Facial nerve:

Applied
Dr. Saleh Mohammad Shoaib
Phase-B resident, MD (Neurology)
National institute of
Neurosciences and hospital
 Facial Nerve Examination: Motor
• Inspect the face –
• Any drooping?
• Asymmetry?
• Differences in blinking
or eye closure on one
side?
• Any involuntary
movement?
• Give the following
commands, demonstrate,
ask the patient to copy
you, then observe any
asymmetry –
 Facial Nerve Examination: Motor
• Stapedius muscle: Contracts to
tighten the ossicular chain,
Dampens vibrations passed to the
cochlea via the oval window, thus
protects the inner ear from loud
noises.
• Nerve supply: Nerve to stapedius
(motor branch of CN VII).
• Effect of lesion: Hyperacusis
(high-pitched sounds appearing
unpleasantly louder than normal).
 Facial nerve examination: Taste
• Taste sensation from anterior 2/3rd
of tongue (except vallate papillae)
is carried by chorda tympani branch
of CN VII.
• Ask the patient to protrude the
tongue, and test one side at a time
• Sugar for sweet
• Salt for salty
• Vinegar/lemon juice for sour
• Quinine for bitter sensation
• Rinse the mouth with water after
each step.
 Reflex testing: Corneal reflex
• Afferent: Ophthalmic division of
trigeminal nerve (CN V1).
• Efferent: Facial nerve (CN VII).
• Method:
• Gently depress the lower
eyelid while the patient looks
up.
• Lightly touch the lateral edge
of the cornea with a wisp of
damp cotton wool.
• Look for both direct and
consensual blinking.
 Corneal reflex: Interpretation

Stimulate Direct blinking Consensual

blinking
V nerve Involved eye Absent Absent
lesion Opposite eye Normal Normal
VII nerve Involved eye Absent Normal
lesion Opposite eye Normal Absent
 Examination of facial
nerve in a comatose/non-
cooperative patient
• Inspect for any obvious
asymmetry, droop or deviation.
• Give a painful stimulus
(supraorbital pain), and see the
facial response.
• Test for corneal reflex.
Patterns of facial weakness
• UMN type
• LMN type
Effect of Supranuclear (UMN) Lesions
• Paresis of voluntary movements
of the lower portion of the face
• Contralateral to the affected
hemisphere
• Peri-oral muscles are especially
affected
• Relative sparing of the frontalis
and orbicularis oculi
(sometimes, lower or even the
upper segment of the
orbicularis oculi may be paretic).
 Volitional/voluntary facial paresis
• Volitional facial paresis
(VFP) affects facial
movements with voluntary
effort, sparing activation
on emotion.
• Site of lesion: Cortico-
bulbar tract, at lower
precentral gyrus, internal
capsule, cerebral
peduncle, or upper pons.
• Can be examined by giving
commands as described Fig: (A) VFP (showing the teeth), (B) symmetric
before. activation with emotion (laughing).
 Emotional facial paresis
• EFP = Impaired activation of
face muscles with emotion but
normal voluntary activation.
• Far less common than VFP.
• Sites of lesion: Anterior to the
precentral gyrus, especially if
they involve the right cerebral
hemisphere; and also others.
• Can be tested by provoking a
spontaneous smile by asking
funny questions and telling
hilarious stories.
Fig: (A) Symmetric voluntary activation (showing
the teeth); (B) right EFP while smiling.
Effect of complete unilateral LMN lesions
• While UMN lesions may result in selective
VFP or EFP, LMN facial weakness from
facial nerve palsy affects both equally.
• Unilateral paralysis of all mimetic facial
muscles
• Bell phenomenon: On attempting closure
of eye, the eyeball may deviate up and
out due to relaxation of the inferior
rectus and contraction of the superior
rectus. It represents a normal response,
but seen due to impaired eye closure.
• Food crumbs tend to be retained
between the teeth and the cheek on the
affected side.
 Levels of LMN lesions
• Pons (nuclear and fascicular lesions)
• Posterior Fossa Lesions (Cerebellopontine Angle Lesions)
• Intratemporal lesions
• Lesions distal to the Stylomastoid Foramen
 Nuclear and Ventral
Fascicular
Lesions (Pontine
Lesions)
• Neighboring structures
may occasionally be
involved.

