SEMINAR

Facial Nerve Palsy

Dr. SHOUVIK CHOWDHURY

 CONTENTS
 INTRODUCTION OF FACIAL NERVE
 FACIAL PALSY
 BELL’S PALSY
 Facial nerve
 VII cranial nerve
 Supplies muscles of facial expression
 Some treated as intermediofacial nerve
 Willis-portiodura(facial),
portiomollis(auditory)
 Soummering seperated 2 and numbered
seperately
Embryology
 Nerve of 2nd branchial
arch
 Facial nuclei are derived
from neural crest
 Migrates ventrally
 Ventrolateral aspect of
hindbrain
 Motor fibres are axons of
cells in ventrolateral
lamina of midbrain &
grows outwards to
muscle fibres of their
distribution
Nucleus

 Facial nucleus-
special
visceral/branchial
efferent
 Superior salivatory
nucleus-general
visceral efferent
 Lacrimatory n-
GVE & GSA fibres
 Nucleus of Tractus Solitarius

 SVA nuclei
 GVA nuclei
 Site-medulla
oblongata
 supply
 Facial nerve is a mixed nerve, having
a motor root and a sensory root.
 Sensory root “nervus
intermedius of Wrisberg” carries taste
fibers from the anterior 2/3 of the
tongue, lacrimal, palatine mucosa and
general sensation from the concha and
retroauricular skin,submandibular &
sublingual salivary gland
 Motor root supplies the muscles of the
face, auricle, stapedius,
stylohyoid,digastric(post.belly)
Branches
Branches on face
Brancial Supplies the muscles of
motor facial expression; posterior
(special belly of digastric muscle;
visceral stylohyoid, and stapedius.
efferent)

Visceral Parasympathetic
motor innervation of the lacrimal,
(general submandibular, and
visceral sublingual glands, as well
efferent) as mucous membranes of
nasopharynx, hard and soft
palate.

Special Taste sensation from the

sensory anterior 2/3 of tongue; hard
(special
afferent) and soft palates.
General General sensation from the
sensory skin of the concha of the
(general auricle and from a small
somatic area behind the ear.
afferent)
 Neurones
 1- Upper motor neuron: Primary motor
cortex (Precentral gyrus)
 The axons of these neurons enter the
Corticonuclear fiber bundle to reach
the second lower motor neuron in the
Pons.
 2- Lower motor neuron: Facial motor
nucleus.
 The facial nucleus is divided into two
parts:
 The upper part receives bilateral
innervations, and supplies the muscles
of the forehead and eyebrows
(temporal branches).
 The lower part receives innervations
mainly from the contra lateral
hemisphere, and supplies the muscles
of the lower part of the face through
the facial nerve.
Ganglion
 Blood supply to facial nerve –
clinical relevance
 Courses between the epineurium and periosteum – making the blood
supply at risk when mobilizing at the first genu
 Extrinsic
 Stylomastoid artery (branch of the postauricular artery of external
carotid artery)
 Greater petrosal artery (branch of middle meningeal artery)
 Labyrinthe segment - lacks anastomosing arterial cascades thereby
making the area vulnerable to ischemia

