15.1Introduction

Facial nerve palsy may arise from a myriad ofconditions, some benign and some potentiallylife-threatening. Depending on the etiology, theparalysis and facial disfigurement may be tem-porary or permanent. Often a multidisciplinaryteam approach is needed for patient care. Theoculoplastic surgeon plays a crucial role in theevaluation and rehabilitation of patients withfacial palsy. Immediate attention must be aimedat corneal protection and maintenance of vi-sion; however, long-term management of facialdisfigurement, epiphora, and secondary effectsof aberrant regeneration are significant ele-ments in patient care. Use of a systematic andmethodical approach to evaluation and man-agement of facial paralysis, as described in thisreview, provides the oculoplastic surgeon withthe ability to coordinate care for patients withthis complex condition.

15.2Diagnosis

The most common cause of facial nerve weak-ness is Bell’s palsy, named after the British neu-rologist, Sir Charles Bell. This unilateral, lowermotor neuron facial palsy of acute onset occurswith an incidence of 15–40 per 100,000 and a re-currence rate of up to 10% [1]. Bell’s palsy is adiagnosis of exclusion, however, and shouldonly be proposed after all other possible causeshave been reviewed and eliminated. The possi-ble causes of facial palsy are numerous, but thethree most common categories of etiology after

Facial Paralysis:A Comprehensive Approach to Current Management

Roberta E. Gausas

15

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∑ The causes of facial paralysis are myriad,but the most common etiologies are idio-pathic, infectious, traumatic, or neoplastic

∑ A thorough patient history including onset,duration, and associated symptoms is es-sential in establishing the correct etiology

∑ The facial nerve is a mixed nerve carryingmotor, sensory, and parasympathetic in-formation

∑ Anatomically, the facial nerve runs a com-plex course divided into four segments:the supranuclear, nuclear, fascicular, and peripheral nerve

∑ Patients with facial paralysis suffer bothfunctional and esthetic deficits, and bothmay lead to altered self-image and socialhandicap

∑ Examination of the face is simplified by sub-dividing the face into four functional units;the brow complex, the periorbital complex,the midface complex, and the lowerface/oral complex. Each unit has specificfunctional and esthetic considerations

∑ Reversible facial paralysis is managed withsupportive care consisting of lubricationand enhancement of corneal coverage

∑ Irreversible facial paralysis is managed surgically and tailored to the individualfunctional and esthetic desires of each patient and each of his or her facial func-tional units.These procedures are generallycategorized as those aimed at dynamic reanimation, which involve repair or graft-ing of the nerve, or muscle grafting, andthose aimed at static rehabilitation, whichinvolve repositioning and resuspension ofsoft tissues

Core Messages

idiopathic are infection, trauma, and neoplasm,or the sequelae of its treatment (Table 15.1).

15.2.1Patient History

A meticulous history can be critical in uncover-ing the cause of facial palsy. A patient may notvolunteer pertinent historical information un-less appropriately questioned.The onset and theduration of the palsy should be established. As-sociated symptoms such as pain or facial numb-ness should be recorded. The patient should beasked about changes in hearing, taste, or tear-ing. Hyperacusis results from impairment of thestapedius muscle. Decreased sense of taste mayoccur with distal lesions. Excessive tearing is acomplex issue and may have more than onecause. Tearing may result from dryness second-ary to poor tear production or corneal expo-sure, from poor outflow secondary to ectropionor tear pump mechanism loss, or from gustato-ry reflex tearing secondary to aberrant regener-ation.A history of a rash or vesicles may suggestcertain diagnoses, such as Lyme disease orRamsay-Hunt syndrome. It is important to elic-it a full history of previous skin cancer or headand neck cancer, and any surgical interventionfor cancer. An immunization history is perti-nent since recent immunizations for influenzaor polio have also been linked to facial palsy(Table 15.2).

A carefully obtained history aids tremen-dously in determining the cause and location ofa palsy. For example, a 6-month history of non-resolving facial paralysis that was preceded byfacial numbness in a patient with distant histo-ry of facial skin cancer, despite lack of a recur-rent cutaneous component, suggests perineuralinvasion of skin cancer, rather than Bell’s palsy,and warrants further work-up (Fig. 15.1).

