Facial Nerve Paralysis

Chapter
Facial Nerve
Paralysis
Otology could be a dull way of life without 7th cranial

nerve arrogantly swerving through the temporal bone to
the muscles of facial expressions
John Grooves
Introduction
Facial nerve is a mixed nerve containing motor, sensory (nervus
intermedius or nerve of Wrisberg), secretomotor and taste fibers.
It is the most common cranial nerve to be paralyzed. Its long
bony course makes the nerve prone to trauma by temporal
bone fractures while its shortest and narrowest labyrinthine
segment is more vulnerable to vascular injury (ischemia). This
makes the labyrinthine segment the most common segment
to be involved in Bells palsy. Abnormalities like dehiscence of
fallopian canal can make it prone to infection and iatrogenic
trauma. Regardless of the cause, facial nerve paralysis is
associated with loss of emotional and voluntary facial
expression, thus inflicting psychological trauma to the patient.
Surgical Anatomy
It is a nerve of 2nd branchial arch having motor and sensory
(nervus intermedius) roots. It contains voluntary fibers from
precentral gyrus, which course down through the internal
capsule to brainstem that involuntary emotional fibers
originating in more central areas of brain (Thalamus and
Hippocampus). It also has secretomotor relay fibers from
salivatory nucleus (Nucleus Tractus Solitarius).
Facial Nerve Paralysis
Fig. 8.1: Facial nerve segments
Intracranial Course (Fig. 8.1)

Facial nerve originates in Pons in facial motor nucleus, which has
two halves. In upper half, impulses are received from precentral
gyrus of both sides and innervate upper part of face. Lower
half receives impulses from opposite precentral gyrus only
and innervates lower half of face. Root of the facial nerve after
leaving its nucleus in pons, hooks around 6th nerve nucleus
forming the Facial Colliculus. This first bend is also known as
the internal genu. Hence, facial nerve nuclear paralysis is always
associated with paralysis of 6th nerve.
After leaving pons, facial nerve crosses cerebellopontine
angle with 8th nerve and nerve of Wrisberg (nervus inter
medius). The latter has secretary fibers to lacrimal, sublingual,
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Otology an Overview
submaxillary salivary gland and also contain the fibers carrying

back to Pons, taste sensation from anterior 2/3rd of tongue and
sensations like pain, temperature and touch from posterior
wall of EAC.
Intratemporal Course (Fig. 8.2)

In Internal auditory canal (IAC), facial nerve and nervus
intermedius join to form a common trunk and lies above the
acoustic nerve, i.e. anterosuperior in internal auditory meatus
(IAM). At the fundus of IAC, facial nerve enters a separate 33
mm long bony canal named after anatomist Gabriel Fallopius
who called this canal as fallopian aqueduct. Facial nerve is also
covered with a fibrous sheath (prolongation of dura mater)
from IAM to the terminal branches of facial nerve. Part of facial
nerve between its entrance into fallopian canal and geniculate
ganglion is called labyrinthine segment because it lies between
cochlear and vestibular labyrinth. It is shortest (5 mm) and
narrowest (0.68 mm) of all the segments of facial nerve.
Fig. 8.2: Intratemporal course
Labyrinthine segment gives way to the tympanic part,

proximal end of which is marked by geniculate ganglion and
distal end by pyramidal eminence. Tympanic segment begins
at geniculate ganglion where it makes a right angle turn known
as the 1st genu. Length of tympanic segment is 12 mm.
Frequent dehiscences are seen in this part. Two branches
arise from geniculate ganglion:
1. Greater superficial petrosal nerve (secretomotor fibers to
lacrimal gland).
2. Lesser superficial petrosal nerve (secretary fibers to parotid
gland).
At pyramidal eminence, the fallopian canal makes another
right angled but more gentle turn called the 2nd genu.
This area of facial nerve is prone for injury during surgery.
3. A branch of facial nerve, i.e. nerve to stapedius arises from
here.
Vertical segment or mastoid segment begins at second
genu and ends at stylomastoid foramen. It is 13 mm in
length and is the longest intratemporal segment (Table 8.1).
4. Chorda tympani the fourth branch arises from distal 3rd
of mastoid segment containing secretomotor fibers to the
submaxillary and sublingual gland and taste sensation
from anterior 2/3rd of tongue (Fig. 8.3).
Extracranial Course
Facial nerve comes out of funnel shaped stylomastoid foramen
giving rise to other branches.
Table 8.1: Length of various segment of facial nerve

Part
Length in mm
Brainstem to entrance of IAC
2324 mm
Internal auditory meatus
512 mm
Labyrinthine segment
2.56 mm
Tympanic segment
711 mm
Mastoid segment
916 mm
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Otology an Overview
Fig. 8.3: Facial nerve components

1. Posterior auricular nerve supplying small muscles of
auricle.
2. Branch to posterior belly of digastric.
Both above branches can be severed without causing
subjective disability allowing facial nerve, after being freed from
its attachments, to be displaced upwards several millimeter
in the fallopian canal for approximation of ends when a small
segment is missing. Extracranial segment gives rise to two main
branches that divides into several small branches forming Pes
Anserinus or Goose foot (Fig. 8.4).
A. Temporal
B. Zygomatic
C. Buccal
D. Mandibular
E. Cervical
Fig. 8. 4: Pes anserinus