* Parhizkar N, Hiltzik DH and Selesnick SH. Facial nerve rerouting in skull base
surgery. Otol Clin N Am. 2005; 38(4): 685-710
 variation
 Facial nerve
 10,000 fibers
 7,000 myelinated
 Facial muscles
 3,000
 Secretomotor
 Sensory
 (leave main trunk
proximal to
stylomastoid
foramen)
Site of lesion & manifestations
 Applied anatomy
 Facial paralysis
 Cerebral stroke- paralysis of lower m. of face
 occlusion of blood vessels
 Reflexes-tectobulbar fibres from superior
colliculus-eyelid closure
 Fibres from trigeminal sensory n.- corneal reflex,
suckling, chewing
 Fibres from superior olivary nucleus on auditory
pathway-reflex contraction of stepedius
 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.
 Pathogenesis – Neural injury due
to edema at point between the
meatal foramen and the geniculate
fossa.
 Shooting pain in auditory canal,
soft palate
 Trigger zone-pinna
Melkersson-Rosenthal
syndrome
 Triad
 Recurrent orofacial edema
 Recurrent facial palsy (50-
90%)
 Lingua plicata (fissure
tongue) – 25%
 Lips become chapped,
fissured and red-brown in
appearance
 Facial nerve
decompression may be
indicated if facial paralysis
is severe and recurrent
 Superficial musculoaponeurotic
system
 Support mechanism for
various soft tissue envelope
 Continuous with posterior
frontalis & platysma inferiorly
 Anterior-inv.fascia of
orbicularis oculi, zygomaticus,
levator labii superioris
 Dissection should be sub
SMAS at level of zygomatic
arch
 Above arch-dissection-s.c or in
loose areolar plane deep to
temporoparietal fascia.
Frey’s syndrme/gustatory sweating/crocodile
tear syndrome-
Hystronic spasm-constant twitching of
some/all facial muscles.
tonic contraction of orbicularis oculi m.with
constant blinking of eye.
Red zone of webster
Facial palsy
 Facial palsy
 Total flaccidity of facial muscles to perform
motor function.
 Etiology –
 Over 40 causes; broadly classified into
three major groups
 Central or intracranial region
 Vascular abnormalities
 Central nervous system degenerative diseases
 Myasthenia gravis
 multiple sclerosis
 Guillain Barre syndrome
Tumors of the intracranial
cavity-
scwanomma
neurofibroma
neurogenic sarcoma.
Glomus tumour
 Intratemporal

 Bacterial (e.g., otitis media; malignant otitis externa) and viral

(e.g., herpes zoster) infections, diptheria, TB, mumps,
infectious mononucleosis.
 Cholesteatoma
 Trauma
 Longitudinal and horizontal fractures of the temporal bone
 Gunshot wounds
 Tumors invading the middle ear, mastoid, and FN
 Iatrogenic causes (surgical injury)
 Congenitial – osteopetrosis (hereditary)
 Extracranial

 Parotid gland region

 Malignant tumors of the parotid gland
 Trauma (lacerations and gunshot wounds)
 Iatrogenic factors
 Surgical injury
 Parotid – main trunk, branches
 Facelift –marginal
 TMJ – frontal
 Tumor excision – cystic hygroma; hemangioma
 At birth – use of suction or forceps
 Facial palsy

central/
peripheral nuclear
supranuclear
 Upper motor neuron-
originates-cerebral
cortex.
controls- extraocular,
masticatory, lingual,
palatal, pharyngeal &
facial group of
muscles
cerebral cortex-neurons
travelled in crossed &
uncrossed fibres-
terminates at various
level of brainstem-
LMN sends cranial
n.to skeletal m.
 Supranuclear facial paralysis-
Lower part of face chiefly affected.
 Nuclear paralysis-
paralysis of nerve in petrous temporal
bone & motor nucleus-loss of taste in
anterior 2/3 of tongue.
 Paralysis due to fracture base of skull-
involvement of auditory & petrosal n.
most common cause of injury at or after
exit from stylomastoid foramen
Injury
Symptoms
CLASSIFICATIONS OF
FACIAL PALSY
 Rainer schmelzeisen
classification(1999)
 Congenital-
 congenital nuclear aplasia(mobius syn)
 myotonic dystrophy
 Melkersson Rosenthal syndrome
 congenital cholesteatoma
 Neurologic-
 Myasthenia Gravis
 Multiple sclerosis
 Guillan-Barre syndrome
 Neoplastic-

