Facial Nerve Paralysis PPT

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Facial Nerve Paralysis PPT

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Facial Nerve Paralysis

Vanessa S. Rothholtz, M.D., M.Sc.

UCI Department of Otolaryngology – Head and Neck Surgery

May 24, 2007

Chief Complaint

My Starbucks caramel macchiatto dribbled down my chin this morning, and it ruined my white coat.  Now my face isn’t working.  Do I need a face lift?


Unilateral left-sided otalgia (TMJ)

Fever, chills


Generalized fatigue

Conjunctivitis two weeks ago (resolved with antibiotics)

“My eczema acted up again last week, but it looked a little different.”

Travel – Sonoma County for a friend’s wedding a last month


Eyes: Left eye with injected conjunctiva, pupils equal and reactive

Ears: EAC patent, TM c/m/i

Nares: Patent, clear

OC/OP: Dentition intact, tongue midline / mobile, No tonsillar hypertrophy


Normal tone and symmetry at rest

Obvious facial asymmetry with effort

No perceptible forehead movement

Incomplete eye closure

Asymmetrical motion of mouth with maximal effort

What grade of paralysis is this based on the House-Brackmann facial nerve grading scale?





House-Brackmann Facial Nerve
Grading Scale

I           Normal

II         Normal tone and symmetry at rest

Slight weakness on close inspection

Good to moderate movement of forehead

Complete eye closure with minimum effort

Slight asymmetry of mouth with movement

III        Normal tone and symmetry at rest

Obvious but not disfiguring facial asymmetry

Synkinesis may be noticeable but not severe

+/- hemifacial spasm or contracture

Slight to moderate movement of forehead

Complete eye closure with effort

Slight weakness of mouth with maximum effort


IV        Normal tone and symmetry at rest

Asymmetry is disfiguring or results in obvious facial weakness

No perceptible forehead movement

Incomplete eye closure

Asymmetrical motion of mouth with maximum effort

V         Asymmetrical facial appearance at rest

Slight, barely noticeable movement

No forehead movement

Incomplete eye closure

Asymmetrical motion of mouth with maximum effort


Differential Diagnosis

V         Anomalous sigmoid sinus, benign intracranial hypertension, intratemporal aneurysm of internal carotid artery, embolization for epistaxis (external carotid artery branches)

I           Malignant otitis externa, otitis media, cholesteatoma, mastoiditis, meningitis, parotitis, chicken pox, Ramsay Hunt syndrome, encephalitis, poliomyelitis (type I), mumps, mononucleosis, leprosy, HIV/AIDS, influenza, Coxsackie virus, malaria, syphilis, scleroma, TB, botulism, mucormycosis, Lyme disease

T          Cortical injuries, basilar skull fractures, brainstem injuries, penetrating injury to middle ear, facial injuries, altitude paralysis (barotrauma), SCUBA diving (barotrauma)

A         Temporal arteritis, periarteritis nodosa, Multiple sclerosis, myasthenia gravis, sarcoidosis, Wegener granulomatosis, eosinophilic granloma

M         Paget disease, osteopetrosis, diabetes mellitus, hyperthyroidism, pregnancy, alcoholic neuropathy, bulbopontine paralysis, oculopharyngeal muscular dystrophy

I           Bell palsy, Melkersson-Rosenthal syndrome (recurrent facial palsy, furrowed tongue), hereditary hypertrophic neuropathy, (Charcot-Marietooth disease, Dejerine-Scottis disease), Landry-Guillain-Barre syndrome, Sarcoidosis, Kawasaki disease, surgery, embolization

N         Acoustic neuroma, glomus jugulare tumor, leukemia, meningioma, hemangioblastoma, hemangioma, pontine glioma, sarcoma, hydradenoma, gacial nerve neuroma, teratoma, fibrous dysplasia, von Recklinghausen’s disease, carcinomatous encephalitis, cholesterol granuloma, carcinoma (invasive or metastatic)

C         Molding, forceps delivery, myotoic dystrophy, Moebius syndrome

D         Vaccine for rabies, Antitetanus serum, mandibular block anesthesia

Course of the Facial Nerve

Intracranial – Arises at the pontomedullary junction and courses with CNVIII to the internal acoustic meatus – 12mm

Meatal – Anterior to the superior vestibular nerve and superior to the cochlear nerve – 10mm

Intratemporal –

Labyrinthe segment

Passes through narrowest part of fallopian canal – 12mm

Narrowest part of facial nerve.  The most susceptible to compression secondary to edema.