192 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

Table 15.1. Causes of facial palsy

IdiopathicBell’s palsyMelkerson-Rosenthal syndrome

InfectiousHerpes zoster oticus (Ramsay-Hunt syndrome)Varicella virusOtitis mediaMastoiditisLyme diseaseTuberculosisHIV/AIDSPoliomyelitisMumpsMononucleosisLeprosySyphilisCat scratchBotulismInfluenza

NeoplasticParotid gland tumorFacial nerve schwannomaGlomus jugulare tumorNasopharyngeal carcinomaPerineural invasion of skin cancerMetastatic cancer

TraumaticBlunt and penetrating craniofacial traumaScuba divingLightning

Birth/congenitalBirth traumaMoebius syndromeDysgenesis of infratemporal facial nerve

IatrogenicPostimmunizationPostsurgical sequelae of removal of braintumor or parotid gland tumor

InflammatorySarcoidosisHeerfordt’s disease (uveoparotid fever)

InfiltrativeAmyloidosis

NeurologicGuillain-Barré syndromeMyasthenia gravis

MetabolicPregnancyDiabetes mellitusHypertension

15.2.2Anatomy and Function

Ability to perform a thorough physical examina-tion of facial paralysis is facilitated by an under-standing of the anatomy and function of the facialnerve. This knowledge is also critical in develop-ing a surgical plan for facial rehabilitation.

15.2.2.1Facial Nerve Pathophysiology

The facial nerve is a mixed nerve in that it carriesmotor,sensory,and parasympathetic information.It serves a predominantly motor function, howev-er, and is responsible for all facial motion exceptmastication. Of its approximately 10,000 neurons,7,000 fibers innervate muscles of facial expression.For the oculofacial surgeon, muscles of particularimportance innervated by the facial nerve are thefrontalis, which lifts the eyebrows and forehead;the orbicularis oculi,which closes the eyes; and theorbicularis oris, which closes the lips.

The remaining 3,000 fibers of the facialnerve form the nervus intermedius, which con-veys sensory and parasympathetic fibers. Thesensory fibers carry taste from the anterior two-thirds of the tongue. The parasympathetic se-cretomotor fibers innervate the lacrimal,parotid and salivary glands. Facial nerve injuryaffects non-motor function by producing ab-normalities not only in taste and hearing, but

15.2 Diagnosis 193

Fig. 15.1. A Seventy-year-old patient who presentedwith a 6-month history of unresolving left-sided facial paralysis associated with facial numbness.

B Physical examination revealed old scar and subcuta-neous mass along left jawline. Biopsy of site revealedsquamous cell carcinoma with perineural invasion

Table 15.2. Pertinent patient history for facial palsy

1. Onset and duration of palsy: rapid vs. gradual

2. Status of palsy: resolving, persistent, worsen-ing

3. Associated symptoms: facial numbness, pain,change in hearing, loss of taste, epiphora

4. Associated physical findings: vesicles, rash,swollen lymph node

5. Past medical and surgical history: previousskin cancer, previous head and neck cancer,surgical treatment for cancer, recent immu-nizations

A B

also in lacrimation, most important for the ophthalmologist. Facial nerve lesions above the geniculate ganglion may cause decreasedlacrimal secretion with subsequent epiphorafrom dry eye. Central lesions may result in aber-rant regeneration with gustatory reflex tearing.

15.2.2.2Facial Nerve Anatomy

In its complex course through the posterior fos-sa, temporal bone, and parotid gland, the facialnerve is vulnerable to many neoplastic, trau-matic, and infectious disorders. It may be divid-ed into four anatomic segments: supranuclear,nuclear, fascicular, and peripheral nerve.

Supranuclear Pathway

Neural activity within the facial motor area of thefrontal lobe initiates voluntary movement of theface. The supranuclear neurons that innervatethe facial nerve nucleus lie in the precentralgyrus of the frontal lobe. Upon leaving the pre-central gyrus, these axons coalesce to becomepart of the corticobulbar tracts that descendthrough the internal capsule towards the cerebralpeduncle [2].It is just below this level that most ofthe supranuclear fibers cross over to the oppositeside of the pons to innervate the facial nerve nu-cleus.Some fibers,however,do not cross over andsynapse in the ipsilateral facial nerve nucleus.This anatomic feature explains why the upperface is supplied with innervation from both cere-bral hemispheres and why supranuclear lesionsinvolving the descending motor pathways causepalsy of the contralateral lower face only.