scwanomma
 neurofibroma
 neurogenic sarcoma.
 Glomus tumour
 Acoustic Neuroma
 parotid tumours
 Temporal/external acoustic canal tumours
 Infections-
 otitis media, viral (e.g., herpes zoster) infections,
diptheria, TB, mumps, infectious mononucleosis.
 Iatrogenic-
 Parotidectomy
 Rhytidectomy
 lateral skull base surgery
 Traumatic-
 Temporal bone #
 gunshot
 facial lacerations
 Other causes-
 toxic
 metabolic
 idiopathic-Bell’s palsy
 Brainstem infarction
 Seddon (1943) classification of nerve
injury
 Neurapraxia –
 Only the myelin sheath is affected
 The conduction of impulses is blocked but
axoplasmic transport continues
 The nerve distal to the site of the lesion has
abnormal voluntary motor function but retains
normal electrical stimulability
 This usually occurs for several days after trauma
and disappears spontaneously and completely
 Seddon (1943) classification of nerve
injury
 Axonotomesis
 Axonal continuity is lost
 Wallerian degeneration distally (3-5 days)
 Although the neural element is separated and
damaged, the myelin sheath remains intact
 Spontaneous but incomplete recovery may be
expected
 If the endoneural tube is also disrupted, aberrant
regeneration of axonal sprouts may randomly enter
distal endoneural tubes
 Seddon (1943) classification of nerve
injury
 Neurotmesis
 Allcomponents of the peripheral nerve are
transected
 Wallerian degeneration distally (3-5 days)
 The epineural sheath is disrupted, allowing axon
sprouts outside the nerve sheath to produce
neuromas
Seddon (1943) classification of nerve
injury
Axonotomesis & neurotmesis
 Axons begin to regenerate about 3 weeks after
injury
Axon may regenerate at a rate of 1 mm/day
 Recovery begins within 2-4 months
 Sunderland Classification(1978)
 Sunderland expanded Seddon's system by
subdividing type 3 injuries and proposed the following
classification types:
 Sunderland I (Neuropraxia) - as in Seddon.
 Sunderland II (Axonotmesis) - as in Seddon.
 Sunderland III (Neurotmesis) - loss of continuity of
endoneurial tubes, with intact perineurium, distal Wallerian
degeneration occurs.
 Sunderland IV (Neurotmesis) - loss of continuity of
perineurium, distal Wallerian degeneration occurs.
 Sunderland V (Neurotmesis) - loss of continuity of
epineurium, distal Wallerian degeneration occurs.
 Evaluation of acute facial paralysis

 House-Brackman grade system(1985)

 I, Normal: Normal facial functioning all areas
 II, Mild dysfunction: slight weakness
noticeable only on close inspection
 Atrest: normal symmetry and tone
 Motion: some to normal movement of forehead
 Ability to close eye with minimal effort
 Ability to move corners of mouth with minimal effort and
slight asymmetry
 Mild synkinesis, contracture, or hemifacial spasm
Evaluation of acute facial paralysis
 House-Brackman grade system
 III, moderate dysfunction:
 obvious but not disfiguring difference between two side
 No function impairment
 Noticeable but not severe synkinesis, contracture, and hemifacial
spasm
 At rest: normal symmetry and tone
 Motion:
 slight to no movement of forehead
 Ability to close eye with maximal effort and obvious asymmetry
 Ability to move corners of mouth with maximal effort and obvious
asymemetry
Evaluation of acute facial paralysis
 House-Brackman grade system
 IV, moderate severe dysfunction:
 Obvious weakness and disfiguring asymmetry
 At rest: normal symmetry and tone
 motion:
 no movement of forehead
 Inability to close eye completely with maximal effort
 Asymmetrical movement of corners of mouth with maximal effort
Evaluation of acute facial paralysis
 House-Brackman grade system
 V, severe dysfunction:
 Only barely perceptible motion
 At rest: possible asymmetry with droop of corner of mouth and
decreased or absent nasolabial fold
 Motion:
 No movement of forehead
 Incomplete closure of eye
 Slight movement of corner of mouth

