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Ростовский Государственный Медицинский Университет

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Duration of symptoms: determine viability of the affected facial musculature—muscle may be reinnervated 18-24 months following denervation Prognosis: Determine likelihood of spontaneous recovery based on facial nerve status (ie, intact or not), signs of any clinical recovery 6-12 months after onset

Neuromuscular Examination

Ask for a baseline photo of the patient; subtle facial asymmetries may exist prior to diagnosis of facial paralysis

Assess for type of facial palsy

Central vs peripheral etiology

Upper motor neuron lesion: contralateral facial paralysis that is forehead sparing Lower motor neuron lesion: ipsilateral total facial paralysis

Flaccid paralysis vs partial palsy vs synkinesis

Flaccid paralysis: no facial movement on affected side Partial palsy: weakness from decreased neural input/muscular atrophy Synkinesis: postparalytic phenomenon thought to be caused by aberrant facial nerve regeneration, results in involuntary facial movements with volitional facial activation (eg, eye closure with smile)

Flaccid facial palsy exam

Smooth forehead with absence of wrinkles Brow ptosis Lagophthalmos—check for protective Bell phenomenon (superior rotation of globe with attempt at eye closure) C-shaped nasal deformity with tip and philtral deviation away from paralyzed side, lack of nostril dilation during inspiration Effacement of the nasolabial fold Down-turned oral commissure, inability to smile or expose lower dentition

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Lower lip of paralyzed side can be more elevated due to lip depressor paralysis

Inability to whistle or puff out cheeks

Partial facial palsy exam: decreased facial movements due to intrinsic weakness, can also involve synkinesis

Synkinetic facial palsy exam

Activation of non-native facial muscles on affected side Smile asymmetry, oral commissure malposition, and oral incompetence due to tethering from simultaneous activation of antagonist muscles

Associated with significant facial and neck tightness Other physical findings include xerophthalmia (greater superficial petrosal nerve), hyperacusis (nerve to stapedius), dysgeusia (chorda tympani nerve), and gustatory lacrimation (“crocodile tears”; hyperlacrimation during salivation caused by “miswiring” of general visceral efferent fibers to the lacrimal gland instead of the salivary glands)

Facial Nerve Grading Systems

House-Brackmann scale: one of the most common

classification schemes—I (normal) to VI (complete facial paralysis), III signifies complete eyelid closure

Evaluates gross appearance and motion at the

forehead, eye, and mouth

Limitations include its generalized assessment of facial

nerve function, inability to detect small changes in

facial nerve recovery, and lack of metrics for synkinesis Sunnybrook facial grading system: measures zonal symmetry at rest and with voluntary motion, includes assessment of synkinesis eFACE: electronic assessment that uses a visual analog scale to rate static, dynamic, and synkinetic function and zonal symmetry as well as overall facial disfigurement; scored from 0 to 100 (0 = severe asymmetry/palsy, 100 = normal symmetry/function) with −100 to 100 used for bidirectional parameters (eg, −100 = ptotic, 0 = normal, 100 = hyperelevated)

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Electrodiagnostic Studies: assist with prognostication and decision between surgical intervention vs observation

Normal side of the face is used as a control (ie, less useful in bilateral cases) Perform >72 hours after symptom onset (ie, after Wallerian degeneration has occurred) to ensure accurate result

Electroneurography (ENoG)

Compares differences in compound muscle action

potentials between normal vs affected side after

transcutaneous stimulation of facial nerve

>90% axonal degeneration representing a poorer

prognosis

Most predictive test for facial nerve recovery

Electromyography (EMG)

Performed 2-3 weeks after symptom onset—at rest,

with needle insertion, and with voluntary muscle

contraction

Fibrillation potentials: muscle denervation

Polyphasic potentials: muscle reinnervation

Nerve excitability test (NET)

Transcutaneous stimulation over the stylomastoid

foramen until contraction of the paralyzed side is

visualized

Difference >3.5 mA with the normal side is significant

Easy to perform, but highly subjective and examiner

dependent Maximal stimulation test (MST) is similar to the NET, except maximal current is used

Additional Workup

In cases of trauma, use computed tomography to assess for temporal bone fractures An audiogram should be obtained in all patients and, if abnormal, the next step is magnetic resonance imaging and referral to an otolaryngologist For lagophthalmos—monitor for keratoconjunctivitis, corneal ulceration

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TREATMENT OF FACIAL PALSY

NONSURGICAL MANAGEMENT

Acute Management

Oral corticosteroids ± antivirals treat

edema/compression of the nerve, depending on etiology. For Bell palsy, begin treatment within 72 hours of symptom onset. Eye care: corneal ulceration and potential blindness can result if corneal sensation is impaired and eyes are not adequate protected.

