Approach to Facial Weakness

Primary Category

Essential Neurology

P-Category

Secondary Category

S-Category

Authors

Anas Zahid MBBS ,
Awais Khan MD

Introduction

Facial nerve palsy can be defined as paralysis of any structure innervated by the facial nerve, thus inhibiting facial expression.

Deficits in normal social interactions is a major psychosocial effect.

Paralysis of facial muscles can also lead to the following clinical effects, besides deficits in facial expression:

Eyelid closure deficits
Oral incompetence and drooling
Deficits in phonation of labial sounds such as /b/ or /p/
Obstructed gaze that is progressive with age
Exposure and drying of the cornea
Lack of protection of the eye from foreign material
Nasal obstruction unilateral or bilateral and potential shift of the nasal base toward the nonparalyzed side
Pocketing of food in the buccal sulcus
Severe dental caries

Facial palsy is a broad term encompassing the entire spectrum of facial movement disorders caused by lower motor neuron / axonal injury of the facial nerve, including:

Flaccid facial palsy

Can be defined as total or near-total absence of facial movement and tone without synkinesis or hyperactivity.

Facial paresis
Postparalytic facial palsy

Can be defined as a facial movement disorder of postparalyic facial nerve syndrome comprising varying degrees of zonal synkinesis, hypoactivity, and hyperactivity.
Postparalytic facial nerve syndrome includes symptomatic gustatory epiphora (also known as Bogorad syndrome or crocodile tears) and facial discomfort.

The syndrome is thought to result from aberrant axonal regeneration or ephaptic transmission following a facial nerve insult.

A thorough investigation must be done to determine the etiology of the FP and to direct management.

An insult leading to acquired facial palsy usually leads to acute flaccid facial palsy (FFP).

The eventual outcomes range from total and persistent FFP to complete functional recovery.
Between these extremes of range, combinations of hypoactivity and hyperactivity and synkinesis exist;

Facial synkinesis can be defined as involuntary and abnormal facial muscle activation with volitional or spontaneous expression.
Oculo-oral and the oro-ocular are the most common general forms of synkinesis.
Oculo-oral synkinesis may coexist with other types of synkinesis.
Other types of facial synkinesis include chin-oral synkinesis, platysma synkinesis, ocular-chin synkinesis, ocular-nasal synkinesis and chin-ocular synkinesis.

These combinations of facial palsy may also be accompanied by postparalytic facial nerve syndrome

Epidemiology

Acquired facial nerve palsy is uncommon overall in the general population; affecting 20 to 32 per 100,000 people per year in the general population.

In children the incidence is even lower, estimated at 2.7 per 100,000 per year in children younger 10 years and 10.1 per 100,000 per year in children 10 to 20 years old.

There is a bimodal distribution of infectious and traumatic facial nerve palsy;

peaks are at 1 to 3 years and at 8 to 12 years old.

Males and females are affected equally.

Both sides of the face are affected equally.

The lifetime risk is 1 in 60

It is more common in pregnancy and diabetes mellitus..

History

Arriving at a diagnosis for the underlying cause of the facial movement disorder is paramount.

A complete and careful history is valuable in establishing the diagnosis.

Bell’s Palsy is the most common cause of facial paralysis followed by trauma to the facial nerve.

Timely recognition of facial weakness is important to detect causes that require early intervention, such as stroke.