Covering of the facial nerve includes:
a. EndoneuriumLayer around each nerve fiber.
b. PerineuriumMany tubules are held together in bundles
by perineurium.
c. EpineuriumMany bundles are held together by
epineurium to form nerve trunk.
Blood Supply
Stylomastoid artery (stylomastoid branch of postauricular
artery)
Superficial petrosal branch of middle meningeal artery
Labyrinthine artery
Anterior inferior cerebellar artery.
Anomalies of Facial Nerve

Dehiscence of facial canal
The most common in tympanic portion
Geniculate ganglion
Mastoid segment
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Otology an Overview
Nerve crossing tympanic cavity between oval and round

window
Nerve emerging from temporal bone at pyramidal eminence
Nerve crossing promontory inferior to both oval and round
window
Nerve divided and embracing crura of stapes
Backward hump at pyramidal eminence
Bifurcated or trifurcated mastoid segment
Facial nerve represented by fibrous strand
Trunk may occasionally divide within temporal bone prior
to exiting the stylomastoid foramen.
In view of these anomalies, every patient undergoing ear
surgery must be informed about possibility of facial paralysis
even though it is rare.
High Points
1. Facial
Sinus plate
nerveisisthicker
a nervethan
of 2nd
thebranchial
dural plate
arch.
2.
2 Type
The nerve
III pneumococci,
consists of influenza
10,000 motor
B, Type
and
B haemophillus
sensory fibersinfluenzae
of which have
70%
dubiousare
(7000)
reputation
myelinated
for motor
causingaxons
complications.
to facial muscles and 30% (3000)
3 are
Typesensory
III pneumococcal
and parasympathetic
infection is common
fibers. in infancy, old age, diabetics.
3.
4 33
Intracranial
mm longcomplications
passage for facial
cannerve
be multiple
in the temporal
in 1/3rd bone
of patients.
was described
5 by
Dura
Anatomist,
is tightly Gabriel
bound Fallopius.
to bone inFallopius
posterior
called
fossathis
and
canal,
loosely
an aqueduct.
bound in
4. Intracranial
middle fossasegment of facial nerve from brainstem to IAM is 24 mm and
6 intratemporal
Extradural abscess
from fundus
between
of IAM
lateral
to stylomastoid
sinus and bone
foramen
is called
is 2830
perisinus
mm.
5. Sheath
abscess of facial nerve begins in the internal auditory meatus as a
7 prolongation
In osteothrombophlebitic
of dura, as extension
the nerve leading
enters the
to lateral
labyrinthine
sinus thrombosis,
segment
bony
of
fallopian
sinus plate
canal.and
Thisouter
sheath
dural
becomes
wall mayprogressively
be found intact.
strong and well
8 developed
Normal lateral
as the
sinus
nerve
is soft,
approaches
compressible
stylomastoid
and glistening
foramen.
bluish in color
6. Greater
while diseased
superficial
sinus
petrosal
is firm,nerve
opaque
is the
andfirst
white.
branch of facial nerve that
9 arises
Normalfrom
pressure
geniculate
of CSFganglion.
is 80-120 mm H2O
10
7. Labyrinthine
Ratio of frequency
segment
of temporal
(part oflobe
facial
abscess
nerveand
between
cerebellar
its entrance
abscess isinto
2:1
11 fallopian
Cerebral abscess
canal and
of otogenic
geniculate
variety
ganglion)
is pearisshape
the shortest
(narrow(5
near
mm)
contex
and
and wider towards
narrowest
(0.69 mm)
ventricle)
part of fallopian
and cerebeller
canal.abscess is ovoid or irregular.
12
8. Area
Hypodense
proximalarea
to the
surrounded
geniculatebyganglion
enhancing
is prone
ring to
is called
ischemia
Ring
for sign
two
(radiological appearance) which is seen in brain abscess.
reasons:
13 Anatomical
It is narrowest
asymmetry
part ofoffallopian
mastoidcanal
process is seen in 12% of population.
14 30 %
Unique
of thevascular
petroussupply,
bonesi.e.
have
poor anastomosis
air cells extending
between
to apex.
arterial system.
15
9. 33
Raremm
symptoms
long fallopian
of petrositis
canal isare
oneTransient
of the most
facialconsistent
palsy, mild
landmark
recurrent
of
vertigo and
temporal
bone.
fever.
Facial Nerve Palsy

Classification Depending on Site of Lesion (Fig. 8.5)
A.

B.

C.
Supranuclear type
On opposite side of causative lesion
Upper part of the face is spared
Spastic type
Emotional movement and muscle tone is preserved.
Infranuclear type
Same side of the causative lesion
Flaccid type
Upper part of face is also involved.
Nuclear type: Features similar to infranuclear type.
Etiological Classification
Intracranial
Intratemporal
Extratemporal.
Fig. 8.5: Facial nervesupranuclear and infranuclear lesions
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Otology an Overview
Classification Depending on the Cause

Congenital (inherited or developmental)

Infectious
Traumatic
Neoplastic
Miscellaneous.
Classification Based on Degree of

Pathological Damage
A. Neuropraxia: Physiological and reversible block with no
anatomical disruption. It is temporary and associated with
full return of function.
B. Axonotmesis: Axon sheath is intact but axon is divided.
Distal degeneration of nerve fibers occurs.
C. Neurotmesis: Whole nerve is severed. Degeneration of
distal segment occurs. Greater propensity to mismatch
and neuroma may form.
Sunderlands Classification (1951)