Pons

The motor nucleus of the facial nerve lies withinthe reticular formation of the pons. It may besubdivided into four cell groups, one of which,the intermediate cells, innervates the frontalis,orbicularis oculi, and corrugator muscles. Motoraxons constituting the facial nerve exit the facialnucleus, travel towards the fourth ventricle, bendaround the sixth nerve nucleus,and exit the pons.

The parasympathetic component of the fa-cial nerve arises in the superior salivatory nu-

cleus, above the facial motor nucleus. Theparasympathetic component of the facial nervesupplies secretomotor fibers to the lacrimal,sublingual and submandibular glands.

The nervus intermedius consists of boththese parasympathetic fibers and sensoryfibers. The sensory fibers subserve taste to theanterior two-thirds of the tongue, and somaticsensation to the external auditory meatus andpostauricular region.Afferent fibers to the facialnucleus also derive from the trigeminal nucleusas part of the corneal reflex, and the acousticpathways as part of the stapedius reflex.

Cerebellopontine Angle

The facial motor root and nervus intermediusexit the brain stem along with the vestibularacoustic nerve at the cerebellopontine angle.The facial nerve then travels through the tem-poral bone via the internal auditory canal withthe nervus intermedius and auditory nerve.

Fallopian Canal

The facial nerve separates from the acousticnerve to enter its own canal, the fallopian, or fa-cial, canal. It then winds its way along an ap-proximately 30-mm path through the laby-rinthine, tympanic, and mastoid segments. Thelabyrinthine segment contains the geniculateganglion and the first branch of the facial nerve,the greater petrosal nerve. This nerve carries se-cretomotor fibers to innervate the lacrimalgland and nasopalatine glands after synapsingin the sphenopalatine ganglion. The mastoidsegment is where the nerve to the stapediusoriginates and the chorda tympani nervebranches off. The chorda tympani nerve carriestaste fibers from the anterior two-thirds of thetongue, parasympathetic fibers to the sublin-gual and submaxillary glands, and somatic sen-sation from the external auditory meatus.

Extracranial Course

The motor branches of the facial nerve exit thefallopian canal at the skull base via the stylo-mastoid foramen. The facial nerve then pene-trates the parotid gland and divides into superi-

194 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

or (temporofacial) and inferior (cervicofacial)divisions. These divisions may be further sub-divided from top to bottom into the temporal,zygomatic, buccal, mandibular, and cervicalbranches [3].The branching patterns of these fivesubdivisions vary among individuals and exten-sive interconnections exist among the branches.This accounts for the variety of aberrant regener-ation phenomena that may occur following re-covery from facial nerve palsy. Such phenomenainclude gustatory reflex tearing (crocodile tears)where salivary gland nerve fibers are redirectedtowards the lacrimal gland and involuntary tear-ing occurs with salivation while eating.

Summary for the Clinician

∑ A thorough patient history is crucial in establishing an accurate diagnosis andshould include associated symptoms suchas facial pain or numbness, and changes in hearing, taste, or tearing

∑ Motor, sensory and parasympathetic fibersconstitute the facial nerve. The nervus intermedius carries facial nerve sensoryand parasympathetic information and is responsible for tearing, salivation, and taste

15.3Facial Nerve: Physical Examination

Patients with facial paralysis suffer both func-tional and esthetic deficits. The degree of deficitwill depend on the amount of facial weakness,which can vary from mild paresis to completeparalysis, and the patient’s age.Younger patientswith greater tissue tone and support may ex-perience a lesser degree of functional abnor-mality, whereas older patients with the samemedical condition but weaker tissue tone willexperience more significant dysfunction. How-ever, problems encountered by these patientsare not just limited to physical findings, but alsoinclude altered self-image and social handicap.Patients experience chronic eye pain and tear-ing, difficulty breathing, impaired speech, diffi-culty eating and drinking, and drooling. Addi-tionally, there is the obvious facial asymmetrywhich is made worse during facial animationand laughter. These problems may lead the pa-tient to feel stigmatized and to avoid social con-tact. Therefore, the surgeon responding to theneeds of the facial paralysis patient must be