Causes of Acute Facial Palsy (FP) include:

Bell’s palsy

Thought to be mostly caused by Herpes Simplex Virus infection

Trauma, including:

Temporal bone fractures (most common)
Soft tissue injuries
Birth trauma
Iatrogenic injuries

Ramsay-Hunt syndrome (Varicella zoster virus)
Lyme disease
Otic infections and cholesteatomas
Postsurgical insult, for example:

Following vestibular schwannoma extirpation

Adjuvant treatments for disease adjacent to or involving the facial nerve, for example:

Radiation
Chemotherapy

Benign tumors, for example:

Facial nerve schwannomas
Venous vascular malformations of the facial nerve
Geniculate ganglion hemangiomas

Malignant tumors, for example:

Parotid or hematogenous primaries
Facial nerve squamous cell carcinomas
Regional spread of cutaneous malignancies
Solid tumor metastases
Sarcomas

Congenital malformations
Systemic infections, for example:

Human immunodeficiency virus
Syphillis
Poliomyelitis

Autoimmune conditions, for example:

Guillain-Barre syndrome
Antiphospholid antibody syndrome
Sarcoidosis
Systemic lupus erythematosus
Sjogen’s

Sarcoidosis
Genetic syndromes

Melkersson-Rosenthal Syndrome
Albers-Schönberg Disease (Osteopetrosis)
Möbius Syndrome
Goldenhar Syndrome (Oculoauriculovertebral Dysplasia)

Hypertension

Believed to be due to hemorrhage into the facial nerve canal

Pontine infarcts or hemorrhages may present with isolated FP, although rare.

Factors of the history that have a significant effect on facial function and quality of life and are well documented include:

Time course of onset of palsy
Progression
Previous therapies
Resultant symptoms

The presence of the following symptoms in the history may help narrow down the diagnosis:

Otovestibular symptoms

Hearing loss
Hyperacusis
Vertigo
Imbalance
Otorrhea
Otalgia

Other focal neurologic deficits

Diplopia
Facial anesthesia

Constitutional symptoms

Fever
Chills
Fatigue
Malaise
Sweats
Weight loss

Meningitic

Headache
Nuchal rigidity

Lyme-specific symptoms

Recent tick bite or exposure
Erythema migrans rash,
Arthralgias
Myalgias
Low back pain

Inflammatory symptoms

Orofacial swelling or parotitis
Uveitis
Known autoimmune conditions

In the case of palsy at or shortly following birth:

Prolonged labor
Forceps use
Facial and periauricular ecchymoses (at delivery or shortly thereafter)

In the case of acute idiopathic FP, certain ‘red flag’ features point to an alternate diagnosis to Bell’s palsy, including:

Bilateral paralysis
Slow onset of facial weakness;

Weakness in Bell’s palsy fully progresses over 24–72 hours

Asymmetric weakness across facial zones at onset
Constitutional symptoms;

Fever, lethargy, malaise, myalgias

Headache;

Other than retroauricular pain and otalgia, which occur frequently in Bell palsy

Presence of other focal neurologic deficits;

Diplopia, hearing loss, vertigo

Absence of recovery of facial tone within 4 months of palsy onset

Variations in facial symptoms exist with respect to the timing of presentation and degree of recovery.

Newly acquired deficits from neurapraxic or axonotmetic injuries may continue to resolve for 12 months or longer without surgical intervention.

Successful muscle recovery is highly correlated with denervation time

FFP results in:

Paralytic lagophthalmos and ocular irritation
Loss of facial symmetry at rest
Collapse of the external nasal valve
Oral incompetence

Postparalytic facial palsy (PFP) presents with:

Facial synkinesis
Muscle hyperactivity
Contracture
Epiphora

Platysmal synkinesis results in:

Neck discomfort
Facial fatigue

Periocular synkinesis results in:

A narrowed palpebral fissure width

Lack of meaningful smile occurs in severe cases

Although facial sensation is preserved, some patients may complain of a sensation of numbness

One important difference between FP of HSV origin and that of VZV origin is that the former may recur whereas recurrence of zoster is very rare in immuocompetent individuals

Family history is of particular importance in diagnosing autoimmune causes, along with a personal history of:

Other autoimmune conditions
Rashes
Orofacial edema
Nasal septal perforation
Multiple miscarriages

Physical Examination

An exhaustive head and neck examination is indicated along with otoscopy and a complete cranial nerve examination.