Class I (1st degree) Akin to the physiological block (neuro
praxia). Only axonal flow is affected.
Class II (2nd degree) Division of individual axon but not of
surrounding perineurium.
Class III (3rd degree) Axon and perineurium are divided but
not endoneurium.
Class IV(4th degree) Axon, perineurium and endoneurium
are all divided but not nerve sheath
(class II, III, IV corresponds to axo
notmesis).
Class V (5th degree) Total severance of nerve (Neurotmesis).
(Note: Class IV and class VScarring prevents regrowth of
axon. Hence, no spontaneous recovery is seen).
Classification of Recovery and its Grading by House

and Brackmann (HB)
HB Grade I Recovery complete.
HB Grade II Recovery fair with noticeable abnormality.
HB Grade III Incomplete, moderate recovery

HB Grade IV Incomplete poor recovery
HB Grade V No recovery.
Pathology of Nerve Injury

After injury, axoplasm is gradually depleted by catabolism at
a constant rate, which needs to be replenished by the parent
neuron. If it is not replenished, loss of axon will occur in
approximately 29 days. Rate of flow of axoplasm from parent
neuron is 1 mm/day or 1 inch/month. This is also a rate of
degeneration of axon when nerve is cut.
Axon of peripheral segment of nerve, unable to feed fresh
axoplasm because of pressure or sectioning, live on for 23 days
with continued electrical excitability but without conduction
of impulses across the site of injury.
1. Neuropraxia: Little axoplasm can be siphoned off and
hence temporary but reversible loss of conductivity.
2. Axonotmesis: Pressure sufficient to block replenishment
of axoplasm completely. After several days, death of axons
results.
3. Neurotmesis: Entire nerve trunk dies due to continued
severe pressure or sectioning.
Regeneration
Single regenerating axon is likely to branch out and enter
Schwann cells of several tubules whereas single Schwann
cell may be shared by many small axons. Thus, the axon that
supplied a single muscle previously, now supplies widely
separated muscles causing synkinesis or disassociated
movements (e.g. crocodile tears).
Etiology

Congenital
Infective
Neoplastic
Traumatic.
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Otology an Overview
Congenital facial palsy or facial palsy at birth can be

Traumatic (birth trauma)
Inherited or developmental.
Birth Trauma
Prolonged or difficult labor
Use of forceps.
Search should be made for signs of temporal bone or facial
injury such as hematoma or laceration, hemotympanum or
ecchymosis over the mastoid.
Investigations:
CT scan for fracture of fallopian canal or concealed fracture
Brainstem evoked response audiometry (BERA) for hearing
assessment
Progressive decline in amplitude of compound action
potential.
Birth trauma is generally associated with I, II, III degree
injury and spontaneous recovery will occur. IIIrd degree injury
in patients later life may manifests as hyperkinesis or synkinesis.
Inherited or Developmental Disorder

Inherited
Associated with abnormality of craniofacial structures
Ear, palate, maxillary deformities with other cranial nerves
deformity
Myotonic dystrophy and Albers Schenberg disease are two
types of facial paralysis that may be inherited.
Developmental
Developmental disorders (Fig. 8.6) like
Moebius syndrome: Multiple cranial nerve palsy especially
6th nerve palsy with unilateral or bilateral facial palsy.
CHARGE syndrome: Coloboma, Heart defect, Atresia
choana, Retarded growth, Genital hypoplasia, Ear
abnormalities.
Oculo-auriculo-vertebral (OAV) syndrome.
Fig. 8.6: Facial nerve palsy due to developmental disorder

In contrast to traumatic causes, inherited or developmental
cases are associated with

1. No response to electromyography (EMG)

2. No change with serial testing.
Infections
Bells palsy (Viral)
Herpes zoster cephalicus/Herpes zoster oticus/Ramsay Hunt
syndrome
Lyme disease
Acute and chronic otitis media (cholesteatoma or granulation
tissue)
Malignant otitis externa
Mastoiditis (acute or acute exacerbation of chronic mas
toiditis)
Infectious mononucleosis.
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Otology an Overview
Neoplastic
Tumors of facial nerve Schwannoma (sites CP angle, IAM,
temporal bone, chorda tympani)
Meningioma
Angioma
Intraosseous hemangioma
Tumors of parotid gland
Adenoid cystic carcinoma
Mucoepidermoid tumor
Acoustic neuroma causing facial palsy
Others like
Squamous cell carcinoma
Basal cell carcinoma
Metastatic tumor
Adenocarcinoma
Mesodermal neoplasm, hemangioma, primary chole
steatoma.
Traumatic
Iatrogenic injury:
Parotid surgery
Otologic surgery
Temporal bone fracture:
Immediate or late
Complete or incomplete
Longitudinal fracture 10% chances of palsy
Transverse fracture 40% chances of palsy
Gunshot Injury
Birth trauma.
Causes
A. Intracranial Palsy
a. Brainstem

VascularThromboembolism, hemorrhage

TraumaBrainstem trauma due to head injury

InfectionPoliomyelitis, diphtheria, infective poly
neuritis

b.