15.3 Facial Nerve: Physical Examination 195

Table 15.3. Facial functional units

Facial unit Physical findings Functional, esthetic and social impairment

1. Brow complex Brow ptosis Impaired superior visual field

Heavy upper eyelid

Brow asymmetry

2. Periorbital complex Upper lid retraction Epiphora

Lower lid retraction Photophobia

Paralytic lagophthalmos Eye pain

Lower lid/punctal ectropion Blurred vision

Decreased blink Lid asymmetry

Exposure keratitis

3. Midface complex Descent of malar eminence Facial asymmetry

Loss of nasolabial fold Impaired breathing

Collapse of nostril

4. Perioral complex Ptosis (lengthening) of lip Impaired eating/drinking

Inferomedial rotation Impaired speechof oral commissure

Jowling Oral incompetence/drooling

Inability to smile

cognizant of both the desire for functional reha-bilitation and the desire for esthetic restoration,and include the patient’s concern about theirsocial handicap in the evaluation.

Detection of subtle weakness and aberrantregeneration requires careful observation,whereas severe paralysis is obvious from a dis-tance. The surgeon should observe the patient’sentire face both during rest and during con-versation throughout the examination, notingvoluntary and involuntary facial movements.Certain grading systems have been described to quantify facial paralysis, such as the House-Brackman classification of facial nerve dys-function. The House grading system is used to document the degree of paralysis in latestages of the process and the Brackman modifi-cation attempts to include early stages of paral-ysis [4].

The physical examination can be simpli-fied by subdividing the face into four func-tional units. These units are the brow complex,the periorbital complex, the midface complex,and the lower face/oral complex. Each unit hasspecific functional and esthetic considerations(Table 15.3).

15.3.1Brow Complex

Evaluation of the face should begin with deter-mination of whether the facial palsy is central orperipheral. Therefore frontalis muscle functionshould be tested first, by asking the patient tolook up. If frontalis muscle function is intact bi-laterally, the palsy is central. If frontalis musclefunction is unilaterally impaired, the palsy isperipheral.

The physical findings of the brow complexobserved in patients with frontalis muscle im-pairment include: loss of forehead rhytids,lengthening of the forehead, and brow ptosis.These features combine to apply weight to theupper eyelid and may accentuate pre-existingupper lid dermatochalasis (Fig. 15.2A). The pa-tient may complain of superior visual field im-pairment and heaviness of the eyelid, making itdifficult to open the eye or sustain activitiessuch as reading or driving. Esthetically, facial

asymmetry is noticeable both in the resting andin the animated position.

Brow ptosis is measured by manually elevat-ing the brow to the desired level, and measuringthe amount of descent in millimeters after re-leasing the brow.Attention should be paid to thedegree of both medial and lateral droop, as wellas the ultimate brow shape desired, keeping inmind that a male brow tends towards a flat archcompared to the more curved arch of a femalebrow. The amount of brow ptosis can be docu-mented photographically. The degree of superi-or visual impairment can be documented withformal visual field testing.

15.3.2Periorbital Complex

Patients with facial paralysis often complain ofpain, burning, photophobia, epiphora, and lidasymmetry. These complaints are directly relat-ed to loss of orbicularis muscle tone, and are at-tributable to excessive corneal exposure. Expo-sure keratitis is a serious sequela of facialparalysis, and will dictate the urgency of treat-ment. Several physical findings may contributeto corneal exposure.

Retraction is the most common finding inthe upper eyelid. With loss of the usual protrac-tor function of the orbicularis oculi muscle,the action of the levator palpebrae muscle isunopposed, and therefore the lid elevates. Lidretraction may be partially masked by signifi-cant dermatochalasis and brow ptosis, becom-ing evident only when the brow is manuallyelevated. Functionally, upper eyelid retractionincreases corneal surface exposure and con-tributes to lagophthalmos. Esthetically, it cre-ates an unnatural and asymmetrical facialappearance.