Dorsal
Patterns of pontine lesions
Millard–Gubler Syndrome (Ventral pontine syndrome)
• Site of lesion: ventral pons.
Ventral
• Affected structures:
• Fascicles of the CN VII
• Fascicles of the CN VI
• Corticospinal tract
• Features:
• 1. Ipsilateral peripheral facial
paralysis
• 2. Ipsilateral lateral rectus
paralysis
• 3. Contralateral hemiplegia Dorsal
Millard-
Gubler
Syndrome
Fig: Axial T2-weighted
sequence shows
hyperintense infarct
located ventromedial
on the left part of
pons (white arrow)
and stenosis of basilar
artery (black arrow
head).
 Foville Syndrome (Inferior Medial Pontine
Syndrome)
• Site of lesion: pontine
tegmentum/dorsal pons.
• Affected structures:
• Fascicles of the facial nerve
• PPRF/CN VI nucleus
• Corticospinal tract
• Features:
• Ipsilateral peripheral facial
paralysis
• Ipsilateral lateral gaze palsy
• Contralateral hemiplegia
Foville
Syndrome
Fig: DWI showing an
area of diffusion
restriction is noted at
the left medial aspect
of inferior pons
(green arrow)
indicating acute
infarction.
 Eight-And-A-Half Syndrome
• Site of lesion: Dorsal
paramedian inferior pons.
• Affected structures:
• PPRF or abducens nucleus,
• Medial longitudinal fasciculus
(MLF)
• Nucleus and fascicles of the
facial nerve
• Features:
• Internuclear ophthalmoplegia
(INO) [ipsilateral]
• Horizontal gaze palsy [same
side]
• Ipsilateral peripheral facial palsy
Ipsilateral
involvement of –
1. 7th nerve
nucleus/ fascicle = 7
2. PPRF/CN VI
nucleus = ipsilateral
lateral gaze palsy =
1
3. MLF = ipsilateral
INO = ½
7+1+½ = 8½
Previous patient’s MRI: T2
showing paramedian
tegmental pontine infarct
(arrow).
Common brainstem lesions involving CN VII
• Infarct
• Hemorrhage
• Demyelination
• Infection
• Neoplasm
Fig: Pontine hemorrhage
causing unilateral facial
nerve palsy
Fig: Pontine demyelination
causing left sided facial
nerve palsy
Pontine
tuberculoma
may also
cause facial
palsy!
Fig: Pontine glioma
causing left facial
nerve palsy
 Facial palsy in Lateral
medullary syndrome
• Ipsilateral LMN facial weakness:
Extension of the lesion to inferior pons
to involve CN VII nucleus/ fascicle
(lateral ponto-medullary syndrome e.g.
due to occlusion of VA)
• Ipsilateral UMN facial weakness:
Involvement of supranuclear
corticobulbar fibres, which descend
down in contralateral ventromedial
medulla, decussate at upper medulla,
then ascent up in ipsilateral
dorsolateral medulla to reach CN VII
nucleus.
Subarachnoid space lesions causing CN VII
palsy
• Meningitis –
• Infectious (e.g. TB)
• Inflammatory
• Neoplastic
• CP angle tumours –
• Vestibular schwannoma
• Meningioma
• Epidermoid
• Metastasis
• AVM
• Facial nerve schwannoma etc.
TB meningitis with multiple CN palsy
Vestibular schwannoma (acoustic neuroma)
• 80-90% of CPA mass lesions
• Clinical:
• VIII N: Progressive unilateral hearing loss, usually with tinnitus. Progression results in
unsteadiness, with true vertigo being rare.
• VII N: Late involvement.
• V N: Involvement may occur with tumors > 3 cm (check corneal reflex), with tic douloureux-
like symptoms being unusual.
• Imaging:
• Often heterogeneous signal and nonuniform enhancement.
• Medium size tumors look like ice cream in a cone (IAC is the cone).
• Rarely calcified.
• Except for very small tumors, IAC is frequently enlarged.
• Look for an acute angle between the tumor and the petrous bone (meningiomas usually have
an obtuse angle)
Fig: Vestibular schwannoma. There is an extra-axial abnormal signal
(heterogeneous hyperintense in T2) mass lesion in the right CP angle
with extension into the internal auditory canal and heterogenous avid
enhancement after contrast injection.
The ice cream cone sign in
vestibular schwannoma

Cone: IAC component

Ice cream ball: CP angle
(cisternal) component.
 Meningioma
• 5 – 10% of CPA mass lesions
• Clinical:
• Since they often arise from the superior anterior edge of the IAC, early facial
nerve involvement is more common, and hearing loss is usually late.
• Trigeminal neuralgia-like pain is more common than with VSs.
• Imaging:
• Homogeneous signal and enhancement.
• The tumor may enter the IAC but it tends not to enlarge it.
• IAC often eccentric in tumor.
• Tumor is flat against petrous bone with an obtuse angle to the bone.
• Calcification and bony hypertrophy may occur (which occasionally narrows the
IAC).
CP angle
meningioma
Fig: Left CP angle dural
based solid mass
extending into and mildly
expanding the left IAC.
It has vivid and
homogeneous contrast
enhancement.
Dural tail sign in
CPA
meningioma

