FACIAL PALSY

Lecturer : Vivien Puspitasari

This teaching material is copyrighted.

No part of this work may be reproduced, including photocopied, without written permission of UPH.
 Learning Objective

Student should be able to

• Describe anatomy of facial nerve from its nucleus in
the pons until its distal component
• Describe the component and organs innervated by
facial nerve
• Understand the pathological process on facial nerve
• List the disease that cause dysfunction of facial nerve
What’s happen with the baby?
 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?
 Cranial Nerve VII - Facial Nerve

 Brancial motor
Supplies the muscles of facial
expression; posterior belly of digastric
muscle; stylohyoid, and stapedius.
 Visceral motor
(general visceral efferent)
Parasympathetic innervation of the
lacrimal, submandibular, and
sublingual glands, as well as mucous
membranes of nasopharynx, hard and
soft palate.
 Special sensory
(special afferent) Taste sensation from
the anterior 2/3 of tongue; hard and
soft palates.
 General sensory
(general somatic afferent) General
sensation from the skin of the concha
of the auricle and from a small area
behind the ear
 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
 FACIAL NERVE DISORDER

• Reduce function (palsies)

• Excessive activation of facial nerve-innervated muscles
e.g hemifacial spasm

Facial neuropathy
• Infectious
• Inflammation
• Neoplastic
• Trauma
Diagnosis of facial weakness
First step : determine central or peripheral

Cells of the facial nucleus that

innervate the lower face receive
corticobulbar fibers primarily
from the contralateral cerebral
hemisphere

Cells of the facial nucleus that

innervate the upper face receive
corticobulbar fibers originating
from both cerebral hemisphere
 Central facial palsy

• lesion above the level of the facial

nuclei in the pons of the
contralateral hemisphere
• A unilateral lesion in the cortex or
underlying corticobulbar fibers
usually produces contralateral
voluntary central-type facial
paralysis and contralateral
hemiplegia but does not affect
salivary & lacrimal secretions or
the sense of taste
 Peripheral facial palsy

• Weakness or paralysis of all

muscles of facial expression
• Due to a lesion of the ipsilateral
facial nerve but can also be
produced by a lesion of the
ipsilateral facial nucleus or facial
nerve in the pons
• Hyperacusis : paralysis of the
stapedius muscle
• Lesions proximal to the
geniculate ganglion : permanent
loss of taste & unable to produce
tears
• The most common cause of acute facial
paralysis :
– Central : Stroke (hemisphere)
– Peripheral :
• Bell’s palsy
• Herpes zoster oticus
• Stroke (brainstem)
 Peripheral facial nerve palsy

• Primary (75%) /idiopathic → Bell’s palsy

• Secondary (25%)
– Systemic viral infection
– Trauma
– Surgery
– Diabetes
– Local infection
– Tumor
– Immunological disorder
 Bell’s Palsy

• ~ 75% of all acute facial palsy

• Highest incidence 15 – 45 years old
• Incidence in UK 20/100000
• In pregnant women 45/100000
 Bell’s Palsy
Risk Factor
– Pregnancy

– Diabetes mellitus

– Age >30

– Exposure to cold temperatures

– Upper respiratory infection (e.g., coryza, influenza)

– Will it recurrent ?
 Bell’s Palsy
ETIOLOGY

• Inflammation of the facial nerve causes swelling and subsequent

compression of both the nerve and the associated vasa nervorum

• May arise secondary to reactivation of latent herpes virus (herpes

simplex virus type 1) in cranial nerve ganglia

• May arise secondary to ischemia from arteriosclerosis associated

with diabetes mellitus
 Bell’s Palsy
SIGNS AND SYMPTOMS

• Weakness on affected side of face, often sudden in onset

• Pain in or behind the ear in 50% of cases (may precede the palsy in 25% of cases)

• Subjective numbness on the ipsilateral side of the face

• Alteration of taste on the ipsilateral anterior 2/3 of the tongue (chorda tympani
branch of the facial nerve)

• Hyperacusis (nerve to the stapedius muscle)

• Decreased tear production

Diagnostic Approach acute facial weakness
History

• Time course of the illness (e.g., rapid vs. slow onset)

• Any predisposing factors (e.g., recent viral infection, trauma, new

medications, hypertension, diabetes mellitus)

• Presence of hyperacusis or history of recurrent Bell palsy (both

associated with poor prognosis)

• Any associated rash (suggestive of herpes zoster, Lyme disease, or

sarcoid)
 Physical Exam
Neurologic examination to determine if the weakness is due to a problem in
either the central or peripheral nervous systems

• Flaccid paralysis of muscles on the affected side, including the forehead

– Impaired ability to raise the ipsilateral eyebrow

– Impaired closure of the ipsilateral eye

– Bell phenomenon: Upward diversion of the eye with attempted closure of the
lid

– Impaired ability to smile, grin or purse the lips

• Patients may complain of numbness, but on sensory testing, no deficit is present.

• Examine for involvement of other cranial nerves.

Bell’s phenomenon in facial palsy
If a patient tries to close their eyes but is unable to do so on the affected side,
the globe will still move upwards in the usual fashion. The resut is that the
white sclera fills most of the palpebral fissure.
 Skin
• Examine for vesicular
• Examine for rash (herpes zoster
erythema migrans virus).
(Lyme disease) and
 TESTS

• Electromyography

– Nerve conduction on affected and nonaffected sides can

be compared to determine extent of nerve injury.

