, risorius, levator anguli oris, and depressor anguli oris come together. Deep fibers of the zygomaticus major are angled upward from the modiolus to fuse with the levator anguli oris, whereas caudal fibers continue into the depressor anguli oris. The main nerve to the zygomaticus major enters the deep surface of the upper third of the muscle.
The levator labii superioris originates along the lower portion of the orbital margin above the infraorbital foramen. The muscle courses inferiorly, partially inserting into the nasolabial crease. The lateral fibers pass inferiorly into the orbicularis oris, and the deepest fibers form part of the modiolus. The nerve to this muscle reaches it by first passing underneath the zygomaticus major muscle to supply the levator labii superioris on its deep surface.
The levator anguli oris is the third lip elevator. It takes origin from the maxilla below the infraorbital foramen and inserts into the modiolus. Because this muscle belongs to the deepest layer, it is innervated on its superficial surface by the same branch that supplies innervation to the buccinator.
Three muscles along with the zygomaticus minor serve to elevate the lip. The zygomaticus muscles move the commissure at an angle of approximately 45°, the levator anguli oris elevates the commissure vertically and medially, and the levator labii superioris elevates the lip vertically and laterally to expose the upper teeth.
The orbicularis oris is a complex muscle that functions as far more than a sphincter of the mouth; it serves to pucker and purse the lips. It makes up the bulk of the lip, as skin overlies it superficially and mucous membrane is attached on its deep surface. Philtral columns are formed by the insertion of the orbicularis, and a portion of levator labii superioris, into the skin.11 The levator labii superioris fibers reach the philtral columns by coursing above the surface of the orbicularis oris to insert into the lower philtral columns and vermilion border as far medially as the peak of Cupid’s bow. Anatomically and functionally, the orbicularis oris muscle consists of two parts, superficial and deep. The deep layers of the muscle encircle the orifice of the mouth and function as a constrictor. The superficial component also brings the lips together, but its fibers can contract independently to provide expression.12
The lower lip depressors consist of the depressor labii inferioris, also known as the quadratus labii inferioris, and the depressor anguli oris, also known as the triangularis (Fig. 11.3). The mentalis, however, is not a lip depressor. Its indirect action on the lip is to elevate it.8 The depressor labii inferioris arises from the lateral surface of the mandible, which is inferior and lateral to the mental foramen. It runs medially and superiorly to insert into the lower border of the orbicularis oris and its surface. Through fibrous septa, it attaches to the vermilion and the skin of the middle third of one side of the lip.9 Its action is to draw the lower lip downward and laterally and to evert the vermilion (e.g., as in showing the lower teeth). The depressor anguli oris arises from the mandible laterally and is superficial to the depressor labii inferioris. The medial fibers insert directly into the skin at the labiomandibular crease; the remainder blend into the modiolus.13 It depresses the angle of the mouth (e.g., in frowning).
Fig. 11.3 The depressor anguli oris can be seen in the corner of the mouth. Muscle contraction pulls the corner of the mouth down as in the expression of sadness. The depressor labii inferioris goes into the orbicularis oris of the mid lateral portion of the lower lip and pulls the lip down. The muscle’s function is apparent in an open-mouth smile showing the lower teeth. The mental nerve lies on the deep surface of the depressor labii inferoris.
Facial paralysis is a complex clinical problem with numerous consequences affecting the function, self-image, and social interactions of those afflicted and their families (Fig 11.4). Function of the muscles vital for the protection of the eye, maintenance of the nasal airway, oral continence, and clear speech may be lost. These muscles support the face at rest and enable an individual to wink, pucker the lips, and express emotions of surprise, joy, anger, and sorrow.
Brow ptosis is more commonly a problem in the older patient. The weight of the forehead tissue may cause sagging of the eyebrow inferiorly over the superior orbital margin, which causes an asymmetric shape and obstructs the upward gaze. This may be complicated by overactivity of the contralateral frontalis muscle, which increases the discrepancy between eyebrow height. At rest, the depressed eyebrow gives the impression of unhappiness or excessive seriousness. With animation, the asymmetry of the brows and wrinkling of the forehead are accentuated.
The orbicularis oculi muscle is crucial for the protection of the eye. It enables eyelid closure and provides a physical barrier against wind and foreign matter. Repetitive blinking is also important for control of the even spread of tear film in a lateral to medial direction to prevent drying of the cornea. The effective drainage of tears is also dependent on a functioning orbicularis oculi muscle; its action on the lacrimal sac establishes a pump-like effect that facilitates the efficient clearance of tears.
When the eyelids are open, the distance between the upper and lower eyelid is 9–11 mm at its widest point. In the neutral gaze position, the upper eyelid covers 2–3 mm of the superior corneal limbus; the lower eyelid lies at the level of the inferior corneal limbus. Thus, there is normally no sclera showing.
