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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
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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?
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History
Unilateral left-sided otalgia (TMJ)
Fever, chills
Headache Generalized fatigue
Conjunctivitis two weeks ago (resolved withantibiotics)
“My eczema acted up again last week, but itlooked a little different.”
Travel – Sonoma County for a friend’s wedding alast month
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Physical
Eyes: Left eye with injected conjunctiva, pupils equaland reactive
Ears: EAC patent, TM c/m/i
Nares: Patent, clear
OC/OP: Dentition intact, tongue midline / mobile, Notonsillar hypertrophy
Face:
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
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What grade of paralysis is this
based on the House-Brackmann
facial nerve grading scale?
IV
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House-Brackmann Facial Nerve
Grading ScaleI 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 contractureSlight to moderate movement of forehead
Complete eye closure with effort
Slight weakness of mouth with maximumeffort
IV Normal tone and symmetry at rest
Asymmetry is disfiguring or results inobvious facial weakness
No perceptible forehead movement
Incomplete eye closure
Asymmetrical motion of mouth withmaximum effort
V Asymmetrical facial appearance atrest
Slight, barely noticeable movement
No forehead movement
Incomplete eye closure
Asymmetrical motion of mouth withmaximum effort
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Differential DiagnosisV 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 (typeI), 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, diabetesmellitus, 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-Barresyndrome, 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, vonRecklinghausen’s disease, carcinomatousencephalitis, cholesterol granuloma,carcinoma (invasive or metastatic)
C Molding, forceps delivery, myotoicdystrophy, Moebius syndrome
D Vaccine for rabies, Antitetanus serum,
mandibular block anesthesia
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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 tocompression 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
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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
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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
Extrinsic
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
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Work Up
Basic labs, thyroid function panel, Lyme titersELISA for antibodies
Audiogram Stapedial reflex
EKG
MRI with gadolinium / CT
Nerve Excitability Test, Maximal StimulationTest, Electroneuronography (EnoG) - Useful 72hours post-injury
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Topognostic Testing
Schirmer test for lacrimation
Stapedial reflex test (stapedial branch)
Taste testing (chorda tympani nerve)
Salivary flow rates and pH (chorda
tympani)
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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 isconsidered abnormal.
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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 evokes a reflex movement of thestapedius muscle changes the tension on the TM (whichmust be intact for a valid test) resulting in a change in theimpedance of the ossicular chain
If intact stapedial reflex, complete recovery can beexpected to begin within six weeks
Absence of the stapedial reflex during the first two weeks
in Bell’s Palsy is common
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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.
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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 Flow Rate
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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.
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Nerve Excitability Test (NET)
Benefits:
Easy to perform
More comfortable for patient
Drawbacks
Subjectivity (relies on operator’s visualdetection of response)
May exclude smaller fibers (current thresholdsare likely to selectively activate larger fiberswith lower thresholds and not those smaller fivers closer to stimulating electrode)
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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
Response
Equivalent to contralateral side
Minimally diminished (50%)
Markedly diminished (< 25% of normal)
Absent
Symmetric response within first ten days – completerecovery in > 90%
No response within first ten days – incomplete recoverywith significant sequelae
Superior to NET - test becomes abnormal sooner, butdrawback is subjectivity
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Evoked electromyography (EEMG) or
Electroneuronography (EnoG) Records compound muscle
action potential (CMAP) withsurface electrodes placedtranscutaneously in thenasolabial fold (response) andstylomastoid foramen(stimulus)
Waveform responses areanalyzed to compare peak-to-
peak amplit`udes betweennormal and uninvolved sideswhere the peak amplitude is
proportional to the number of intact axons
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Evoked electromyography (EEMG) or
Electroneuronography (EnoG)
Most reliable in first 2-3 weeks post event (as neuropraxic fibersrecover or regenerate, they discharge asynchronously and theresponse 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 Disadvantages:
Uncomfortable
Cost
Test-retest variability due to position of electrodes
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Electromyography (EMG)
Measures post-synaptic membrane di/triphasic(polyphasic) potentials with voluntary muscle contractionthat are present 6-12 weeks prior to visible return of function
Assesses reinnervation potential of muscles two weeksafter 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
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More Methods
Antidromic (retrograde) Conduction – F-wavesrepresent activated motor neurons in facialmuscles.
