Facial Nerve Paralysis
Facial Nerve Paralysis
Facial Nerve Paralysis
Facial Nerve
Paralysis
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).
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Otology an Overview
Extracranial Course
Facial nerve comes out of funnel shaped stylomastoid foramen
giving rise to other branches.
Length in mm
2324 mm
512 mm
Labyrinthine segment
2.56 mm
Tympanic segment
711 mm
Mastoid segment
916 mm
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Otology an Overview
Blood Supply
Stylomastoid artery (stylomastoid branch of postauricular
artery)
Superficial petrosal branch of middle meningeal artery
Labyrinthine artery
Anterior inferior cerebellar artery.
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Otology an Overview
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.
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.
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Otology an Overview
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
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.
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%)
C. Extracranial
Trauma: Birth trauma
Prolonged and difficult labor
Forceps delivery
Facial injury
Postoperative
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Otology an Overview
D. General
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...
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
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.
Topognostic Tests
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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.
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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.
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.
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Otology an Overview
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.
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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Otology an Overview
Allergy
Positive family history (14%)
History of viral prodrome.
Pathogenesis
Primary ischemia Edema Rigid inelastic bony canal
Secondary ischemia Ischemic neuropathy.
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:
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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Otology an Overview
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
Predictors of Recovery
Complete or incomplete palsy
Response to ENoG or MST
Time when recovery first began.
Pain
Bells palsy in pregnancy
Old age
Dry eye
Complete palsy
Postauricular pain.
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Otology an Overview
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).
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Otology an Overview
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.
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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Otology an Overview
Benign Tumors
Schwannoma
CP angle tumor, acoustic neuroma
Meningioma
Hemangioma
Angioma
AV malformation.
Malignant
Adenoid cystic carcinoma
Mucoepidermoid carcinoma.
Traumatic
Rarely bilateral
Upper and lower part of face is equally affected.
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.
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Otology an Overview
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.
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