Assessment of the zones of facial function is essential, both at rest and with movement.

The following aspects of the facial structures should be evaluated:

The postion of the brow

The effect of the brow position on the periocular complex

The degree of paralytic lagophthalmos
Whether or not Bell’s phenomenon is present
Palpebral fissure width
Lower lid position
Laxity using methods such as:

Distraction
Snap-back test

Depth and Orientation of the Nasiolabial Fold (NLF)
Oral commisure position
The degree and presence of synkinesis of the following muscle groups:

Brow
Ocular
Midface
Depressor
Mentalis
Platysma

The contralateral hemi-face is assessed to look for weakening of paired muscle groups;

If present, it is likely to produce improved symmetry

Spontaneous smile may be assessed;

Humorous video clips may be used for this purpose, for example

The appearance of the face is documented in the following 9 movements, using photography and videography:

Face at rest
Pucker
Complete eye closure
Brow elevation
Grin
Nose wrinkling
Whistling
Pouting and lower lip depression
Profile view for the assessment of the platysma action

Figure 1: The nine standard frontal views, as described above, beginning at top row, on the far left, respectively.

Figure 3: de Sanctis Pecora C, Shitara D. Botulinum Toxin Type A to Improve Facial Symmetry in Facial Palsy: A Practical Guideline and Clinical Experience. Toxins (Basel). 2021 Feb 18;13(2):159. doi: 10.3390/toxins13020159. PMID: 33670477; PMCID: PMC7923088.

Functional integrity of the muscles of the forehead is helpful to differentiate a central from a peripheral lesion of the facial nerve;

A central nervous system lesion will show normal tone and movement of both sides of the forehead
A peripheral facial nerve lesion will show abnormal motor tone and movement on the affected side of the forehead

Systems for identifying and quantifying facial weakness in relation to stroke from static frames or video data have emerged over the course of the previous decade.

However, video or in-person examination by a neurologist remains the gold standard.

These systems rely on varied techniques to extract relevant features from static frame pixel data;

In general they can be categorized into landmark-based features and intensity-based features
Landmark-based features encode information generally associated with position of key facial features such as shape
Intensity-based features focus on information such as skin color, creases, texture, etc

Investigations

In cases where the signs and symptoms are indicative of Bell’s Palsy, no further investigations are required.

Exceptions include titers to confirm specific diagnoses that have specific therapies such as Lyme-disease.

Imaging studies are indicated in cases where there is suspicion of benign/malignant tumors or signs of infection.

Examples of such studies include:

Fine-cut CT of the temporal bone without contrast
Gadolinium-enhanced MRI of the temporal bones and parotid glands

Imaging of the facial nerve must be accompanied by images of:

The brain and pons
The cerebellopontine angle
The internal auditory canal
All 3 portions of the facial canal
The geniculate ganglion
The stylomastoid foramen
The parotid gland

Indications in such cases include:

Abnormal otoscopy or tuning fork findings
Palpable parotid or neck mass
Slow- or asymmetric-onset of FP
Slowly progressive FP
Unilateral recurrent FP
Recent FP with absence of recovery at 4 months

Not recommended as part of the initial evaluation for patients whose history is otherwise consistent with BP as it is relatively rare for masses to present with acute FP.
Abnormalities in addition to facial palsy should also lead to imaging studies of the brain.

Blood studies are used in cases that are recurrent or are suspected to be autoimmune in nature; examples are:

Complete blood count
Erythrocyte sedimentation rate
C-reactive protein
Rheumatoid factor
Antinuclear antibody
Antineutrophil cytoplasmic antibody
Antiphospholipid antibodies
Angiotensin converting enzyme

Electrophysiologic testing can be helpful in predicting functional recovery in acquired deficits.