Tympanic segment

From geniculate ganglion to pyramidal turn – 11mm

Mastoid segment

Exits the stylomastoid foramen – 13mm

Extracranial – From stylomastoid foramen to pes anserinus



The longest segment of the facial nerve is:

A.        Vertical of mastoid portion

B.        Cisternal portion

C.        Tympanic portion

D.        Portion in the IAC




Captier G.  Organization and microscopic anatomy of the adult human facial nerve: Anatomical and histological basis for surgery

Blood supply to facial nerve – clinical relevance

Courses between the epineurium and periosteum – making the blood supply at risk when mobilizing at the first genu


Stylomastoid artery (branch of the postauricular artery of external carotid artery)

Greater petrosal artery (branch of middle meningeal artery)

Internal auditory artery (branch of the AICA)

Labyrinthe segment – lacks anastomosing arterial cascades thereby making the area vulnerable to ischemia


* Parhizkar N, Hiltzik DH and Selesnick SH. Facial nerve rerouting in skull base surgery.  Otol Clin N Am. 2005; 38(4): 685-710

Work Up

Basic labs, thyroid function panel, Lyme titers ELISA for antibodies


Stapedial reflex


MRI with gadolinium / CT

Nerve Excitability Test, Maximal Stimulation Test, Electroneuronography (EnoG) – Useful 72 hours post-injury

Topognostic Testing

Schirmer test for lacrimation

Stapedial reflex test (stapedial branch)

Taste testing (chorda tympani nerve)

Salivary flow rates and pH (chorda tympani)


Topognostic Testing

Schirmer Test

Greater superficial petrosal nerve

Filter paper is placed in the lower conjunctival fornix bilaterally

3- 5 minutes

Value of 25% or less on the involved side or total lacrimation less than 25 mm is considered abnormal.

Topognostic Testing

Stapedial Reflex


Stapedius branch of the facial nerve

Most objective and reproducible

A loud tone is presented to either the ipsilateral or contralateral ear à evokes a reflex movement of the stapedius muscle à changes the tension on the TM (which must be intact for a valid test) resulting in a change in the impedance of the ossicular chain

If intact stapedial reflex, complete recovery can be expected to begin within six weeks

Absence of the stapedial reflex during the first two weeks in Bell’s Palsy is common

Topognostic Testing

Taste Testing

Chorda tympani

Extremely subjective

Papillae generally disappear within 10 days post injury –  middle 1/3 of the tongue is most indicative, because the anterior 1/3 may receive bilateral input.


Topognostic Testing

Salivary flow rates

Chorda tympani

Cannulation of Wharton’s ducts bilaterally

5 minute measurement of output

Significant if 25% reduction in flow of the involved side as compared to the normal side

Salivary pH µ Flow Rate


Nerve Excitability Test (NET)

Most predictive prognostic factor for recovery of facial nerve function*

Hilger nerve stimulator over stylomastoid foramen

Reflects elevated thresholds for neuromuscular stimulation due to degeneration / disruption of axons (comparison to contralateral side)

Difference > 2.5 milliamps – poor prognosis


* Ikeda M et. al. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence.  Laryngoscope. 2005; 115:855-860.


Nerve Excitability Test (NET)


Easy to perform

More comfortable for patient


Subjectivity (relies on operator’s visual detection of response)

May exclude smaller fibers (current thresholds are likely to selectively activate larger fibers with lower thresholds and not those smaller fivers closer to stimulating electrode)

Maximal Stimulation Test (MST)

Electrical impulse administered to saturate the nerve with current and to compare it to contralateral side

Test is repeated periodically until definitive response


Equivalent to contralateral side

Minimally diminished (50%)

Markedly diminished (< 25% of normal)


Symmetric response within first ten days – complete recovery in > 90%

No response within first ten days – incomplete recovery with significant sequelae

Superior to NET – test becomes abnormal sooner, but drawback is subjectivity

Evoked electromyography (EEMG) or Electroneuronography (EnoG)

Records compound muscle action potential (CMAP) with surface electrodes placed transcutaneously in the nasolabial fold (response) and stylomastoid foramen (stimulus)