Eyelid position is measured by recording thedistance from the corneal light reflex to the lidmargin with the patient’s face in the frontalplane and a light directed at the cornea. This isreferred to as the marginal reflex distance, orMRD. The position of the upper lid relative tothe corneal light reflex is designated as MRD1,whereas the position of the lower eyelid isdesignated as MRD2.

196 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

Lower eyelid physical findings include: re-traction, ectropion, and punctal eversion. Ectro-pion describes an outward turning of the eyelidmargin, separating it from the globe. This mayoccur along the entire length of the eyelid, ormedially affecting only the punctum. Both ec-tropion and punctal eversion lead to impairedtear drainage and accumulation of tear debris,resulting in epiphora and irritation. The degreeof ectropion will be related to the amount ofpre-existing lower lid laxity, which is dependenton the patient’s age.

Loss of orbicularis oculi muscle tone leadsnot only to eyelid retraction, but also to paralyt-ic lagophthalmos and incomplete blink reflex(Fig. 15.2B). Paralytic lagophthalmos is meas-ured in millimeters as the vertical interpalpe-bral distance during gentle eyelid closure. Thepresence or absence of a Bell’s phenomenon

should be noted by gently lifting the eyelids dur-ing forced closure. A poor Bell’s phenomenonworsens the usual risk of corneal exposure dur-ing sleep.

Examination of the eye should includecorneal sensation. Decreased corneal sensitivitycan be seen in facial nerve palsy, but when coex-istent with hypoesthesia of adjacent eyelid skin,fifth cranial nerve involvement should be sus-pected.

15.3.3Midface and Perioral Complex

The midface complex is closely related to thelower eyelid and affects lower eyelid positionand function. Physical findings in this region in-clude: descent of the malar tissues with loss of

15.3 Facial Nerve: Physical Examination 197

Fig. 15.2 A, B. Physical findings of brow and periorbital functional units include brow ptosis, paralyticlagophthalmos, and ectropion

Fig. 15.2 C, D. Physical findings of perioral and lower face functional units include loss of nasolabial fold,lengthening of lip, and rotation of nose and mouth. These findings are exaggerated with facial animation

A B

DC

the malar eminence, loss or flattening of the na-solabial fold, and inferomedial rotation of thenasal ala (Fig. 15.2C).This leads to collapse of thenostril and interference with normal breathing.

Malar descent can be evaluated by manuallyelevating the midface to the desired level tomatch the opposite side, and noting the amountof vertical shift in millimeters. The distancefrom the nasolabial fold to the vermilion borderof the upper lip on the unaffected side should bemeasured in order to appropriately plan for sus-pension of the nasolabial fold on the affectedside. Older patients with paralysis are particu-larly prone to jowling of the lower face. If leftunaddressed, the persistent downward pull ofthe weight of the lower face will diminish thelong-term effect of any midface or nasolabialfold suspension.

Physical findings of the perioral complex in-clude lip ptosis, which is lengthening of the up-per lip with inferior and medial rotation of theoral commissure (Fig. 15.2C).Loss of orbicularisoris muscle tone leaves the effect of gravity un-opposed, resulting in inferior displacement.This muscle weakness also leaves the contrac-tion of the opposite orbicularis oris muscle un-opposed, resulting in medial displacement ofthe lips. These forces combine to create a twist-ing or rotation of facial structures which is evi-dent at rest and exaggerated during speech(Fig. 15.2D). Patients may complain of drooling,difficulty eating, and difficulty speaking. Thismay lead to social handicap.

Summary for the Clinician

∑ Examination of facial paralysis is simpli-fied by subdividing the face into four functional units, each with distinct findingsproducing physical, esthetic, and social impairment

∑ The brow complex will exhibit brow ptosisimpairing the superior visual field

∑ The periorbital complex will be charac-terized by paralytic lagophthalmos causingdiscomfort and epiphora due to exposurekeratitis

∑ The midface complex will exhibit efface-ment of the nasolabial fold and impairedbreathing due to collapse of the nostril

∑ The lower face/oral complex will be charac-terized by ptosis and rotation of the mouthcausing impairment of speech and eating

15.4Treatment Strategies (Table 15.4)

Normal facial tone exists in the presence of adelicate balance between vertical and horizon-tal forces, between gravitational pull and mus-cular contraction. Clearly understanding theorientation and function of each facial muscleand the orientation of the forces acting upon itleads to a full understanding of the affects of fa-cial paralysis. The physical results of facialparalysis represent a disruption of the balanc-ing act between vertical and horizontal forcesthat normally exists.