Tumor
Disseminated sclerosis.
Between brainstem and IAM
Trauma: Fracture skull base
Excision of acoustic neuroma
Surgery of trigeminal ganglion
Meningitis
Nonspecific
Tubercular
Syphilitic.
Tumors
Acoustic neuroma
Tumors of CP angle.
B. Intratemporal (90%)

Idiopathic Bells palsy (66%)

Trauma: Head injury with fracture of temporal bone
Contusions
Postoperative
Mastoidectomy
Stapedectomy
Tympanoplasty
Penetrating injury of middle ear
Infections
Complications of acute or chronic otitis media
Mastoiditis
Herpes zoster oticus
Tumors
Benign
Malignant tumor
Iatrogenic.
C. Extracranial
Trauma: Birth trauma
Prolonged and difficult labor
Forceps delivery
Facial injury
Postoperative
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Otology an Overview
Ear or parotid surgery

Low postaural incision in children
Tumors: Metastatic lymph node in upper part of posterior
triangle of neck
Parotid tumor.
D. General

Congenital agenesis of nerve

Diabetes
Lead poisoning
Infection like poliomyelitis, diphtheria, syphilis, sarcoidosis
Fungal infections
Granulomatous lesion.
E. Syndromal Association
Moebius syndrome
Bilateral facial nerve palsy
Unilateral or bilateral 6th nerve palsy
Abnormalities of extremities
Involvement of other cranial nerves VIIIXII
Dystrophica myotonica
Thalidomide embryopathy
Melkersson Rosenthal syndrome.
High Points
1. Sir Charles Bell (1829) demonstrated that motor innervation of the
muscles of expression is by 7th cranial nerve.
2 For many years after Bells demonstration, all cases of facial palsy were
called Bells palsy.
3 Delay in blinking may be the earliest manifestation of facial palsy.
4 Vascular flaring of posterosuperior aspect of tympanomeatal area is seen
due to red Chorda tympani nerve in Bells palsy.
5. Taverner (1959) gave criteria for Bells palsy
Paralysis of all the muscle group of one side of face
Sudden onset
Absence of signs of CNS disease
Absence of signs of ear or CPA disease
6. In 90% of patients, facial palsy is due to disease within temporal bone.
7. Seddon (1943) and Sunderland (1951) classified facial palsy depending
on the degree of pathological damage.
Contd...

Contd...
8. After facial palsy, i.e. injury to facial nerve, Wallerian degeneration takes
place in 34 days following injury and distal nerve excitability is preserved
for 34 days.
9. Other cranial nerve palsy if seen along with facial nerve, systemic or
central cause should be suspected.
10 Regenerating axons grows at the rate of 1 mm/day.
Evaluation of Facial Nerve Palsy

The aim is to know the cause, site of lesion and fate of facial
palsy.
History and evaluation is done to explore following areas:
Is palsy idiopathic or with some cause?
Is it incomplete or complete?
Is it sudden or delayed (in case of trauma)?
Is it recurrent? Is it progressive?
Is it unilateral or bilateral?
Non-degenerating or degenerating (degree and depth of
injury).
Causes of bilateral facial nerve palsy
Guillain Barre syndrome
Leukemia, sarcoidosis
Skull fracture
Moebius syndrome
Rabies, lyme disease
Infectious mononucleosis
General Evaluation
A. Facial examination
Observing patients face at rest and during movements
Looking for emotions, asymmetry, hemifacial spasm, tics
Blink test:
Delay in blinking at rest may be the earliest manifestation
of facial palsy. Patient is asked to stare at the examiner
who then suddenly taps patient on glabella with forefinger. Resulting blink is studied and delay in blinking on
one side may be due to facial weakness.
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Otology an Overview
Testing facial movements

Wrinkling the forehead and elevating eyebrows (Tem
poral branch)
Screwing up eyes (Zygomatic)
Wrinkling nose (Buccal)
Showing teeth and blowing out cheek (Mandibular).
B. Ear examination
Careful examination for cholesteatoma (attic), ASOM, CSOM,
malignant otitis media, tubercular otitis media and for any
other signs of middle ear disease.
Red chorda tympani (vascular flaring of posterosuperior
aspect of tympanomeatal area) is seen in Bells palsy.
C. Audiometry
Unilateral SNHL-CP angle tumor and acoustic neuroma
Investigations to rule out cochlear and retrocochlear lesion,
BERA.
D. Vestibular function test; useful in

Ramsay Hunt syndrome
Tumors in IAM
CNS disorder.
E. X-ray evaluation of temporal bone for tumor/trauma/

tuberculosis/cholesteatoma (congenital or acquired).
F. Carotid or vertebral arteriogram.
G. High resolution CT scanTumors in facial canal, CP
angle.
H. MRI scan.
I. X-ray chest, mastoid.
Topognostic Tests

Tearing (greater superficial petrosal nerve)

Salivation (greater superficial petrosal nerve)
Taste (chorda tympani)
Stapedial reflex (nerve to stapedius).
Fig. 8.7: Schirmers test

a. Tearing (Schirmer test )
Dry piece of blotting paper, 0.1 mm thick, 5 mm wide
and 30 mm long is hooked on to lower eyelid for 5
minutes (Fig. 8.7). Distance of filter paper, which is wet
is compared with normal side. Abnormal Schirmer test
is decrease of lacrimation of 75% or more on affected
side as measured by amount of paper soaked by tears
on each side or a bilateral decrease in lacrimation. This
should be less than 10 mm for both sides at 5 minutes
(Lambert and Brackmann). At times unilateral injury to
geniculate ganglion can paradoxically cause B/L reduction
in lacrimation.
b. Submandibular salivary flow after cannulating submandibular salivary duct
Salivary flow is tested for:

Consistency

Flow

pH

Secretion rate.
These are also prognostic indicator for facial palsy
Sialometry
Polythene tube is passed into Whartons duct and salivation
is provoked by stimulation with 6% citric acid. Measurement
of number of drops of saliva from each side during one
minute or until total flow reaches 25 drops is done.
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Otology an Overview
c. Taste test

For manual test of taste sensation salt (NaCl), sweet
(sugar), bitter (chloroquine tablet) can be used. Tongue
is gently rubbed with the cotton bud soaked in the
solution being tested after patient is asked to protrude
tongue (chemical gustometry).

Electrogustometry: Small current is applied to the
lateral border of protruded tongue in its anterior 2/3rd
via a metal rod. Current is slowly increased till patient
receives metallic taste. Normal threshold is 1 mA, which
may be raised to 4 mA if chorda is involved.
d. Stapedial reflex
Loud noise is put in either ipsilateral or contralateral ear.
Reflex causes stapedial tendon to contract suddenly.
This may be seen on tympanometry as a flick. However,
absence of the reflex may be result of many other
disorders. If the reflex is absent in view of normal hearing,
then the site of lesion is likely to be between the geniculate
ganglion and the stapedius muscle.
These topognostic tests have little value in localizing site of
lesion. In acute conditions, this has limited value while in chronic
conditions, no or very little value due to following reasons:
Variable anatomy or branches of facial nerve allowing axon
to take a variety of alternative pathways to reach their
destination
Different components of nerve at various level with different
degree of severity
Recovery of various components may occur at different
times
Techniques used to measure the various facial nerve
functions may not be completely reliable.
Electrophysiological Tests
Aim
1. To know degree of degeneration
2. To know potential for recovery.
Prognosis in acute facial palsy can be determined by serial
electrical testing. However, electrical tests cannot provide
status of the facial nerve in the immediate post-injury state.
Three types of test are:

1. Maximal stimulation test.
2. ElectromyographyUseful when degeneration has
already occurred and done by 10th or 14th day following
onset.
3. ElectroneuronographyThis is done in 1st week following
paralysis when early or immediate degeneration is known.
Maximal Stimulation Test (MST)

Duchenne for the first time suggested an excitability test but it
was first described by May et al. in 1971.
MST is of limited value until 35 days after onset of
paralysis
Once the nerve degenerates and response to electrical
excitability is lost, the test is no longer useful
Since, it need comparison with the other side, it is not
useful in recurrent, alternating and bilateral paralysis.
Nerve Excitability Test (Minimal Excitability Test)

Commercially available nerve stimulator is used. Ground
electrode is placed over stylomastoid foramen and active
electrode is used to stimulate individual nerve fiber. Two sides
are compared and 3.5 mA differences between two sides
suggest severe injury. It has prognostic value up to 8595%,
but is handicapped by:
Failure to reflect degeneration
High false negative rate
Low sensitivity.
Maximum Nerve Excitability Test

By giving suprathreshold maximal stimulation, all fibers capable
of responding are brought into action and improve the low
sensitivity of minimal response version of nerve excitability test.
This is of no value in 1st 72 hours. Stimulus is always greater
than 5 mA and is based on pain.
Response of involved side is compared with normal side
and evaluated as;
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Otology an Overview
Table 8.2:Electromyography
Muscle activity
Response
Amplitude
Duration Conclusion
Normally at
rest
No activity
Voluntary
contraction
Voluntary motor
unit potential
100200
uv
310
ms
Normal biphasic
In facial palsy
Fibrillation
potential appear
on 10th14th
day of paralysis
> 100 uv
12 ms
Fibrillation
potential
indicate
degeneration
Recovery of
facial paralysis
Polyphasic
potential
Indicate
recovery and
precedes
return of facial
movement by
12 weeks
Note: Since fibrillation potential occurs late, early phase decisions are not
possible on the EMG.
Equal response indicates neuropraxia as it does not raise

threshold
Reduced response due to increased threshold indicates
partial degeneration
Absent response due to total loss of excitability indicate
severe degeneration.
Electromyography (EMG) (Table 8.2)

Electrical activity in any striated muscle is recorded via needle
electrodes inserted in muscle.
Normally at rest
No activity
Voluntary contraction Voluntary motor units
Facial paralysis Fibrillation potential (suggests
Wallerian degeneration)
Onset of recovery
Polyphasic potentials are seen.
Evoked Electromyography
It is also called electroneuronography (ENoG), was described
by Esslens and popularized by Fisch. Test should be done on
3rd or 4th day of trauma and not useful for 1st 72 hours after
injury.One may use the term evoked electromyography, which
is more apt because it is compound action potential of muscle
fibers that is measured.
Compound action potential generated by maximal
simulation is analyzed with the healthy side as a reference.
Percentage of amplitude of compound action potential of the
involved side is the basis of this test. This percentage expresses
the ratio of blocked fibers to those undergoing degeneration.
ENoG 50% of normalFunctional recovery is uniformly
excellent
10% of normalRecovery is prolonged but satisfactory
2% of normalUnsatisfactory recovery.
Use of Supramaximal Voltage