Transcranial magnetic stimulation – Enablescentral activation via a transcranial application of induce current via an electromagnetic coil
Trigeminofacial Reflex – Records action potentials reflexively generated in the orbicularisoculi muscle in response to an electrical stimulusapplied to V1
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Lyme Disease - Borrelia Burgdorferi
Ten percent of patients have facial nerve paralysisafter 1-4 weeks incubation period
ELISA to search for IgG and IgM antibodies
Facial paralysis resolves in 6 to 12 months
Treatment
Early antibiotics
• Reduce symptoms
• Event long-term sequelae
Children - IV penicillin, ceftriaxone or cefotaxime
Adults - tetracycline
Muscular therapy
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Bell’s Palsy
60-70% cases
Pathophysiology – Impaired “axoplasmic” flowfrom 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, tongueand taste disturbances
Recurrences are more likely (2.5x) in patients withfamily history, immunodeficiency or diabetes
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Bell’s Palsy
Treatment
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 tubulesoccurs (two weeks), will allow for axonal regeneration to occur
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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
Controversy:
Lack of randomization, controls and definitivedosing 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.
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Facial Nerve function recovers to HB gradeI 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.
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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.
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What is this Condition?
Ramsay Hunt Syndrome
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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, dysacusisand 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 thegeniculate fossa in the labyrinthe segment
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The most common etiology of facialnerve 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.
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Which of the following infections is mostlikely to cause facial paralysis in a
pediatric patient?A. Acute otitis media
B. Mastoiditis
C. Mycobacterium infection
D. Disseminated herpes
infection
* Evans AD et. al. Pediatric facial nerve paralysis: Patients, management
and outcomes. Int J Ped Otol. 2005; 69:1521-1528.
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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
Treatment
Myringotomy
Otic antibiotic drops containing topical steroids
IV antibiotics and steroids
If not improved… mastoidectomy
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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, limbmalformations)
Pathogenesis – Genetic
cause vs. Ischemic cause
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Melkersson-Roenthal syndrome
Triad Recurrent orofacial edema
Recurrent facial palsy (50-90%)
Lingua plicata (fissuretongue) – 25%
Lips become chapped,fissured and red-brown inappearance
Biopies identifygranulomatous changes
Facial nerve decompressionmay be indicated if facial
paralysis is severe andrecurrent
N l ti
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Neoplastic
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
Adenopathy
Palpable neck or parotid mass
Most common benign tumor - facial nerveschwanomma
Most common malignant tumors - mucoepidermoidcarcinoma and adenoid cystic carcinoma of the
parotid gland.
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Temporal Bone Fractures
Longitudinal fractures
80% incidence but 10-20% with facial nerveinjury
Transverse fractures
20% incidence, but 50% with facial nerveinjury
Most common site of fracture
Perigeniculate region
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Temporal Bone Fractures
Penetrating injury to extratemporal facial nerve
branches
Injuries medial to a line perpendicular to thelateral 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
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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
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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 paralysisD. Partial weakness of the facial nerve
* Bento RF and de Brito RV. Gunshot wounds to the facial nerve. Otol
Neurotol. 2004; 25: 1009-1013.
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Following surgical repair of facial nerve injurydue to a gunshot wound, the typical facial
nerve function outcome is House Brackmanngrade:
A. I or II
B. III or IV
C. V
D. VI
* Bento RF and de Brito RV. Gunshot wounds to the facial nerve. Otol
Neurotol. 2004; 25: 1009-1013.
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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
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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)
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Complications
Keratitis
Emotional/Social Issues
Synkinesis