 VI, total paralysis: no movement

 Diagnostic
Evaluation of
Facial Palsy
 History
 Physical
examination
 Evaluation of facial paralysis
 A careful history of the patients illness
 Sudden in onset and frequently evolve over 2-3
weeks after onset-infl/infctn
 Any palsy progression over 3 weeks should be
evaluated for a neoplasm
 Any palsy persist for 6 month without any
recovery should be considered for a neoplasm.
 Patients may also mention otalgia or aural
fullness and facial or retroauricular pain,
Physical examination
 Physical exam:
 Polyposis or granulations
in the ear canal may
suggest cholesteatoma or
malignant otitis externa.
 Vesicles in the conchal
bowl, soft palate, or
tongue suggest Ramsay
Hunt syndrome
Diagnostic Evaluation of Facial Palsy
Topognostic tests
Hearing and balance tests-stapedial reflex
Schirmer test
Submandibular flow test
Taste test

As the quality of radiographic studies, primarily

high resolution CT scan, has improved, the
importance of topognostic testing has fallen off
 Topognostic Testing
 Schirmer test for lacrimation
 Stapedial reflex test (stapedial branch)
 Taste testing (chorda tympani nerve)
 Salivary flow rates and pH (chorda
tympani)
 Topognostic Testing
Schirmer Test
 Greater superficial petrosal nerve
 Filter paper is placed in the lower
conjunctival fornix bilaterally
 3- 5 minutes
 Value of 25% or less on the involved side
or total lacrimation less than 25 mm is
considered abnormal.
 Topognostic Testing
Stapedial Reflex

 Stapedius branch of the facial nerve

 Most objective and reproducible
 A loud tone is presented to either the ipsilateral or
contralateral ear  evokes a reflex movement of the
stapedius muscle  changes the tension on the TM
(which must be intact for a valid test) resulting in a
change in the impedance of the ossicular chain
 If intact stapedial reflex, complete recovery can be
expected to begin within six weeks
 Topognostic Testing

Taste Testing
 Chorda tympani
 Extremely subjective
 Papillae generally disappear within 10
days post injury - middle 1/3 of the
tongue is most indicative, because the
anterior 1/3 may receive bilateral input.
 Topognostic Testing

Salivary flow rates

 Chorda tympani
 Cannulation of Wharton's ducts bilaterally
 5 minute measurement of output
 Significant if 25% reduction in flow of the
involved side as compared to the normal side
 Salivary pH  Flow Rate
 Electrodiagnostic testing
 Conduction test:
 F.nerve is stimulated at angle of mandible
 Recording electrode- frontalis & o.oculi m.
 Latency of muscle measured from onset of
stimulus on both sides
 latency>3.8 msec considered abnormal
 Nerve Excitability Test (NET)
 Most predictive prognostic factor for recovery of facial
nerve function*
 Hilger nerve stimulator over stylomastoid foramen
 Reflects elevated thresholds for neuromuscular
stimulation due to degeneration / disruption of axons
(comparison to contralateral side)
 Difference > 3.5 milliamps - poor prognosis

* Ikeda M et. al. Clinical factors that influence the prognosis of facial nerve paralysis
and the magnitudes of influence. Laryngoscope. 2005; 115:855-860.
 Nerve Excitability Test (NET)
 Benefits:
 Easy to perform
 More comfortable for patient
 Drawbacks
 Subjectivity (relies on operator’s visual detection of
response)
 May exclude smaller fibers (current thresholds are
likely to selectively activate larger fibers with lower
thresholds and not those smaller fibers closer to
stimulating electrode)
 Maximal Stimulation Test
(MST)
 Electrical impulse administered to depolarize the
nerve with current and to compare it to contralateral
side
 Test is repeated periodically until definitive response
 Response
 Equivalent to contralateral side
 Minimally diminished (50%)
 Markedly diminished (< 25% of normal)
 Absent
 Symmetric response within first ten days – complete
recovery in > 90%
 No response within first ten days – incomplete
recovery with significant sequelae
Electroneuronography (EnoG)
 Records compound muscle
action potential (CMAP) with
surface electrodes placed
transcutaneously in the
nasolabial fold (response)
and stylomastoid foramen
(stimulus)
 Waveform responses are
analyzed to compare peak-
to-peak amplitudes between
normal and uninvolved sides
where the peak amplitude is
proportional to the number
of intact axons
 Electroneuronography (EnoG)