With eye closure, the majority of movement occurs in the upper eyelid while the lower lid remains relatively static. However, with squinting or smiling, there is up to 2 mm of upward movement in the lower eyelid. The main function of the inferior orbicularis oculi is the maintenance of lid margin contact with the globe and assistance with tear damage.
Patients with facial paralysis are troubled by significant discomfort in the eye because of corneal exposure and desiccation. This drying frequently produces a reflex tear flow. Excessive tears poorly managed by the paralyzed eyelids result in overflow. Therefore, patients with dry eyes often present with excessive tearing. This tearing problem can be distressing and is exacerbated by the downward inclination of the face (e.g., during reading).
The appearance of the paralyzed eye is also of concern to the patient. The eye has a widened palpebral aperture and is unable to convey expression. Thus, when the patient smiles, the paralyzed eyelids remain open instead of slightly closing. With the passage of time, the lower eyelid develops an ectropion, causing the inferior lacrimal punctum to pull away from the eye. An ectropion further exacerbates tearing and increases the risk of excessive corneal exposure.
The other major concern for patients with facial paralysis is the inability to control their lips. This affects the patient’s ability to speak, eat, and drink properly. For example, many patients with facial paralysis have difficulty producing b and p sounds. Buccinator paralysis leads to problems in the control of food boluses. Food tends to pocket in the buccal sulcus of the paralyzed portion of the face; therefore, many patients chew only on the contralateral side. This type of paralysis also severely affects normal facial expressions. The main complaint heard from patients is their inability to smile. This should not be regarded as an aesthetic issue. It is a functional disability because it directly impairs communication. Paralysis of the orbicularis oris results in drooling and difficulty in controlling the mouth (e.g., drinking from a glass).
The emotional effects of facial paralysis cannot be underestimated. The unilaterally paralyzed face presents obvious asymmetry at rest, exacerbated by an attempt to smile (Fig. 11.5). As a result, these patients avoid situations in which they are required to smile. They become characterized as serious and unhappy, and their psychosocial functioning is frequently poor. A patient with bilateral facial paralysis has severe disability because his or her face cannot convey emotion.
Fig. 11.5 (A) At rest, the right-sided partial facial paralysis in this young woman is minimally evident, as seen by a slight deviation of the mouth to her left and a slightly wider palpebral aperture in her right eye. (B) With smiling, the asymmetry becomes more apparent.
In the formulation of a treatment plan, it is helpful to have a practical and clinically oriented classification. This will facilitate sound decision making and realistic surgical planning. Facial paralysis can take many forms. It can be classified anatomically and as congenital or acquired, and it can be broken down further into unilateral or bilateral categories.14 In addition, the degree of muscle involvement varies from total to partial paralysis. More than 50% of patients with facial paralysis suffer from Bell’s palsy and often recover fully.
Congenital facial paralysis is present at birth. This is the most common form of facial paralysis seen in a pediatric setting. It may be isolated with the involvement of the facial nerve and its musculature only, or it may be part of a syndrome.
It is estimated that facial paralysis occurs in 2.0% of live births.15 In the majority of patients, it is believed to be the result of intrauterine pressure on the developing fetus from the sacral prominence. The facial nerve is superficial and easily compressed. This leads to the panfacial type and buccal branch variety of congenital facial paralysis. It is believed, however, that the mandibular branch component and syndromic forms of facial paralysis may have a different etiology. In the authors’ experience, the cause of unilateral facial paralysis was congenital in two-thirds of patients encountered and acquired in one-third of patients. Acquired facial paralysis resulted from intracranial tumors in 50% of patients; and acquired facial paralysis from extracranial trauma. The majority of traumas were related to surgical procedures, most commonly cystic hygroma excision. In infants, the nerve is superficial at birth and can easily be traumatized through external compression or surgical misadventure. In contrast, the cause of facial paralysis for the majority of adults is acquired, from either intracranial lesions or inflammatory processes, such as Bell’s palsy.
Congenital facial paralysis may be syndromic. The most common unilateral syndromic condition associated with facial paralysis is hemifacial microsomia. All tissues of the face can be affected to a variable degree, including the facial nerve musculature. The most common bilateral congenital facial paralysis is a result of Möbius syndrome. The functional effects of congenital facial paralysis tend to worsen gradually as the influence of gravity and aging prevails.
Bilateral facial paralysis may be the result of bilateral intracranial tumors or bilateral skull base trauma, but it is usually found to be the congenital bilateral facial paralysis or Möbius syndrome. Various cranial nerves accompany the seventh nerve’s involvement, specifically the sixth, ninth, 10th, and 12th. Möbius syndrome is also associated with trunk and limb anomalies in about one-third of patients, the most common being talipes equinovarus and a variety of hand anomalies, including Poland syndrome. Cranial nerve involvement is usually bilateral and severe but often incomplete. There is frequently some residual function in the lower component of the face (the cervical and mandibular branch regions). The incidence of Möbius syndrome is estimated to be about 1 in 200 000 live births.