Waveform responses are analyzed to compare peak-to-peak amplit`udes between normal and uninvolved sides where the peak amplitude is proportional to the number of intact axons

Evoked electromyography (EEMG) or Electroneuronography (EnoG)

Most reliable in first 2-3 weeks post event (as neuropraxic fibers recover or regenerate, they discharge asynchronously and the response is subsequently diminished)

Response < 10% of normal in first 3 weeks – poor prognosis

Response > 90% of normal within 3 weeks of onset – 80-100% probability of recovery

Testing every other day

Advantages: Reliable




Test-retest variability due to position of electrodes

Electromyography (EMG)

Measures post-synaptic membrane di/triphasic (polyphasic) potentials with voluntary muscle contraction that are present 6-12 weeks prior to visible return of function

Assesses reinnervation potential of muscles two weeks after onset

Limited value early in evaluation because fibrillation potentials indicating axonal degeneration do not appear until 10 – 14 days post onset

Detection of motor units in 2 of 3 muscle groups – 87% satisfactory outcome

Detection of motor units in 1 muscle group – 11% satisfactory

More Methods

Antidromic (retrograde) Conduction – F-waves represent activated motor neurons in facial muscles.

Transcranial magnetic stimulation – Enables central activation via a transcranial application of induce current via an electromagnetic coil

Trigeminofacial Reflex – Records action potentials reflexively generated in the orbicularis oculi muscle in response to an electrical stimulus applied to V1

Lyme Disease – Borrelia Burgdorferi

Ten percent of patients have facial nerve paralysis after 1-4 weeks incubation period

ELISA to search for IgG and IgM antibodies

Facial paralysis resolves in 6 to 12 months


Early antibiotics

Reduce symptoms

Event long-term sequelae

Children – IV penicillin, ceftriaxone or cefotaxime

Adults – tetracycline

Muscular therapy

Bell’s Palsy

60-70% cases

Pathophysiology – Impaired “axoplasmic” flow from edema of facial nerve within fallopian canal

Rapid onset and evolution  < 48 hours

May be associated with acute neuropathies of cranial nerves V- X

Pain or numbness affecting ear, mid-face, tongue and taste disturbances

Recurrences are more likely (2.5x) in patients with family history, immunodeficiency or diabetes

Bell’s Palsy



Oral antivirals – Acyclovir –  10mg/kg (500mg)  q8hrs x 7 days

Corticosteroid taper 1mg / kg / day for 10 days

Eye protection – lacrilube

Follow progression with serial exams

Facial nerve decompression

Progression to > 90% degeneration on ENOG

Performed before irreversible injury to the endoneural tubules occurs (two weeks), will allow for axonal regeneration to occur

Treatment of Bell’s Palsy with Steroids: A controversial closer look

Steroids may have the following effects:

Reduce risk of denervation

Preventing / lessening synkinesis

Preventing progression to complete paralysis

Hastening recovery


Lack of randomization, controls and definitive dosing in most studies

Stankiewicz J.  Steroids and idiopathic facial paralysis. Otlaryngol Head Neck Surg.  1983; 91: 672.

Wolf S. Wagner J. Davidson S. et.. al. Treatment of Bell’s palsy with prednisone: a prospective randomized study.  Neurology. 1978; 28: 158.

Facial Nerve function recovers to HB grade I function in what percentage of patients with Bell’s Palsy?

A. 50%

B. 70%

C.  85%

D.  95%



* Ikeda M et. al. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence.  Laryngoscope. 2005; 115:855-860.

Which of the following factors is a predictor of poor facial nerve outcome following Bell’s Palsy?

A.        Age over 50 years

B.        Male Gender

C.        Loss of lacrimation

D.        Hypothyroidism


* Ikeda M et. al. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence.  Laryngoscope. 2005; 115:855-860.

What is this Condition?

Herpes Zoster Oticus
(Ramsay Hunt syndrome)

10-15% of acute facial palsy cases

Lesions may involve the external ear, the skin of EAC or soft palate

Associated symptoms – hearing loss, dysacusis and vertigo

Additional involvement of CN V, IX and X and cervical branches 2, 3 and 4

Pathogenesis – Neural injury due to edema at point between the meatal foramen and the geniculate fossa in the labyrinthe segment

The most common etiology of facial nerve paralysis in children is:

A.        Infection

B.        Congenital

C.        Trauma

D.   Iatrogenic



* Evans AD et. al. Pediatric facial nerve paralysis: Patients, management and outcomes.  Int J Ped Otol.  2005; 69:1521-1528.