 Most reliable in first 2-3 weeks post event (as neuropraxic

fibers recover or regenerate, they discharge asynchronously
and the response is subsequently diminished)
 Response < 10% of normal in first 3 weeks – poor prognosis
 Response > 90% of normal within 3 weeks of onset – 80-
100% probability of recovery
 Testing every other day
 Advantages: Reliable
 Disadvantages:
 Uncomfortable
 Cost
 Test-retest variability due to position of electrodes
 Electromyography (EMG)

 Assesses reinnervation potential of muscles two

weeks after onset
 Limited value early in evaluation because fibrillation
potentials indicating axonal degeneration do not
appear until 10 – 14 days post onset
 Detection of motor units in 2 of 3 muscle groups –
87% satisfactory outcome
 Detection of motor units in 1 muscle group – 11%
satisfactory
 Trigeminal-facial reflex testing (Blink
reflex)
 Stimulate the supraorbital division of the
ophthalmic branch of trigeminal nerve
 Record EMG from orbicularis oculi muscle
 Diagnostic Evaluation of Facial Palsy
 Radiographic studies
 CT scans (brain stem, cerebellopontine
angle, temporal bone, skull base)
 Sialography of parotid
 Chest radiographic survey to detect
sarcoidosis, lymphoma, carcinoma
 Treatment plan
 Goals
 Normal appearance at rest.
 Symmetry at involuntary motion
 Restoration of oral, ocular & nasal
sphincter
 No loss of other significant functions
 Repair
 Immediate(0-3 weeks)
 Delayed(3 wk-2 yr)
 Late(over 2 yrs)
 Requirement of innervation
 Viable ipsilateral facial nucleus
 Proximal nerve segment capable of
supporting axonal regeneration
 Distal nerve segment through which the
axon may regenerate into facial muscles
 Direct nerve repair
 In primary repair, careful
realignment of fascicles,
epineural vessels & other
identifying landmarks are
attempted to re-establish
original relationship to nerve
ends.
 Epineural sutures are used for
small distal branches
 Avoidence of tension at suture
line
 Use of fine caliber suture
 In nerve coaptation, fibrous
tissue proliferation at sutured
area may endanger axon
arising from central nerve
stumps
 Fibrous tissue formation initiated by
trauma of nerve, interpositioning of blood
clots between nerve stumps & application
of tension.
 Extratemporal nerve grafting
 Baker & Conley(1979)
 Indications:
 to reconstruct the defect to reconstitute
the system without tension
 Loss of main trunk or peripheral division
secondary to trauma, scarring or resection
 indications