Acquired facial paralysis may also be unilateral or bilateral through local disruption of the nerve at various locations. Damage to the nerve may be intracranial in the nucleus or the peripheral nerve, extracranial in the peripheral nerve, or the result of damage to the muscle itself. Intracranial and extracranial neoplasms, Bell’s palsy, and trauma are the most common causes seen in the adult setting. Although recovery is the rule in Bell’s palsy, at least 10% of patients are left with some degree of paralysis. Bilateral acquired facial paralysis is usually the result of skull base fractures, intracranial lesions, usually in the brainstem, or intracranial surgery.
Throughout all of these areas, however, facial paralysis constitutes a spectrum of involvement. It may be complete or incomplete to varying degrees, obvious in some patients, and subtle in others (Table 11.2).
|Congenital absence of facial musculature|
|Neoplastic – benign, malignant, primary, metastatic|
|Absence of motor units|
Facial paralysis patients present with a broad spectrum of signs and symptoms. Thus treatment varies from individual to individual. A thorough history and examination will reveal the presence of a complete or partial seventh-nerve paralysis and, if the paralysis is partial, the specific muscles affected and the extent of the paralysis. Has there been any return of function? Is this improvement continuing or has it reached a plateau? The history must include any eye symptoms, such as dryness, excessive tearing, incomplete closure, discomfort when the patient is outdoors, and use of artificial tears. The patient should be questioned about the nasal airway, oral continence, speech, and level of psychosocial functioning and social interactions.
The patient’s concerns and expectations must be sought. For some, attaining a symmetric appearance at rest is more important than achieving a smile. In comparison to the younger patient, the older patient is more likely to be worried about brow ptosis, ectropion, and drooping of the cheek.
The level of injury to the nerve, if it is not known, can be assessed clinically. Injury to the nerve within the bony canal may result in loss of ipsilateral taste appreciation, hyperacusis, and facial weakness because the chorda tympani and nerve to the stapedius may be injured at this level. Injury to the seventh cranial nerve near the geniculate ganglion will also result in decreased secretory function of the nose, mouth, and lacrimal gland.
The eye must be thoroughly assessed. Visual acuity in each eye should be documented. The height of the palpebral aperture should be measured and compared with the nonparalyzed side. The degree of lagophthalmos and the presence of a Bell reflex will indicate the risk of corneal exposure. The lower eyelid position should be measured. Tone in the lower eyelid can be assessed by the use of the snap test. This is done by gently pulling the eyelid away from the globe and releasing it. The eyelid normally snaps back against the globe; however, this fails to occur in the patient with poor lid tone. The position of the inferior canalicular punctum should be assessed. Is it applied to the globe or is it rolled away and exposed? In addition, the patient should be examined for corneal irritation or ulceration.
The nasal airway is examined next. Forced inspiration may reveal a collapsed nostril due to loss of muscle tone in the dilator naris and drooping of the cheek. An intranasal examination should also be done.
Examination of the mouth and surrounding structures documents the amount of philtral deviation, the presence or absence of a nasolabial fold, the amount of commissure depression and deviation, the degree to which the upper lip droops, and the presence of vermilion inversion. With animation, the amount of bilateral commissure movement is recorded; it is also noted how much of the upper incisors show when the patient is smiling. Speech should be assessed. An intraoral examination is performed to check dental hygiene and to look for evidence of cheek biting.
The presence of synkinesis, the simultaneous contraction of two or more groups of muscles that normally do not contract together,16 should be documented. Synkinesis is thought to occur from a misdirected sprouting of axons. The most common types of synkinesis are eye closure with smiling,17 brow wrinkling when the mouth is moved,18 and mouth grimacing when the eyes are closed.
An assessment of the other cranial nerves, particularly the fifth, is also performed. Cranial nerve involvement may exacerbate the morbidity of facial nerve paralysis. These nerves should also be assessed as possible donor motor nerves.
As has been stressed previously, treatment must be individualized. However, in general, the aims of treatment are to protect the eye, to provide symmetry at rest, and then to provide movement. The ultimate goal is to restore involuntary, independent, and spontaneous facial expression. The goals of treatment for the eye are to maintain vision, to provide protection, to maintain function of the eyelids, to improve cosmesis, and to enable the eye to express emotion. The goals for the mouth are to correct asymmetry, to provide oral continence, to improve speech, and to provide a balanced symmetric smile that the patient will use in social settings. Clearly, the accomplishment of all these gals is difficult, and they cannot be achieved completely.