15.4.1Supportive Care

Facial paralysis can be categorized as reversibleor irreversible. Patients with reversible facialpalsy can be treated with supportive care, whilethose with irreversible palsy are candidates forsurgical intervention. In either situation,corneal decompensation dictates the urgency ofintervention. Therefore, testing for corneal sen-sation cannot be emphasized enough.

Initial supportive therapy consists of fre-quent ocular lubrication. This is achievedthrough the use of artificial tears, usually a min-imum of four times a day and as frequently asevery hour while awake, and lubricant gel orointment at night. Additionally, a moisturechamber can be created at night by fashioning acircular piece of cellophane wrap over the or-bital rim,use of an eye patch over the cellophane,or use of a pre-manufactured moisture bubble.

Temporary interventions can be consideredin situations in which the cornea requires short-term added protection. External lid weights(Meddev Co., Palo Alto, CA) fixed to the uppereyelid pretarsal skin aid in lid closure. A tempo-rary suture tarsorraphy is useful for acute situa-tions of corneal decompensation or for patientswho are unable to instill lubricating drops or gel.

198 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

15.4.2Surgical Strategies

For patients with irreversible facial palsy, such asthose who have lost facial nerve function afterresection of a head and neck cancer, surgical re-habilitation should be considered. Each individ-ual patient will have a unique situation in whicheither some or all of the facial units are involvedand either some or all of the facial units are caus-ing symptoms. The surgical plan must be tai-lored to each individual patient, and take intoconsideration the patient’s needs and desires forboth functional and social rehabilitation.

The following is an outline of the surgicalstrategies available for each facial unit. The goalsof facial rehabilitation can be aimed at either re-animation or static resuspension. Proceduresthat have the goal of facial reanimation includedirect or indirect hypoglossal-facial nerve anas-tomosis, facial nerve grafts, cross-face seventhnerve grafts, and temporalis muscle transfers.This chapter focuses on surgical procedureswith the goal of static facial suspension(Fig. 15.3A, B). Proper coordination between theorbitofacial surgeon and other disciplines, in-cluding neurosurgery, head and neck surgery,and plastic surgery, is needed to provide affectedpatients with the optimal surgical plan and care.

15.4 Treatment Strategies 199

Table 15.4. Treatment strategy by involved facial functional unit

Facial unit Treatment strategy

1. Brow complex Brow lift:– Direct approach: suprabrow, midforehead, pretricheal– Endoscopic approach– Coronal approach– Browpexy

2. Periorbital complex Lubrication

Tarsorraphy:– Temporary: suture– Permanent: lateral intermarginal adhesion

Correction of upper lid retraction/lagophthalmos:– Gold weight placement– Lid spring placement

Correction of lower lid/punctual ectropion:– Horizontal lid shortening: lateral tarsal strip, medial canthal placation– Punctal inversion: excision conjunctival diamond, cauterization

Correction of lower lid retraction:– Placement of spacer graft: hard palate, tarsus, banked sclera, Alloderm

3. Midface complex Reanimation procedures:– Facial nerve repair, nerve grafting, nerve transfer– Temporalis muscle transfer– Microvascular free flap transfer

Static support procedures:– Midface lift:

Subperiosteal or supraperiosteal suspension sutures– Lateral rotation of nasal ala– Recreation of nasolabial fold:

Suspension suturesDirect lift

4. Perioral complex Oral commissure lift:– Suspension sutures– Wedge resection

15.4.2.1Surgical Strategies: Brow Complex

Of the number of surgical techniques which areavailable to obtain a brow lift in the paralyzedbrow, some are more effective than others. Eachof them is a compromise between esthetic andfunctional outcome. The advantages and disad-vantages of each technique should be reviewedwith the patient. Esthetically, an endoscopicbrow lift, or browpexy, avoids a visible scar, butin the paralyzed brow tends not to provide a ro-bust or durable elevation. The most effectivemeans of elevating the weight of a paralysedbrow is through a direct approach, which car-ries the risk of some form of scar. A unilateraldirect brow lift via a suprabrow, midforehead,or pretricheal incision provides significant and durable elevation with minimal scar ifclosed in multiple layers with attention to detail(Fig. 15.4A, B).