Facial nerve resection preservation

 Frequently use donor site
 Great auricular n.
 Sural n.
 Cervical plexus
 Lateral femoral n.
 Neurorrhaphy
 Graft should lie in
healthy, well vascularized
recipient area
 At least 2 mm. thickness
is identified
 Great auricular n- below
auricle at extn.surface of
sternomastoid m.
 Sural n.-incision behind
lateral malleolus
 Resection of fibrotic
tissue in long standing
paralysis
 Results
 3-12 cm
 Facial tone-movement of middle 3rd of face
 Improvement continues upto 2 years
Reanimation or cross nerve grafting
 Scaramella(1971), smith(1971),
Andrel(1973),Fisch(1974),
Frellinger(1975),
 Principle- cross innervation from non
paralyzed side by sural n. graft that
connects reservoir of healthy peripheral
facial nerve.
 Cross-facial nerve grafting
 Identify branches on normal side
 Two-four sural nerve grafts
 At 9-12 mos surgery performed to coapt
distal ends with selected branches of FN or
facial muscles on paralyzed side
 Disadvatages- surgical intrusion to normal side
of the face with sacrifice of axonal input
 Highly specialized technique
 Longer operating time
 Suture line for each graft increasing probability
of greater loss of sprouting axon
 Longer time for re innervation
 Technical difficulties
 Nerve crossover
 Criteria:
intact peripheral facial n.
intact mimetic muscle system
inaccessible locus of lesion
 hypoglossal, spinal accessory & phrenic
nerves are used
 Hypoglossal Nerve Crossover
 Korte(1903)
 The criteria for use of the hypoglossal nerve
for facial paralysis
 Intact extracranial part of the facial nerve
 Some ipsilateral facial musculature
 A direct VII-to- VII repair of the facial nerve injury
or ipsilateral nerve grafting (VII-graft-VII) is not
possible
 Facial paralysis is irreversible
 Hypoglossal Nerve Crossover
 Patients with denervation of less than 18
months' duration are suitable for this
procedure.
 When the denervation is more prolonged,
fibrosis of the facial musculature prevents
resuscitation, even if powerful ipsilateral
motors are used.
 Indications of hypoglossal
anastomosis
 F.paralysis from radical resection temporal bone
 Intracranial tumours
 Ear/mastoid surgery
 Advantage-
 Direct & uncomplicate technique
 Greater function of tongue movement
 Rapid movt.& better balance
 No discomfort from loss of hypoglossal n.
 Little functional disability
 Inapplicable in mild to moderate paresis
 Regional/segmental nerve paresis
 Hypoglossal Nerve Crossover
 Another chief complaints: Overactivity and mass
movements.
 Synkinesis and mass movements are seen in almost all
patients, especially during talking and eating.
 Involuntary movements of one portion of the face typically
occur while another part of the face moves voluntarily.
 Method to overcome problems: Reeducation; physical
therapy is used to teach the patient to control facial muscles
 Hypoglossal Nerve Crossover
 Another chief complaints: overactivity and
mass movements.
 Other methods attempted are injection of
botulinum toxin, which prevents acetylcholine
release at the neuromuscular end-plate, magnetic
stimulation, and selective myectomy
 Rubin et al. (1984) advised a Z-plasty technique to
restore tongue function.
 The aim of this technique is to provide muscular
neurotization from the normal side across the midline
into the atrophic side.
 Hypoglossal Nerve Crossover
 Disadvantage – if entire hypoglossal nerve
transferred to the ipsilateral facial nerve
 Various
degrees of tongue atrophy and difficulty in
speaking and swallowing
 “Baby-sitter” Procedure
 Partial hypoglossal transfer to ipsilateral FN
during first stage of cross-FN grafting to help
maintain the bulk and tone of facial muscles
 If paralysis >6mos
 Cross-facialnerve grafting must be supplemented
by baby-sitter because the grafts are relatively
weak motor donors.
 “Baby-sitter” Procedure
 40% splitting of XII (preserves tongue
muscles)
 Second stage operation
 Needed for coaptation with contralateral facial
nerve branches for direct neurontization of the
facial muscles, or to supply the muscle transfers.
 Spinal Accessory Nerve
 Transfer of the spinal accessory nerve can
provide good resting tonus
 However, shoulder disabilities are
experienced by almost all patients if the entire
accessory nerve is used.
 Loss of the ability to elevate the abducted
arm, increased shoulder pain during activity,
and frozen shoulder are the main forms of
morbidity associated with this transfer.
 Spinal Accessory Nerve
 Transposition of sternocleidomastoid branch
of the accessory nerve avoids shoulder
paralysis
 Example of a partial accessory transfer - 50%
of the branch to the sternocleidomastoid and