Maximum excitability twitch voltage + 20% to ensure that all
fibers are stimulated and electrical activity in the facial muscles
called action potential is noted. Height of action potential is
compared with the good side and percentage comparison is
done.
Stimulating electrode is kept on the skin over stylomastoid
foramen and supramaximal stimulation is applied to ensure
that all the functioning nerve fibers are stimulated.
Recording electrode is placed in the region of nasolabial
fold. Evoked biphasic compound muscle action potential
(CMAP) is recorded.
Stimulus is gradually increased in magnitude until there is
no further increase in the amplitude of the response.
Normal side is compared with abnormal side.
Amplitude loss on the involved side is directly proportional
to degree of degeneration taking place in the nerve, e.g. if
amplitude of the affected side is 25% of the normal side,
75% degeneration has occurred in the diseased facial nerve,
90% degeneration is indication for surgical decompression
Not useful until 4th day of facial palsy as it takes 3 days for
Wallerian degeneration to reach completion. It is also of less
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Otology an Overview
value after 3 weeks because of nerve fiber desynchronization

(concurrent degeneration and regeneration). It also has
poor value in Ramsay Hunt syndrome due to multiple sites
of nerve involvement.
Limitations of Electrophysiological Test

1. Not useful in incomplete palsy.
2. Not able to discriminate between 2nd and 3rd degree
(axonotmesis, neurotmesis) of injury.
3. No information can be obtained in immediate postparalysis period (1st 72 hours).
Facial Nerve Imaging

CT scan: Labyrinthine segment is banana shape on axial
section
MRI: Investigation of choice for tumor
HRCT: Useful for facial nerve canal and investigation of
choice for temporal bone fractures.
High Points
Prognostically, to know which facial nerve will recover, maximal
stimulation test and electroneuronography are most important. ENoG is
not useful beyond 3 weeks.
Electroneuronography is done to know early or imminent degeneration
and done in 1st week following paralysis whereas EMG is useful by 10th
or 14th day following onset (EMG is useful when degeneration has
already occurred).
In nerve excitability test, comparison is made between normal and
abnormal side and differences of 3.5 mA or greater between two sides are
considered significant.
Maximal stimulation test shows evidence of degeneration as early as 3
days.
Progressive paralysis of face, progressive beyond 3 weeks with no return
of function by 6 months should be diagnosed as tumor/malignancy.
Common Causes of Infranuclear Facial

Nerve Palsy
Bells Palsy
Bells palsy is an acute peripheral facial palsy of unknown
cause though it is believed that viral inflammatory immune
mechanism is a possibility. It is an infranuclear idiopathic
facial nerve palsy, complete or incomplete, diagnosis of which
is made in retrospect. It is a self-limiting and non-progressive
condition.
Probable theories:
Viral
Herpes simplex virus type I (HSVI)
Herpes simplex virus type II (HSVII)
Varicella zoster virus (VZV)
Influenza, adenovirus, coxsackie, EB virus
Vasomotor
Autoimmune
Ischemia or anoxia: Microcirculatory failure of vasa nervorum
leading to ischemic neuropathy
Genetic
Immunologic.
Etiology
Age
3rd4th decade
Incidence increases with each decade of life, maximum
during 1545 years.
Sex
Both genders are affected.
In females, 3.3 times greater risk in pregnancy, more
common in 3rd trimester
Predominantly seen in males more than 40 years and in
females less than 20 years
Stress
Emotional upset
Exposure to cold
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Allergy
Positive family history (14%)
History of viral prodrome.
Pathogenesis
Primary ischemia Edema Rigid inelastic bony canal
Secondary ischemia Ischemic neuropathy.
Possible sites of lesion are:

Chorda tympani
Mastoid segment
Tympanic segment
Labyrinthine segment (physiologic bottleneck)
Brainstem (recently believed).
Clinical Features
Sudden onset, more common during night while sleeping,
pain behind or in the ear may be a warning feature
Weakness of facial muscles (forehead, eye, angle of mouth,
buccinator muscle)
Facial numbness
Taste, lacrimation, salivation decreases (loss of tearing and
taste)
Hyperacusis, dizziness
Ear examination is generally normal but may show red
chorda tympani, vascular flaring of posterosuperior aspect
of tympanomeatal area
CNS examination is normal
Taverners criteria (1959) for Bells palsy:
Paralysis or paresis of all muscle group on one side
Sudden onset
Absence of signs of CNS disease
Absence of signs of ear or CPA disease.
Investigations
Bells palsy is to be diagnosed once trauma, tumor, infections
and other causes of facial palsy are ruled out. Along with the
ENT examination and neurological examination following
investigations are carried out:
Testing all muscle groups of face

Parotid gland examination
Audiogram
Blood sugar, VDRL
X-rayChest and mastoid
CT scan head
Electrophysiological tests
Topognostic tests.
Medical Treatment
A. Reassurance that it is not stroke or intracranial disease
B. Physical therapy

Heat, massage, exercises

Electrical vibrator

Raising eyebrows

Squeezing the eye closed

Wrinkling of nose, whistling

Blowing out cheeks and greening.
C. Physiotherapy

Electrical stimulation to contract muscles passively
(may prevent degeneration of muscles)

Active exercises

Short wave diathermy.
D. Pharmacological therapy

Steroids: This has an empirical role but acts by

Cutting down sequelae like crocodile tears,
synkinesis,

Preventing progression

Hastening recovery

It acts optimally if given in 1st 4 days

To be given in dose of 1 mg/kg body weight in
divided doses and to be tailed off

Steroids in various forms (ACTH, prednisolone,
cortisone) may be given

Vitamins B1, B6 and B12

Vasodilator.
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E.