15.4.2.2Surgical Strategies: Periorbital Complex

The goal of rehabilitation of the periorbitalcomplex is to provide corneal coverage andeliminate lagophthalmos. Lateral tarsorraphyhas been a traditional approach to this problem;however, this procedure creates peripheral fieldloss, often does not entirely alleviate medial andcentral lagophthalmos, and is esthetically unap-pealing.

Upper eyelid retraction is best addressedwith placement of a lid weight in order to over-come unopposed levator muscle action.The most common method used is placement of a gold weight (Meddev Co., Palo Alto, CA) [5, 6]. In a patient with gold allergy, a platinumweight is an alternative [7]. The size of theweight is tested preoperatively incrementallywith the patient in the sitting position. Witheach size of weight tested, the amount oflagophthalmos and induced ptosis should be

200 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

Fig. 15.3. A Preoperative view of irreversible right-sided facial paralysis. B Postoperative view followingstatic facial rehabilitation consisting of direct brow

lift, upper lid gold weight placement, lower lid hori-zontal shortening, midface suspension, and repair ofnasolabial fold

A B

recorded. The selected weight should be the onethat achieves the greatest closure with the leastptosis.

Some surgeons advocate a stainless steelpalpebral spring to reanimate the eyelid.Advan-tages of a spring include a more natural blinkprocess and the esthetically appealing low pro-file of the implant. Disadvantages of this tech-nique include the need for postoperative springtension adjustment, and the risk of spring fa-tigue or extrusion.

The goals of repair for the lower eyelid arethreefold: (1) horizontal shortening to correctectropion or retraction, (2) central support toalleviate lagophthalmos, and (3) inversion of thepunctum to improve epiphora (Fig. 15.4A, B). Ashort lateral intermarginal tarsorraphy can en-hance these steps and not impede peripheral vi-sion.The amount of surgery needed will dependon the degree of lid laxity present, which in turnis dependent upon the patient’s age.

Horizontal lower eyelid shortening is bestachieved through a lateral tarsal strip procedure[8–10]. This is performed via a lateral canthoto-my and inferior cantholysis. A lateral strip oftarsus is fashioned, appropriately shortened,and anchored to the periosteum of the lateralorbital rim as a substitute tendon. If medial can-thal laxity is present, it must be corrected first toavoid significant lateral displacement of thepunctum which interferes with tear outflow [11,12]. The punctum must be in contact with the

tear lake to allow tear outflow. Subtle verticalorientation of the punctum or frank eversion ofthe punctum will inhibit outflow even in thepresence of an adequately tightened lower eye-lid [7, 8]. Punctal inversion can be achieved sur-gically via excision of a small tarsoconjunctivaldiamond or via laser or cautery conjunctivo-plasty [13, 14].

Lower eyelid shortening alone may not cor-rect the central lid sagging often seen in facialparalysis. Such lower eyelid retraction is due toloss of vertical support from loss of orbicularistone. In these cases, a spacer graft is required tobolster the central lower lid position upward,which will help relieve lagophthalmos. A greatvariety of spacer material is available. The sur-geon must decide between autogenous, donor,or alloplastic material. Selection of the materialwill be influenced by any alterations in the hostbed tissue, such as irradiation, previous surgery,or the disease process.Autogenous materials in-clude hard palate graft, tarsal graft, ear cartilagegraft or septal graft [15–18]. Donor materials in-clude banked sclera or Alloderm (Life Cell Co.,Brauchburg, NJ) [19, 20]. Alloplastic materialsinclude a lid spacer implant consisting of Med-por (Porex Surgical Inc., Newman, GA) [21, 22].Donor materials avoid the morbidity associatedwith harvesting tissue, but are susceptible tocontraction [23]. Of these choices, hard palatehas been shown to be an effective and durablegraft material [24–26].