40% of the branch to the trapezius.
 After these delicate splitting procedures,
paralysis does not develop in the
sternocleidomastoid or trapezius muscle.
 Advantage
 Direct & uncomplicated technique
 Greater function as most facial muscles
are associated with conscious or
unconscious tongue movement
 Better facial balance
 During speech movement of mouth is
more natural
 Trigeminal Nerve
 The masseter branch of the trigeminal nerve
can be used as a motor source for local
transposition or free-muscle transfers instead
of a cross-facial nerve graft if it is not involved
in the developmental mishap.
 As with other transfers of chewing muscles,
the patient is retrained by biting for smile.
 Regional muscle transposition
 Baker & conley(1979)
 Indications- absence of mimetic muscles
from long standing atropy
 Need for additional muscle bulk.
 Congenital paralysis
 Complementary to nerve grafting or
crossover
 Transposition of Local Muscles
 Most common: masseter and temporalis muscles
 Their innervation remains the trigeminal nerve
 Therefore, patient must be reeducated after transposition
 Disadvantage of the use of chewing muscles: lack of
synchronization with the healthy side of the face.
 This is lessened by placing a cross-facial nerve graft and
coapting the cross-facial nerve graft to the motor nerve of
these muscles.
 Masseter Muscle-Owens(1951),
Conway(1958), Lexer & Eden(1911)
 A powerful chewing muscle that can be used
to reanimate the mouth
 Disadvantages
 Lateral and posterior displacement of the muscle
because of its deeper location.
 Involuntary facial movements during eating and
talking
 Therefore, poor symmetry and coordination.
 Temporalis Muscle
 The most commonly used muscle for
transposition
 Used to reanimate both oral and eye
sphincters simultaneously,
 Temporalis Muscle
 Transposition
of this muscle empties the entire
temporal fossa and causes a concave deformity.
 Currently, alloplastic materials that can be reshaped
have been used in an attempt to address this problem.
 Another cosmetic sequela of temporalis transfer is
swelling over the zygomatic arch.
 Other complications: involuntary facial
movements during biting, chewing, and
talking and a lack of symmetrical and
coordinated facial movement.
 Advantage
 Elimination of nonvascularized unit that
carries risk of necrosis, breakage, atropy
 Direct insertion of muscle to the area to br
reanimated
 Augmentation of atropic face in long
standing paralysis
 Platysma and Digastric Muscles
 Depression of the paralyzed lower lip must be
included in the overall treatment plan.
 Lack of depression of the lower lip leads to an
unfavorable aesthetic and functional result.
 Pedicled platysma and digastric muscles are
beneficial for providing depression to the
lower lip.
 Platysma and Digastric Muscles
 Platysma is the first choice for depressor
reanimation of the lower lip
 it is innervated by the facial nerve
 When the platysma is absent or paralyzed
 Use the digastric muscle
 A lower cross-facial nerve graft is usually coapted
with the nerve to the anterior belly of the digastric
muscle.
 Allows for coordinated and symmetrical depression
 Transfer of Free Muscles
 Indication - when facial muscles are absent or their
function is substantially diminished.
 Muscle atrophy should be proved with needle EMG
 If the ipsilateral facial nerve is available, the nerve of
the muscle transplant is coapted directly to it.
 In the absence of an available ipsilateral facial nerve,
cross.:facial nerve grafting from the healthy side is
preferred.
 Transfer of Free Muscles
 The results with cross-facial nerve grafting are
always superior to those obtained with other
motor sources
 cross-facial
nerve grafts offer the possibility of
coordinated facial movement.
 If the facial nerves are absent bilaterally
 ipsilateral
hypoglossal, trigeminal, accessory, or
other motor nerves may be used as donors for the
transplanted muscle.
 Transfer of Free Muscles
 When the donor muscle is selected, the
factors to be considered are
 The strength, bulk, and excursion of the
transplanted muscle should be appropriate for the
muscle being substituted.
 The neurovascular pedicle must be reliable.
 Donor site morbidity must be minimal.
 Transfer of Free Muscles
 Smile restoration procedure
 Preoperative measurements and videotapes of the
patient are needed to assess the excursion and
force vectors.
 Direction and degree of pull
 Required at the level of the alar base, upper lip,
commissure, and nasolabial fold should be
considered carefully
 place free-muscle unit accordingly.
 Transfer of Free Muscles