Which of the following infections is most likely to cause facial paralysis in a pediatric patient?

A.        Acute otitis media

B.        Mastoiditis

C.   Mycobacterium infection

D.   Disseminated herpes



* Evans AD et. al. Pediatric facial nerve paralysis: Patients, management and outcomes.  Int J Ped Otol.  2005; 69:1521-1528.

Acute Otitis Media

History and physical exam make the diagnosis

Palsy is progressive over 2 to 3 day period

Infectious agent – Staphylococcus non-aureus, Propionobacterium

CT temporal bone



Otic antibiotic drops containing topical steroids

IV antibiotics and steroids

If not improved… mastoidectomy

Möbius Syndrome

Most frequently sporadic

Congenital facial weakness with impairment of ocular abduction

Dysfunction of other cranial nerves – III, IV, IX, X, XII

Skeletal abnormalities (orofacial, limb malformations)

Pathogenesis – Genetic cause vs. Ischemic cause

Melkersson-Roenthal syndrome


Recurrent orofacial edema

Recurrent facial palsy (50-90%)

Lingua plicata (fissure tongue) – 25%

Lips become chapped, fissured and red-brown in appearance

Biopies identify granulomatous changes

Facial nerve decompression may be indicated if facial paralysis is severe and recurrent


About 5% of cases of facial nerve paralysis are caused by tumors

Characteristics of facial nerve palsy

Slow developing

Additional cranial nerve deficits

Recurrent ipsilateral involvement


Palpable neck or parotid mass

Most common benign tumor – facial nerve schwanomma

Most common malignant tumors – mucoepidermoid carcinoma and adenoid cystic carcinoma of the parotid gland.

Temporal Bone Fractures

Longitudinal fractures

80% incidence but 10-20% with facial nerve injury

Transverse fractures

20% incidence, but 50% with facial nerve injury

Most common site of fracture

Perigeniculate region

Temporal Bone Fractures

Penetrating injury to extratemporal facial nerve branches

Injuries medial to a line perpendicular to the lateral canthus do not need to be explored because they recover spontaneously (draw please)

Immediate paralysis after injury lateral to this line needs to be explored and repaired with an end-to-end anastomosis 48-72 hours after the initial injury

Sunderland Nerve Injury Classification

I  Neuropraxia

Conduction block from compression and loss of axonic flow

Complete recovery

II   Axonotmesis

Axon disrupted but endoneurium preserved

Wallerian degeneration occurs distal to site of injury

Complete recovery

III   Neurotmesis

Complete disruption of axon including its surrounding myelin and endoneurium

Wallerian degeneration

Unpredictable outcome – High risk for synkinesis

IV   Complete disruption of perineurium

V  Complete disruption of epineurium

Risk of a neuroma from nerve sprouts outside of nerve sheath

A patient with facial nerve injury following a gunshot wound to the temporal bone typically presents with which of the following symptoms?

A.        Midface branch paralysis

B.        Complete facial paralysis

C.        Forehead paralysis

D. Partial weakness of the facial nerve



* Bento RF and de Brito RV.  Gunshot wounds to the facial nerve.  Otol Neurotol.  2004; 25: 1009-1013.

Following surgical repair of facial nerve injury due to a gunshot wound, the typical facial nerve function outcome is House Brackmann grade:

A.        I or II

B.        III or IV

C. V




* Bento RF and de Brito RV.  Gunshot wounds to the facial nerve.  Otol Neurotol.  2004; 25: 1009-1013.

A patient presents to the trauma bay after a closed head injury.  He has a unilateral facial nerve paralysis and a CT scan confirms a temporal bone fracture.  The family wants your expert opinion on the prognosis and return of facial nerve function.

Immediate onset – as above

Delayed onset

94%-100% complete recovery

Patients with > 90% degeneration of neural integrity – poor recovery

What if the facial paralysis doesn’t resolve?

End-to-End Anastomosis

Cable Nerve Graft

Hypoglossa-Facial Nerve Anastomosis (Crossover or Jump Graft)

Muscle transposition (Gracilis)

Static Suspension (Gortex, Threads)



Emotional/Social Issues





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