15.4 Treatment Strategies 201

Fig. 15.4. A Preoperative view of brow and perior-bital changes associated with facial paralysis. B Post-operative view following repair consisting of brow

lift, upper lid retraction repair, and lower lid lateraltarsal strip

A B

The surgeon must remember that the lowereyelid is a continuum of the midface and is in-fluenced by and subject to forces acting on mid-face position. Long-term success of correctinglower eyelid position and function greatly de-pends upon correction of midface position.

15.4.2.3Surgical Strategies:Midface and Perioral Complex

The treatment of midface and perioral paralysisis challenging, with many techniques available.The surgeon may select from reanimation pro-cedures that aim to provide some degree of vol-untary facial movement, or those that aim toprovide static facial support. Both the extent

and level of nerve injury will determine theappropriate procedure for each patient.

To achieve dynamic reanimation, the choiceof procedures includes facial nerve repair, facialnerve repair with nerve grafting, hypoglossalnerve transfer, temporalis muscle transfer, or amicrovascular functional muscle transfer, suchas gracilis, latissmus dorsi, or inferior rectusabdominus free flap transfer [27–30].

Static rehabilitation is achieved throughmethods which resuspend soft tissues to fixedstructures. The specific areas of the midface, na-solabial fold, and oral commissure can be ad-dressed via a direct lift or via suspension su-tures. Techniques which resuspend a paralysedface parallel those used for facial rejuvenation.The goals of elevation and anchoring of soft tis-

202 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management

Fig. 15.5. A Intraoperativeview of subperiosteal dissectionwith sparing of infraorbitalnerve during static midface suspension. B, C Intraoperativeview of pre- and postelevationof nasolabial fold and midfacialsoft tissues via suspension sutures anchored at inferior orbital rim.

A

B C

sues are the same as in surgery aimed at rejuve-nation; however, the weight of the tissues andthe effects of gravity in the paralyzed face areoften more difficult to overcome. Several tech-niques of static suspension are available, eachvarying in approach to incision, suspensionmaterial, and anchoring device and location[31–35] (Fig. 15.5A). The orbital rim is an ideallocation for fixation via either an anchoringdevice or suspension sutures passed throughdrill holes. Important aspects of midface eleva-tion include emphasis on vertical lift over later-al lift to avoid joker-like facies [36]. Importantaspects of nasolabial fold elevation include ade-quate outward suspension of the nostril to im-prove breathing, and adequate elevation of theupper lip to improve speech and ability to eat(Fig. 15.5B, C).

Summary for the Clinician

∑ The need for corneal protection dictates theurgency of management. Whether the facialpalsy is temporary or permanent guides themethod of management

∑ The brow complex is surgically managed by a brow lift

∑ Paralytic lagophthalmos is commonly sur-gically managed by gold weight placementin the upper lid and horizontal shorteningof the lower lid, with or without a spacergraft

∑ Mid- and lower-face paralytic descent maybe addressed via dynamic reanimation procedures or via static resuspension offacial tissue to overcome mouth ptosis

15.5Aberrant Regeneration

Aberrant regeneration as a late effect of facialparalysis may occur in two forms: gustatory hy-perlacrimation (crocodile tears) and synkineticfacial movements [37]. Aberrant innervation ofthe lacrimal gland results from misrouting ofpostganglionic parasympathetic secretomotorfibers and produces hypersecretion of tears dur-ing mastication. Facial synkinetic movementssimilar to hemifacial spasm result from misrout-ing of fibers of the orbicularis oris and orbicu-

laris oculi muscles.Both forms of aberrant regen-eration respond to botulinum toxin injection[38–40]. Neuromuscular facial retraining viabiofeedback has also been shown to be effectivetreatment for synkinesis after facial palsy [41,42].

Summary for the Clinician

∑ Gustatory reflex tearing and synkinetic facial movements are two late effects offacial paralysis secondary to aberrant regeneration. Both respond well to botu-linum toxin injection

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204 Chapter 15 Facial Paralysis: A Comprehensive Approach to Current Management