• Electroneurography

– Evoked potentials of affected and nonaffected sides can be

compared.
 Lab

• Lyme titer and IgM, IgG, and IgA for B. burgdorferi

• Salivary PCR for herpes simplex virus type 1 or herpes zoster virus (these
tests are largely reserved for research purposes)

• IgM, IgG, and IgA titers for varicella zoster virus, cytomegalovirus, rubella,
hepatitis A, hepatitis B, and hepatitis C

• ESR

• Blood glucose level

 Imaging

•Facial radiographs
–Rule out fractures

•CT
–Rule out fractures
–Rule out stroke

•Brain MRI
–Not routinely indicated
–Rule out central pontine, temporal bone, and parotid neoplasms
 Treatment of Bell’s palsy
• Without treatment ---- 70% spontaneous recovery
AAN Guideline:
– Early treatment with oral corticosteroid is probably effective in
improving facial-function outcomes
– Addition of Acyclovir is possible effective
– Insufficient evidence exists to recommend facial-nerve
decompression
• The main aims of the treatment in acute phase : to speed
recovery and to prevent corneal complication
• Treatment should begin immediately to inhibit viral
replication and the effect on subsequent
patophysiological processes that affect the facial nerve
 Treatment of Bell’s palsy

Pharmacologic
• Corticosteroid
– Oral prednisone/methylprednisolone
1 mg/kg/day for 7 days
• In 2 – 14 days after the onset
• Antiviral
– Acyclovir 800 mg five daily
– Valacyclovir 1 gr twice daily for 7 days
– Famciclovir 750 mg three times daily for 7 days
• Mecobalamin
Engstrom, dkk
Lancet Neurol 2008:7:993-100
• Prednisolone vs valacyclovir
---- early prednisolone → shorter recovery time
valacyclovir → no effect
• Valacyclovir + prednisolone ----74% recover
• Prednisolone + plasebo -----70 % recover
• Cochraine, 2004 meta-analysis, RCT
– Steroid + placebo ---not effective to decreased
number of patient with complete recovery after 6
months
– Antiviral alone ---- not effective
– Prednisolone + antiviral --- better than prednisolone
alone (2 studies)
– Treatment after 4 days onset ---no benefit
 NON PHARMACOLOGY THERAPY

• Physiotherapy
– Recover muscle strength
– Method: excercise, thermal, electrotherapy,
massage
• Corneal protection:
– Lubricant
– Tarsoraphy
• Decompression surgery
– Still controversial--- not recommended
– Should not performed ≥ 14 days after onset
• If complete facial paralysis is still present after 1
week of medical treatment

Electroneurography
≥ 90% degeneration , only 50% good recovery
< 90%, 80-100% regain excellent function
 Prognosis of Bell’s Palsy

• 70% untreated patient recover completely

• 84% near-normal function
• 20-30% permanent weakness
 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
 COMPLICATIONS

• Crocodile tears syndrome

After acute facial paralysis, preganglionic
parasymppathetic fibers that previously
projected to the submandibular ganglion may
regrow and enter the major superficial petrosal
nerve. Abberant regeneration lead to
lacrimation after a salivary stimulus
• Tonic facial contraction
• Hemifacial spasm ---- Botulinum toxin injection
 DIFFERENTIAL DIAGNOSIS
Infectious

- Lyme disease/lyme borreliosis

- Herpes zoster (Ramsay-Hunt syndrome)

- Acute or chronic otitis media

- Malignant otitis externa

- Osteomyelitis of the skull base

Ramsay Hunt Syndrome
 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
• Without treatment ----35% recovery
• Acyclovir 4000 mg/day for 7 -10 days, streroid --- no
evidence
 Fractures

Trauma injury

- Temporal bone fracture

- Mandibular bone fracture

 Neoplastic
• About 5% of cases of facial nerve paralysis are
caused by tumors
• Characteristics of facial nerve palsy
• Slow developing
• Additional cranial nerve deficits and or headache
• Recurrent ipsilateral involvement
• Adenopathy
• 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
 Cerebrovascular

- Brainstem stroke involving antero-inferior cerebellar

artery

- Aneurysm involving carotid, vertebral or basilar

arteries
 Other
• Multiple sclerosis

• Myasthenia gravis (should be considered in cases of recurrent or bilateral

facial palsy)

• Guillain-Barre syndrome (may also present with bilateral facial palsy)

• Sjogren syndrome

• Sarcoidosis
 Reference

• Gilden GH. Bell’s Palsy. Clinical Practice. N Engl J Med 2004;351:1323-31

• Sullivan FM, Swan IR, Donnan PT, Morrison JM, Smith BH, McKinstry B, et al. Early
treatment with prednisolone or acyclovir in Bell's palsy. N Engl J Med. Oct 18
2007;357(16):1598-607
• Engström M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valaciclovir in
Bell's palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet
Neurol. Nov 2008;7(11):993-1000
• Gronseth GS, Paduga R. Evidence-based guideline update: steroids and antivirals for
Bell palsy: report of the Guideline Development Subcommittee of the American
Academy of Neurology. Neurology. Nov 27 2012;79(22):2209-13