FACIAL PALSY

Vivien Puspitasari

CASE

A 42 year old man noticed while shaving one morning that he was
unable to move the left side of his face. He worried that a serious
problem possibly a stroke might have occurred. He had influenze-like
symptoms the week before this sudden attack.

CASE

General Exam : Normal

Neurologic examination : the patient could not wrinkle his

forehead on the left side or show his teeth or purse his lips on
that side. He had trouble closing his left eye. Taste sensation
was abnormal in the left anterior two-thirds of the tongue, and
a test to determine tear secretion showed that secretion on
the right side was normal, but the left lacrimal gland produced
little fluid. Loud noises caused discomfort in the patient, who
was in good health otherwise, and there were no additional
signs or symptoms.

What is the differential diagnosis?

What is the most likely diagnosis

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

From geniculate ganglion 11mm

Mastoid

segment

segment

Exits the stylomastoid foramen 13mm

Extracranial From stylomastoid foramen

CRANIAL NERVE VII - FACIAL

NERVE

Corticobulbar Tract

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

FACIAL NERVE DISORDER

Reduce function (palsies)
Excessive activation of facial nerve-innervated
muscles e.g hemifacial spasm

Facial neuropathy
Infectious
Inflammation
Neoplastic
Trauma

The most common cause of acute facial

paralysis :
Central : Stroke (hemisphere)
Peripheral :

Bells palsy
Herpes zoster oticus
Stroke (brainstem)

PERIPHERAL FACIAL NERVE PALSY

Primary (75%) /idiopathic Bells palsy
Secondary (25%)

Systemic

viral infection

Trauma
Surgery
Diabetes
Local

infection
Tumor
Immunological disorder

BELLS PALSY
~ 75% of all acute facial palsy
Highest incidence 15 45 years old
Incidence in UK 20/100000
In pregnant women 45/100000

BELLS PALSY
Clinical picture varies, depending on the location
of the lesion of the facial nerve along its course to
the muscles
Symptom:

facial

weakness with maximal onset developing

within two days, associated symptoms : hyperacusis,
decreased production of tears, altered taste,
otalgia/retroauricular pain

BELLS PALSY
Risk Factor
Pregnancy

Diabetes mellitus

Age >30

Exposure to cold temperatures

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

Will it recurrent ?

BELLS 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 and herpes zoster virus) in
cranial nerve ganglia
May arise secondary to ischemia from arteriosclerosis
associated with diabetes mellitus

BELLS 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

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.

Bells 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.

EVALUATION

Laboratory
Not

routinely
Blood glucose/ Hb A1C

Radiology
X-ray
CT

scan / MRI

Electromyography/Electroneurography

TREATMENT OF BELLS PALSY

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 BELLS PALSY

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 facialnerve decompression

TREATMENT OF BELLS PALSY

Corticosteroid
Oral

prednisone 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

Decompression
Still

controversial
Should not performed 14 days after onset

TREATMENT OF BELLS PALSY

Physiotherapy
To

improve muscle contraction

exercise, thermal, electrotherapy, massage

Corneal protection: lucricant

Tarsoraphy,

cosmetic surgery

PROGNOSIS OF BELLS PALSY

71% untreated patient recover completely

84% near-normal function

20-30% permanent weakness

COMPLICATION
Crocodile tears syndrome
Tonic facial contraction
Hemifacial spasm

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

PROGNOSIS OF BELLS PALSY

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

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
IIINormal 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

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

Ramsay Hunt Syndrome

RAMSAY HUNT SYNDROME

Without
Steroid

treatment 35% recover spontaneously

---- no evidence

Acyclovir

4000 mg/hari for 7 10 hari

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