Artificial tears for lubrication

Eyelid taping during sleep for corneal protection

Eye patches, moisture chambers, and scleral lenses

can reduce evaporative losses

Eyelid weight to facilitate eye closure in paralytic

lagophthalmos

Long-term Management

Facial physical therapy

Facial neuromuscular retraining for incomplete

recovery and postoperative training

Can include EMG and mirror biofeedback

Botulinum toxin

Targeted chemodenervation of muscle groups on both

the normal and affected side to achieve facial balance

Commonly used to treat synkinesis and

blepharospasm Facial fillers can be used as an adjunct to correct facial volume asymmetry Determine candidacy for surgical options

SURGICAL MANAGEMENT

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Type of facial palsy, likelihood of spontaneous recovery, and viability of facial muscles dictate surgical options—

muscle remains viable for 18-24 months after denervation

Flaccid facial palsy or weakness

Possible recovery: close observation for 9-12 months

No possible recovery with viable facial muscles: nerve

transfer ± static procedures

No possible recovery with nonviable facial muscles:

muscle transfer ± static procedures Synkinesis: selective neurectomy of nerve branches triggering undesired muscle activation

Static vs Dynamic Procedures

Static procedures re-establish resting facial symmetry and

improve functional deficits but do not restore symmetry in facial movement

Brow lift for brow ptosis

Periocular procedures for paralytic lagophthalmos:

platinum eyelid weight, palpebral spring, lower eyelid

tightening (eg, lateral tarsal strip, tarsoconjunctival flap;

refer to Chapter 23: Eyelid Reconstruction)

Suture suspension/static slings (eg, tensor fascia lata,

palmaris longis, acellular dermis) to resuspend the

nasal valve, nasolabial fold, and oral commissure

Lip depressor resection (eg, DLI, DAO) for smile

asymmetry

Platysmectomy for cervical synkinesis

Asymmetric rhytidectomy to correct asymmetric facial

soft tissue ptosis Dynamic facial reanimation restores facial movement, particularly for smile mechanism

Volitional reanimation: must consciously move face

(eg, masseteric nerve transfer)

Spontaneous reanimation: occurs spontaneously (eg,

cross-facial nerve graft)

Nerve Repair and Nerve Transfer

Primary nerve repair and/or nerve grafting is favored

when possible.

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Repair must be tension-free—interposition grafts

should be used if tension encountered in primary

repair.

Incidence of synkinesis is increased with nerve grafting

due to the presence of two coaptations instead of one

with primary repair. Nerve transfer is used if ipsilateral facial nerve is not viable.

Cross-facial nerve graft (CFNG)

Indicated when proximal ipsilateral nerve stump is unavailable for grafting but distal stump is present and facial muscles are viable for reinnervation. A donor nerve graft (eg, sural nerve) guides regenerating nerve fibers from a redundant facial nerve branch on the normal side to a distal nerve stump on the paralyzed side—potential for spontaneous animation. Nerve growth is monitored by an advancing Tinel sign. Can be less predictable in older patients.

Nerve transfers: V to VII (masseteric), partial XII to VII

Powerful due to a greater number of nerve fibers being transferred compared to CFNG but does not provide spontaneous animation. XII to VII uses 30%-40% of XII to avoid ipsilateral tongue atrophy and synkinesis. Historically also performed with XI and phrenic nerves but no longer used due to significant donor site morbidity.

Babysitter procedure

Used for intermediate duration facial palsy (6-18 months) to prevent muscle atrophy and fibrosis while waiting for CFNG reinnervation. CFNG is combined with a minihypoglossal transfer —XII “babysits” facial muscles until the regenerating nerve fibers arrive from the CFNG.

Muscle Transfers

Regional muscle: temporalis muscle tendon transfer

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Orthodromic transfer of the temporalis muscle (ie, no

muscle inversion) with coronoidectomy, secured to oral

commissure/lips using fascia lata strips

Can also tunnel temporalis under zygoma and transfer

tendon to oral commissure with coronoid still attached

(lengthening myoplasty technique)

Pro: single stage procedure with immediate movement

Con: not spontaneous, fixed oral commissure insertion

with minimal control over smile vector/shape, degree of

oral commissure excursion is variable Free muscle: gracilis free flap (Fig. 19-2)

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Figure 19-2 Free

microneurovascular gracilis muscle

transfer.

Obturator nerve and adductor artery/vein.

CFNG is performed during the first stage and muscle is

transferred 9-12 months later during the second stage.

Pro: spontaneous activation can be achieved, ability to

customize smile vector with reliable oral commissure

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excursion.

Con: requires microvascular expertise, time (performed

6-9 months after CFNG, monitor for movement 1-3

years postop), can create unwanted midfacial bulk.

PEARLS

1. Facial palsy includes a spectrum of facial motor disorders ranging from partial palsy to complete flaccid paralysis to postparalytic synkinesis.

2. Synkinesis refers to the involuntary contraction of facial muscles during volitional movement of other facial muscles, leading to facial asymmetry and/or decreased facial movement due to simultaneous contraction of antagonistic muscle groups.

3. Bell palsy is the most common cause of unilateral facial paralysis in adults (diagnosis of exclusion) and should be treated with oral corticosteroids and antivirals within 72 hours of symptom onset.

4. Facial muscles may remain viable for 18-24 months after denervation.

5. Surgical management of facial palsy depends on the degree and type of facial palsy (eg, flaccid vs synkinetic), potential for spontaneous recovery, and viability of facial muscles.

QUESTIONS YOU WILL BE ASKED

1. What three anatomic landmarks help identify the facial nerve as it exits the stylomastoid foramen? Tragal pointer (lies 1 cm anterior, inferior, and deep), tympanomastoid suture (lies 6-8 mm deep), and posterior belly of the digastric muscle (defines plane of facial nerve).

2. Describe how to find the temporal branch of the facial nerve. Follows the course of Pitanguy line, which is drawn from 0.5 cm below the tragus to 1.5 cm above the lateral brow.

3. What structures are continuous with the SMAS?

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Superficial temporal fascia (temporoparietal fascia) and platysma.

4. What nerves are commonly used to reinnervate paralyzed facial muscles? Contralateral VII, masseteric branch of V, and XII.

THINGS TO DRAW

Draw the course of the extratemporal facial nerve.