For example; following acoustic neuroma resection with a facial nerve thought to be in-continuity.
In such cases, serial electrophysiologic examinations may show early electrical recovery before clinical recovery
Electrophysiologic testing of multiple facial muscle patterns, in patients with Bell palsy, can provide clinically undetectable evidence of neural recovery;

It is useful for mapping available muscle motors before contiguous muscle transfer

Electroneuronography (ENoG) is indicated in cases with delayed traumatic or cases of idiopathic FFP with complete absence of hemi-facial movement on examination.

It is done to ascertain acute facial nerve decompression use for treatment
It is indicated between 3 and 14 days of onset of symptoms

Treatment and Management

Management of FP includes

Diagnosis
Forming a therapeutic plan according to:

The timing of presentation in flaccid cases
Specific pattern of facial dysfunction in patients presenting with aberrant neural regeneration

A wide range of therapeutic options available which can be classified into the following therapeutic strategies:

Pharmaceutical agents
Corneal protective measures
Physical therapy (PT)
Chemo-denervation agents
Fillers
Surgical procedures

In the multidisciplinary management of facial paralysis, every patient should be aware of the potential problems he or she may encounter

Outpatient referrals to neurology, audiology, otolaryngology, and/or ophthalmology and further testing by consultants may be warranted

More urgent consultations may be necessary if:

The FP does not appear peripheral
Other neurological signs or symptoms are present

In case of an anatomically intact nerve or a nerve injury limited to the medial portion of a peripheral branch:

Medical treatment with close observation
Possible electrophysiologic testing for monitoring of progression

In case of a transected nerve, immediate exploration with direct anastamosis provides the best chance of recovery.

In case of an injury to a large segment of the nerve, an interposition graft should be placed immediately.

If the injured segment is not easily accessible for repair, nerve transposition is the treatment of choice.

For facial muscles with irreparable damaged or extensive disuse atrophy, muscle transfer procedures are the best option for dynamic facial reanimation.

Corneal protection should be a primary concern and initiated in all causes of FP.

If the cause cannot be determined:

Therapy with prednisone, with or without an antiviral medication can be considered
The above therapy can begin as early as possible after onset of symptoms

It is useful to classify FP cases into 1 of 5 categories for the purpose of narrowing range of therapeutic options.

The categories are based on timing of presentation and status of the facial nerve and musculature.
The categories include:

Acute FFP
FFP with potential for spontaneous recovery
FFP with viable facial musculature with low potential for spontaneous recovery
FFP without viable facial musculature
Paralytic FP (PFP)

It is also useful to group potential interventions by type and side of FP and facial zone to develop a plan for management
Further details on management according to the category of FP are given below

Acute Flaccid Facial Palsy (Intact Facial Nerve)

First 72 hours to 2 weeks following onset of acute facial nerve injury.

Most cases are viral in origin.

Clinician’s role:

Diagnosis
Begin proper medical therapy, for example:

immunosuppressants
antivirals
antibiotics

mitigate risk of exposure keratopathy
determine candidacy for acute surgical intervention

For cases of Bell’s palsy; high-dose corticosteroids, within 72 hours of onset of symptoms, shortens time to recovery

Combination of antivirals and corticosteroids may have further clinical benefit

Particularly in cases with severe to complete paralysis
Significant evidence supports the use of combination therapy in VZV

In cases of Facial Nerve trauma:

Corticosteroids and observation are indicated, in cases of delayed onset or incomplete FP following trauma or iatrogenic insult
Iatrogenic injury resulting in immediate and complete paralysis of one or more FN branches warrants urgent surgical exploration
Patients are referred for neuro-otology consultation for consideration of surgical decompression within 14 days of symptom onset, if there is both of the following:

Total idiopathic or post-traumatic paralysis with an ENoG response demonstrating greater than 90% degeneration
absent voluntary motor units on electromyography (EMG)

FP associated with Lyme disease is treated with

Prolonged course of oral doxycycline or intravenous ceftriaxone
The role of accessory corticosteroid therapy is unclear

FP assoicated with otitis media is treated with:

Wide myringotomy

with or without mastoidectomy

Corticosteroids
Topical and parenteral antibiotics

Autoimmune causes may be a cause but are a diagnostic challenge

Eye lubrication with taping the eye shut at night is done to prevent exposure keratopathy

PT can be done to teach patients upper eyelid stretching

This assists in passive closure of the eye

Correction of paralytic lagophthalmos may be achieved by

Temporary tarsorrhaphy
Upper eyelid weighting
Indications include:

Poor prognosis for rapid recovery
Ocular symptoms with functional interference
Insufficient Bell phenomenon
Absence of recovery at 4 months

Other therapies include mirror therapy

Flaccid Facial Palsy with Potential for Spontaneous Recovery

These are cases in which nerve continuity is thought intact in the setting of FFP

For example, following resection of a vestibular schwannoma where FN stimulation was noted before closure

There is potential for spontaneous recovery in these cases

Return of facial tone and movement are expected within 6 to 12 months

Patients may benefit from therapeutics such as:

PT
Corneal protective measures
Static periocular reanimation
Temporary chemodenervation of the healthy-side depressor labii inferioris muscle

To improve oral competence and articulation during this period
Botulinum Toxin Type A may be used as a chemodenernation agent

Close follow-up (every 3 months) is warranted to ensure recovery of function

Flaccid Facial Palsy with Viable Facial Musculature and Low Potential for Spontaneous Recovery

In such cases, there is discontinuity of the FN or the absence of recovery of facial function is within 6 to 12 months of FP onset

Facial musculature is intact and likely receptive to re-innervation

Common clinical scenarios involve patients presenting with dense FFP resulting from:

Necessary facial nerve resection during surgery for advanced parotid and cutaneous malignancies
Temporal bone tumors such as:

Facial nerve schwannomas
Venous vascular malformations
Cholesteatomas

Cerebellopontine angle tumor extirpations
Pontine hemorrhage

There is evidence that facial musculature remains responsive to re-innervation for periods up to;

24 months following denervation in adults
Possibly for longer periods in children

Options regarding rehabilitation of facial paralysis following nerve transection include:

Grafting procedures
Static suspension
Regional muscle transfer
Free tissue transfer

Nerve grafting is the best option for long-term recovery of tone and function;

However, the effects of nerve grafting may not be noticeable for up to 12 months
This may be significant in the setting of potential tumor recurrence or progression
Combined methods which both mitigate immediate functional deficits and allow for optimal long-term outcomes are ideal.

Interposition graft repair should be considered in the setting of neural discontinuity;

Split-hypoglossal nerve transfer to the main trunk of the facial nerve is an alternative option in cases where:

Interposition graft repair is unfeasible
No recovery is noted within 12 months.

The objective of main trunk repairs and transfers is to:

Restore facial tone
Restore some form of blink
Meaningful reanimation of expression is rare

Voluntary expressions may be restored through targeted nerve transfers during this period, such as:

Nerve-to-masseter transfer to lower zygomatic branches of the facial nerve for smile reanimation
Cross-face nerve grafting to upper zygomatic branches for blink restoration
Considered in patients demonstrating minimal to no improvement in facial function 7 months following vestibular schwannoma resection with facial nerve preservation

As the probability of ultimate recovery of meaningful expression is less than 10%

Static periocular reanimation is offered early in the course of palsy onset where recovery is likely to take several months.

Examples are upper lid weighting and lateral tarsal strip procedure

Methods to improve facial symmetry may be of benefit in patients awaiting facial nerve recovery, including:

Brow lifts
Autologous fat augmentation
Selective and directed chemodenervation

Platysmectomy can be considered in patients with good response to chemodenervation of platysmal banding and spasm, for a more permanent form of treatment

Flaccid Facial Palsy Without Viable Facial Musculature

Facial musculature may be absent;

For example, following resection or congenital absence

Facial musculature may be unlikely to be responsive to re-innervation;

For example, long denervation period or marked distal perineural spread of a malignant tumor

Nerve repair or transfers are NOT indicated in such cases

PT is indicated

Targeted chemodenervation of the healthy side lip depression can be done

Brow elevation can be done

Surgical interventions such as the following are indicated:

Static facial suspensions
Static peri-ocular reanimation
Muscle transfers

Targeted suspensions may be achieved .