Ocular care
Care of the eye is important as patient suffers from
Absence of lacrimation
Drying of conjunctiva
Decreased corneal sensation.
Eye pad, goggles, gold weight implant or insertion of small
spring into upper eyelid will ensure protection of eye and
prevent exposure.
Other measures like:

Artificial tears during daytime and ointment at night

Keeping globe moist (moisture chamber)

Tarsorrhaphy for BAD syndrome (medial or lateral)
BBells phenomenon
AAnesthesia of cornea
DDry eye.
F. Surgical treatment
Role of decompression is controversial. However, if
paralysis does not recover in 68 weeks facial nerve may
be decompressed.

Partial decompression of vertical/horizontal part

Total decompression from IAMstylomastoid foramen
This is done by:

Exposure of nerve

Eggshell bone is removed

Opening sheath

Plastic surgery to improve cosmetic appearance
Dynamic and static.
G. Psychological treatment.
H. Management of common associated problem like
depression and physical pain.
Clinical Course/Outcome

Complete recovery 71%

Recovery with barely noticeable defect 13%
Severe sequealae 4%
Recurrence 12% (same side 36%, opposite side 64%).
Predictors of Recovery
Complete or incomplete palsy
Response to ENoG or MST
Time when recovery first began.
Bad Prognostic Factors

Pain
Bells palsy in pregnancy
Old age
Dry eye
Complete palsy
Postauricular pain.
Herpes Zoster Oticus (Ramsay Hunt

Syndrome/Herpes Zoster Cephalicus/
Geniculate Ganglionitis)
Salient Features
Sudden facial paralysis following viral prodrome
Severe pain in ear and mastoid region
Vesicles appear over auricle, ear canal, palate, anterior
tonsillar pillar (Fig. 8.8)
Paralysis is due to edema of facial nerve in region of
geniculate ganglion
8th cranial nerve is commonly involved with SNHL and
vertigo
Prognosis is worse than Bells palsy
30 to 50% have persistent weakness. Only 60% recover
satisfactorily
Mildest formmay not show neurological sign
More severe form:
SNHL
Vestibular disturbances
Viral encephalitis may ensue
Post-herpetic neuralgia is the sequelae
Evoked EMG (ENoG) response may remain in normal range
beyond 10 days and then lost by 14th day. In Bells palsy,
electrical response may become abnormal by 10th day.
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Otology an Overview
Fig. 8.8: Herpes zoster

It rarely recurs
Acute phase of infection peaks at 1014 days whereas in
Bells palsy, it occurs at 510 days.
Treatment
Control of pain
Treatment of vesicles (steroid and antibiotic ointment)
Oral steroidsPrednisolone 1 mg/kg body weight and to
be tapered off
Antiviral drugsAcyclovir, 10 mg/kg every 8 hour IV)
Pain management of post-herpetic neuralgia.
Trauma
Head injury with fracture (accidental)
Iatrogenic trauma (surgical and also following injection of
local anesthetic)
Penetrating injury (assault, gunshot injury)
Forceps trauma (birth trauma).
Fracture of temporal bone

Two types:
Longitudinal 90% (10% chances of facial palsy)
Vertical 10% (40% chances of facial palsy)
Mixed type
Site of lesion is generally geniculate ganglion
Decision to operate depends on electroneuronography
(ENoG)
More than 90% degeneration of fibers within 2 weeks of
injury indicate poor prognosis

1. Incomplete, delayed palsyConservative treatment as
cause is edema.

2. Complete, immediateSurgical treatment is required.
On exploration
Immediate facial palsy following trauma warrants exploration
sharp pieces of bone impinging into the nerve may be found
which should be removed.
If no fracture is seen but facial palsy is present, paralysis
can be explained by stretching of facial nerve between
brainstem and periosteal epineurial attachment at the distal
end of labyrinthine segment.
Once patient gets medically and neurologically stable, surgical
treatment is decided on the basis of;
HRCT
ENoGexploration is done if ENoG shows more than 90%
denervation within 6 days of onset of paralysis.
Patients coming after month or so ENoG will not be useful
and HRCT and EMG will decide about exploration.
Other reasons for explorations are:
Patient with sudden complete onset
Loss of electrical response
History of major head trauma
Profound SNHL
Radiological evidence of transverse fracture
No return of function of facial nerve in 6 to 12 weeks
No polyphasic potentials (polyphasic potential indicate
recovery).
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Methods
Decompression
No general agreement on the timing of decompression
and exploration
Chang and Cass et al. Within 14 days
May et al. Within 30 days
Removing bony fragments
Establishing continuity

a. End to end anastomosis

b. Interposition grafting
c. Rerouting

d. Reinnervation technique.
Iatrogenic Trauma
Middle ear and mastoid surgery

Trauma to tympanic segment (stapedectomy, tym
panoplasty)

More often than not facial canal is dehiscent.