Fig: Right CPA

meningioma with
extension in the IAC
(arrow). Notice the
linear tail of dural
enhancement (small
arrow).
Fig: Epidermoid cyst in the CP angle. The lesion
has a similar signal intensity to CSF on both T1
and T2 weighted sequences but is 'dirty' on FLAIR.
The diagnosis is confirmed on DWI which
demonstrates very bright signal with intermediate
ADC values similar to brain parenchyma.
Fig: Facial nerve
schwannoma
Intra-temporal lesions causing CN VII palsy

• Bell’s palsy
• Ramsay-Hunt syndrome
• Intratemporal facial nerve schwannoma
• Temporal bone fracture
• Temporal bone neoplasm
• Complicated otitis media with mastoiditis (e.g. Gradenigo
syndrome)
Lesions Affecting the
Meatal (Canal) Segment
of the Facial Nerve in the
Temporal Bone
• In the temporal bone, CN
VII lies close to the CN VIII.
• Lesions at this site e.g.
temporal bone fractures,
10 or 20 tumors, result in
clinical findings similar to Diagram of relationship of nerves in the internal
those seen with the CP acoustic meatus: VII = facial nerve, NI = nervus
angle syndrome, except for intermedius, VIIIc = cochlear nerve, VIIIvs =
lack of hyperacusis. superior division of vestibular nerve, VIIIvi =
inferior division of vestibular nerve
 Bell’s palsy
• Self-limited, typically monophasic facial
nerve palsy of acute-subacute onset.
• Features:
• facial weakness
• Pain (60%)
• Impaired lacrimation (60%)
• Taste changes (30%–50%)
• Hyperacusis (15%–30%).
• Imaging:
• Internal auditory canal MRI often
reveals enhancement of the facial
nerve, most commonly at the
geniculate ganglion.
 Fig: Coronal MRI post-contrast images show
vivid enhancement in the right geniculate
ganglion.

• Etiopathogenesis: Although considered

idiopathic, HSV and VZV reactivation in
the geniculate ganglion have been
implicated in its pathogenesis.
• Rarely, recovery may be followed by –
• Motor synkinesis (e.g. contraction
around the mouth with eye blinking)
• Prognosis: 85% spontaneously recover • Myokymia
normal facial function in 3 weeks. • Blepharospasm-like activity
• Recurrence: Bell palsy may be recurrent,
but alternative causes such as Lyme disease
or sarcoidosis must be considered.

Other effects of
aberrant regeneration
• Crocodile tears (Bogorad syndrome):
Profuse tearing from same sided eye
during eating.
• Cause: Regenerating autonomic fibers
abnormally re-innervate lacrimal gland
instead of salivary gland.
• Gustatory sweating (Frey syndrome):
Profuse sweating and flushing while
eating.
• Cause: Aberrant reinnervation of
postganglionic parasympathetic
neurons to nearby denervated sweat
glands and cutaneous blood vessels.
 Ramsay Hunt syndrome (Herpes zoster oticus)
• Pathology: Reactivation of latent varicella
zoster virus (VZV).
• Involved structure: Geniculate ganglion.
GG
• Features (ipsilateral):
• Peripheral facial paralysis
• Hyperacusis
• Impaired taste
• Geniculate neuralgia
• Herpetic vesicles involving the
eardrum, external auditory meatus,
or palate.
• May accompany hyperemia of the
concha or helix, and
vestibulocochlear dysfunction.
• Facial paralysis may sometimes develop
without the herpetic rash (zoster sine
herpete).

Fig: Unilateral distribution
of clusters of vesicles on
the left side of the face
and tragus of the ear.
Fig: Unilateral distribution
of clusters of ulcers on the
buccal mucosa, labial
mucosa, tongue and palate
Fig: Left complete peripheral facial
on the left side.
nerve palsy.
History of recent
head trauma, now
presented with right
facial palsy.

Fig: Longitudinal
fracture (red
arrows) is seen
traversing the
mastoid portion of
the facial bony canal
(yellow arrow) of
right temporal
bone.
Gradenigo syndrome
• Triad of:
• suppurative otitis media, persistent
otorrhea and ear pain
• CN VI palsy, due to involvement as it
passes through Dorello canal
• retro-orbital pain, or pain in V1 & V2
region
• May involve facial nerve
• Consequence of CSOM spreading to
the petrous apex of the temporal bone,
resulting in petrous apicitis. The Fig: T1 with contrast - left petrous apex is of
inflammation affects nearby structures intermediate to low signal intensity with
(CN V ganglion, CN VI, sometimes CN VII).
peripheral irregular enhancement.
Fig: Facial nerve schwannoma involving the right mastoid segment of the facial
nerve canal.
Fig: CT scan images (axial
view) showing lytic lesion in
the left temporal bone with
erosion of the mastoid air
cells.