Following may be used:

Sutures
Fascia lata
Bioabsorbable or permanent implants.

Areas of the face that may be targeted include:

Brow
Lower eyelid
Midface
Nasal valve
NLF
Oral commissure

Tightening of the lower lid may be achieved by the lateral tarsal strip procedure

With or without medical canthal tendon plication

Dynamic smile reanimation may be achieved through:

Antidromic or orthodromic temporalis muscle transfer
Free muscle transfer with motor innervation provided through cranial nerve transfer

Options for dynamic reanimation of the lower lip include

Anterior digastric muscle transfer
Inlay of a T-shaped fascia graft

Postparalytic Facial Palsy

Develops 6 to 18 months following severe facial nerve insult;

With spontaneous, yet aberrant, regeneration
Or following main trunk nerve grafting

It is permanent

Lagophthalmos is rare

PT is first-line treatment

A comprehensive management program includes

Patient education
Soft tissue mobilization
Mirror and EMG biofeedback
Neuromuscular retraining

Blunting of hyperactivity is indicated through filler injection and weakening of hyperactive muscles through:

Targeted chemodenervation
Neurectomy
Resection in advanced disease

Targeted chemodenervation of diseased side muscles may offer improvement in certain patients.

Examples of the muscles include:

Orbicularis oculi
Mentalis
Platysma

Weakening of the depressor anguli oris muscle on the diseased side can result in dramatic improvement in smile dynamics in select patients.

Done by chemodenervation or resection

Muscle transfer may be done for dynamic smile reanimation

Regional (eg, temporalis) or free (eg, gracilis)
Considered for cases with severe restriction of oral commissure excursion

Targeted nerve transfers are largely ineffective in the setting of PFP

Prognosis

Outcomes and prognosis vary based on the etiology of the disease.

Overall prognosis is good.

Congenital traumatic facial nerve palsy has been shown to resolve spontaneously in 90% of patients within 4 weeks.

Evidence shows 80% to 90% recovery rates in adult and pediatric patients with blunt temporal trauma.

Time to recovery is longer than in patients with an infectious etiology (about 10 months).

Recovery rates of idiopathic facial nerve palsy in children range from 70% to 90%.

Systematic tracking of therapeutic outcomes is a paramount to clinical excellence.

Outcomes tracking in FP may entail:

Patient-reported QoL measures
Clinician-assessed grading of facial function
Objective measurement of facial displacements

QoL impact may be assessed using generalized patient-graded scales such as the SF-36.

The House Brackman Scale is a grading tool universally used to grade recovery of facial nerve function

It consists of a six point scale with patients grouped into 1 of 6 groups
A system made by Brackmann can be used to help place patients in the proper group

It involves making measurements of the movement of the eyebrow and corner of the mouth and comparing the results with those on the unaffected side

Descriptions of patients in each group are as follows:

Group I: Normal facial movement and no weakness or synkinesis
Group II: Slight asymmetry of facial movements with a possible slight synkinesis
Group III: Obvious asymmetry with obvious secondary defects but some forehead movement
Group IV: Obvious asymmetry, no forehead movement, and weakness with possible disfiguring synkinesis or mass action
Group V: Only slight movement of the face, no forehead movement, and not enough facial function return to have secondary defects
Group VI: Absence of any movement or tone

Patient-graded scales specifically designed and validated for use in FP include:

The Facial Disability Index
The Facial Clinimetric Evaluation
The Synkinesis Assessment Questionnaire

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