Trauma at pyramidal bentWhile seeking antrum.
Backward hump at pyramidal eminence

Trauma to vertical segment (cortical mastoidectomy,
MRM)

When retrofacial cells are removed

Low postaural incision in infants

Local anesthesia

Trauma to petrous portionDuring middle fossa
approach.
After acoustic neuroma removal, if facial palsy occurs,
one should wait for one year for spontaneous recovery.
Measures like:

Applying heat to face

Massaging of muscles

Performing facial exercises

Electrical stimulation are employed.
Parotid Surgery
All parotid surgeries should be done with facial nerve
monitoring to cut down the risk of facial palsy.
CP Angle Tumor
Facial nerve is at the risk of paralysis.
Neonatal Facial Nerve Injury

Following findings point towards birth trauma leading to facial
nerve palsy:
Battles sign
Hemotympanum indicate birth trauma
EMG response present at birth but fade later on
EMG response in inherited and developmental disorders
is absent
Neonatal facial nerve injury has excellent prognosis and 90%
recover completely.
Infection
Four major types of infection causes facial palsy:
A. Acute OM with mastoiditis

Cause

1. Congenital dehiscence of fallopian canal in the area
of oval window

2. Coalescent mastoiditis

Myringotomy may be needed

Antibiotics

If paralysis persists beyond 10 days to 2 weeks, mastoi
dectomy is indicated

Decompression has debatable role.
B. Chronic middle ear infection

Cholesteatoma matrix destroys the fallopian canal and
exerts pressure on facial nerve

Granulation tissue also leads to destruction

Treatment is removal of cholesteatoma and granulation
tissue.
C. Malignant otitis externa (skull base osteomyelitis)

Pseudomonas infection in debilitated elderly diabetics
gives rise to granulations leading to osteomyelitis and
facial nerve involvement.
D. Herpes zoster oticus and Bells palsy.
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Tumors of Head and Neck Causing Facial Palsy

About 5% of facial palsies are due to tumor. Tumor may encircle
or invade facial nerve in its course from brainstem to temporal
bone to parotid to facial muscles.
Benign Tumors

Schwannoma
CP angle tumor, acoustic neuroma
Meningioma
Hemangioma
Angioma
AV malformation.
Malignant
Adenoid cystic carcinoma
Mucoepidermoid carcinoma.
General Principles of Management

Removal of tumor
With sparing of nerve in benign tumors
With sacrificing facial nerve in malignant tumors
Possibility of facial reanimation by grafting of FN (only in
benign tumor) may be considered
In malignant tumor, reanimation technique like temporalis
muscle sling may be contemplated.
Indication of Sacrificing FN in Benign Tumor

1. Presence of total facial palsy of 1 year or more duration.
2. Threat to integrity of other structures or to life from tumor
located in posterior fossa.
3. Inability to separate tumor from FN
Some malignant tumors behave like benign tumor so
sparing of FN is possible.
Facial Palsy at Birth

Developmental
Frequently bilateral, so palsy not easily noted
Incomplete
Lower portion of face is usually less affected.
Traumatic
Rarely bilateral
Upper and lower part of face is equally affected.
Syndromes with Congenital Facial Palsy

and Miscellaneous Facial Problem
1. Melkersson Rosenthal syndrome (Melkersson 1928) (Fig. 8.9)
Characterized by
May be
Facial edema
Unilateral or bilateral
Facial palsy
Complete or
Fissured tongue incomplete,
Recurrent facial palsy
Associated with
Migranous
headache
megacolon, facial
swelling, stress
HistologyNon-caseating granulomas.
Complete decompression of facial nerve has been
recommended in case of multiple recurrences.
Fig. 8.9: Melkersson Rosenthal syndrome
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2. Moebius syndrome

Bilateral facial nerve palsy

Unilateral or bilateral 6th nerve palsy

Anomalies of extremities

Involvement of other cranial nerves (VIII to XII).
3. Dystrophica myotonica.
4. Thalidomide embryopathy.
Miscellaneous Conditions
1. Hemifacial spasm

Debilitating condition

Only eye muscles or whole face shows rhythmic spasm

Difficulty in eating and talking

CauseCP angle lesion, tumor or cholesteatoma, loop
of anterior inferior cerebellar artery pressing on facial
nerve

To be differentiated from blepharospasm.
2. Lyme disease

Caused by tick borne spirochete

Bite in head and neck region may result in facial nerve
palsy

Spontaneous recovery is known

ELISA test to detect IgG and IgM antibody to spirochete

Tetracycline is given or 34 weeks.
Other causes of facial palsy
Sarcoidosis
Granulomatous lesion
Vascular lesion
Ingestion of heavy metal
Fungal infection.
Surgeries for Facial Nerve

Dynamic and static procedures
Surgical exploration
Sling of fascia lata
Insertion of graft
End to end anastomosis

Nerve or neuromuscular transfer
Facial nerve decompression
Hypoglossal facial nerve anastomosis.
Other techniques for facial reanimation
Brow lift
Gold implant
Eyelid spring implantation
Lower lid tightening
Temporalis muscle transposition.
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