The patient must be counseled as to what are real and achievable expectations. It is clearly impossible to restore intricate movements to all facial muscles, and the patient who is approximately informed is more likely to be satisfied with his or her outcome.
Nonsurgical management of the patient with facial paralysis applies primarily to the eye and can frequently make the difference between a comfortable eye and a painful one. Nonsurgical maneuvers can protect the eye while surgery is being planned and are regularly used in concert with the surgical management of the eye. In some instances, surgery may be avoided. Nonsurgical management of the eye consists of protecting the eye and maintaining eye lubrication (Table 11.3).
Eye lubrication can be provided by a number of commercially available preparations. This includes clear watery drops containing either hydroxypropyl methylcellulose or polyvinyl alcohol along with other agents including preservatives. These drops function by absorbing into the cornea and lubricating it. Although the duration of action will vary, most are retained on the surface of the eye between 45 and 120 minutes.19 Thus, to be most effective, they should be instilled frequently during the day. Thicker ointments containing petrolatum, mineral water, or lanolin alcohol are retained longer and can be used at night to protect and “seal” the eyelids during sleep. The patient who presents with excessive tearing may in fact have a dry eye and may benefit from the use of artificial tears. Corneal ulceration should be managed with prompt referral for ophthalmologic assessment.
In patients in whom there is incomplete facial nerve paralysis or recovering muscle activity after nerve injury, function may be improved with neuromuscular retraining supervised by an experienced therapist. This consists of various treatment modalities such as biofeedback, electromyography, and self-directed mirror exercises using slow, small, and symmetric movements.20 Patients can often relearn some facial movements or strengthen movements that are weak.
Deciding on a surgical procedure can initially seem daunting. There are a number to choose from, and selecting the most appropriate reconstruction may be confusing. It is important to listen to each patient carefully to identify which aspects of the paralysis are most troublesome and to treat each region of the face separately. The age of the patient, duration of the facial paralysis, condition of the facial musculature and soft tissues, and status of the potential donor nerves and muscles will all influence treatment options. One must consider the patient’s needs carefully and match the needs of the patient with the skill of the surgeon (Table 11.4).
|Brow (brow ptosis)|
|Upper eyelid (lagophthalmos)|
|Lower eyelid (ectropion)|
|Commissure and upper lip|
There are at least three approaches to a brow lift: direct excision of the tissue above the brow (direct brow lift), open brow lift performed through a coronal incision, and endoscopic brow lift. Unilateral frontalis paralysis may cause a difference in brow heights of up to 12 mm. A direct brow lift is best able to correct such a large discrepancy. Direct brow lift involves excision of a segment of skin and frontalis muscle just above and parallel to the eyebrow. If the incision is placed just along the first line of hair follicles, the resulting scar is usually less noticeable. Frontalis shortening by excision and repair provides a reliable correction, which minimally relaxes over time. However, overcorrection is still required. Slight overcorrection is particularly beneficial if the person’s normal side of the forehead is quite active during facial expression. Branches of the supraorbital nerve should be identified and preserved because they lie deep to the muscle (Fig. 11.6).
Fig. 11.6 (A) Assessment of the amount of brow depression on the paralyzed side compared with the normal eyebrow on the patient’s left. (B) Excision of skin and a strip of frontalis muscle to correct brow ptosis. (C) Postoperative appearance.
Brow lift may be performed through a coronal incision with or without a fascial graft to suspend the brow from the temporalis fascia or medially on the frontal bone. Whereas the scar is concealed, this is a larger operation than a direct brow lift and may not achieve as adequate a lift.
The authors have had limited experience with endoscopically assisted brow lifts for facial paralysis. The amount of lift required in the patient with facial paralysis is usually more than can be achieved from a unilateral endoscopic brow lift. It is likely that, with time, there will be gradual drooping. Therefore, the longevity of results in patients with facial paralysis has yet to be demonstrated with this procedure, especially when a large unilateral lift is required.
Several techniques are available for the management of lagophthalmos. These are all directed at overcoming the unopposed action of the levator palpebrae superioris. Because of its relative technical ease and reversibility, lid loading with gold prosthesis is the most popular technique. The patient’s eyelid configuration is important in determining whether the bulge of the gold weight will be visible when the eye is open. If the amount of exposed eyelid skin above the lashes is more than 5 mm when the eye is open, the gold weight is likely to be noticeable to the patient. If the distance is less than 5 mm, the gold weight will roll back and be covered by the supratarsal skinfold (Fig. 11.7).
Because of its inertness, 24-carat gold is used; allergic reactions are rare, but if they occur, platinum weights are also available. Prostheses are available in weights ranging from 0.8 to 1.8 g. Adequate improvement in eye closure can be obtained with a weight of 0.8–1.2 g, giving the patient a comfortable eye without weight-related problems.21