Dx: Left temporal bone

metastasis causing left facial
nerve palsy.
Lesions distal to stylomastoid foramen
causing facial nerve palsy
• Parotid neoplasms
• Surgical procedures
• Infiltration of facial skin cancers along facial motor nerve branches
• Retromandibular lymphadenitis
• Parotitis
• Parotid abscess
• Sarcoidosis
• Infectious mononucleosis
• Lyme disease etc.
 Lesions distal to stylomastoid foramen
causing facial nerve palsy
• All or some individual motor branches may be affected, causing isolated
paralysis of a few individual facial muscles.
• Either the upper or lower facial muscles may be affected in isolation. This
may lead to diagnostic confusion with an UMN lesion when only the lower
facial musculature is involved.
• Taste changes and hyperacusis do not typically occur with these lesions,
given their distal nature.
What are the findings?
Lyme Disease with
Erythema Migrans
& Bell's Palsy
Some causes of bilateral LMN facial nerve
palsy
• Guillain-Barre syndrome
• Lyme disease
• Sarcoidosis
• Bacterial meningitis
• Leprosy
Some interesting syndromes
 Melkersson–Rosenthal
syndrome

• Triad of –
• Persistent or
recurrent orofacial
edema
• Relapsing facial
paralysis
• Fissured tongue

(A) Lips: swollen; Tongue: geographic and fissured.

(B) Same patient afterwards with facial palsy; lips
normal.
Moebius syndrome

• Extremely rare
• Present at birth
• Paralysis of the muscles in the
face which control expression
and lateral eye movements. 
 Parry-Romberg
syndrome
• Progressive facial hemiatrophy
• Over time, the soft tissue
(muscle and fat) gradually
shrinks, the facial bones may
change, and the skin may
become thin.
Some conditions causing bifacial weakness
(but not nerve palsy)
Myasthenia gravis: Weakness of facial muscles results in expressionless
appearance. On smiling, buccinator weakness produces a characteristic
smile (myasthenic snarl).
Myotonic dystrophy: bilateral
face weakness with thin facial
muscles
Abnormal Facial Movements
What is it?

Hemifacial
spasm
Hemifacial spasm
• Painless, irregular clonic contractions on one
side of the face.
• Adult onset (40 – 60 yrs of age, F > M).
• Pathogenesis: Compression of motor root
of CN VII with segmental demyelination.
• Cause: Neurovascular compression at CPA
(AICA commonest, PICA, VA, BA), also other
vascular and non-vascular lesions (tumour,
AVM, aneurysm) compressing CN VII.
• Treatment:
• Medical: Carbamazepine, botox injection
• Surgical: Microvascular decompression
(highly effective). Fig: Preoperative 3T MRI: FIESTA. Red
arrow: AICA loop. White arrow: facial
nerve at root exit zone. 
Pre-operative MRA MRA after 6 months of surgery
Before
surgery
Microscopic
view of the
longitudinal
loop that the
small branch
from the AICA
made around
the facial nerve.
 After
surgery
Microvascular
decompression with
Teflon sponges placed
between the AICA and
the mobilised offending
vessel and the
acousticofacial bundle.
The facial spasm
disappeared in the
immediate
postoperative period. 
What is it?

Facial
myokymia
 Facial Myokymia
• Fine, continuous, rippling, undulating
movements of the facial muscles (“bag
of worms”).
• Pathology: Mostly due to pontine
tegmental lesions involving the
postnuclear, postgenu portion of the
facial nerve, perhaps due to a “release
phenomenon” in the facial nerve
nucleus.
• Cause:
• Multiple sclerosis
• Tumor etc.
Fig: Left sided facial myokymia. Brain MRI: white
matter T2 hyperintensities. Dx: Multiple
Sclerosis.
QUIZ
Q. Which of the following presents with
lower facial weakness with sparing of upper
face?
A. Involvement of cortico-bulbar tract at cerebrum
B. Involvement of cortico-bulbar tract at internal capsule
C. Lateral pontomedullary syndrome
D. Some cases of lateral medullary syndrome
E. Isolated involvement of lower facial branches of facial nerve

Ans: A, B, D, E
What is it?
Ramsay-Hunt syndrome (Left)
What does the
image show?
Bilateral LMN type facial nerve palsy (with
Bell’s phenomenon)
What is it?
Right sided mastoiditis with right facial nerve palsy
 Case scenario
A 59 yrs old female developed sudden right sided weakness and double
vision most prominent in looking leftward. She has facial deviation to
right and isolated abduction failure of left eyeball.

What is the syndrome called?

Millard-Gubler Syndrome (Left)
THANK YOU