 Muscles used as free-tissue transfers include
 Gracilis,
pectoralis minor, rectus abdominis,
latissimus dorsi, and serratus anterior
 To reconstruct two functions, eye closure and
upper lip elevation, with a single muscle flap
usually produce unsatisfactory results
 Exceptin the case of the pectoralis minor
(because of its dual innervation).
 Gracilis
 The first choice for free-muscle
transplantation to reanimate the paralyzed
face in adults
 Advantages: easy access, rare anatomical
variations of the pedicle, easy shaping and
debulking, and appropriate excursion to mimic
the zygomaticus, major muscle during smiling
 Strong adductor muscle, but its absence
results in no functional loss.
 Gracilis
 Disadvantages:
A single direction of pull
 Excess bulk
 easily prevented by meticulous shaping
 Secondary revision is always needed; e.g.,
inadequate pulling force of the free muscle
 a minitemporalis muscle flap
 Pectoralis Minor
 Main indication - developmental facial
paralysis in young children
 The length and width of the muscle at this age
are ideal to fit the involved face
 Bulk at this age is optimal (no sculpting
needed )
 Pectoralis Minor
 Main advantage - can be transplanted as a
whole
 Integrity
of each muscle fiber remains intact
 Minimal donor site morbidity
 Another important advantage: Dual innervation
 Upper third is by a branch of the lateral pectoral nerve
 The lower two thirds by the medial pectoral nerve.
 Allows independent movement of the upper and
lowerparts of the muscle: separate reanimation of the
eye and mouth is possible
 Pectoralis Minor
 Disadvantages
 Deep position and the short and complex neurovascular
pedicle - difficult to harvest.
 Brachial plexus injury in the infraclavicular region.
 The pedicle - much shorter than that of the gracilis and is
variable.
 If debulking necessary, do after muscle is harvested
 Prolongs the ischemia time.
 If necessary, debulking is performed during the revision
stage.
 Pectoralis Minor
 Estimate percentage of bulk loss before the
planned free-muscle flap is transferred
 Despite accurate preoperative planning, free
muscles usually require revision.
 Muscle tension - an important factor in free-
muscle transplantation
 Mark tension in situ so that it can be reproduced
following transfer.
 Muscle tension
 Mark muscle every 1 cm along its longitudinal
axis.
 Rule of thumb in adjusting the tension of the
transferred muscle:
 For facial reanimation, the tension of the muscle
should be the same as the tension in site, or
slightly less.
 In contrast, for extremity reconstruction, the
tension of the free muscle should be greater than
the tension in site.
 Pos-op care
 External immobilization to maintain the
position, e.g., of commissure
 Inadvertent jaw movements do not affect the in
setting of the free muscle.
 Check patency of the vascular anastomosis
every hour with a Doppler flowmeter.
 Diet: NPO, liquid or soft for 2 to 3 weeks
 Speak without opening the mouth.
 Pos-op care
 After the onset of muscle contraction
 Performfacial exercises in front of a mirror, goal:
coordinated animation of both sides of the face
 Mirror/biofeedback
 At 6 weeks
 Ultrasound therapy and manual massage
 To minimize scar formation on the operated side
 To help to avoid scar adhesions between the skin
envelope and the free-muscle unit.
 Factors correlated with the onset of functional
return after free-muscle transplantation for facial
paralysis (Terzis and Noah 1997)
 100 cases
 Key factors: age, sex, and ischemia time in free-flap
transplantation
 No correlation between ischemia time (0 to 3 hours) and the
onset of muscle contraction.
 The onset of contraction was slightly earlier in women than in
men, and the return of function was earlier in young than in
older patients.
 Eye management
 Denervation of the orbicularis oculi muscle -
insufficient eyelid closure
 Gravity pulls the upper and lower eyelids downward
(i.e., lagophthalmos and ectropion, respectively) with
loss of orbicularis oculi tonus
 The ectropion everts the margin of the lower lid and
the punctum lacrimalis
 Tear flow and the lacrimal drainage system are disturbed.
 Eye management
 Constant exposure of cornea gives rise to loss of the
tear film, dryness of cornea, conjunctivitis and keratitis
 If the condition progresses, corneal ulceration and
blindness can develop.
 The age of the patient, presence of the blink reflex
and corneal sensation, the degree of lagophthalmos,
and the experience of the surgeon are critical factors
in determining the method of treatment.
 Nonsurgical Methods
 In the early period, the following nonsurgical methods
protect the eye from the detrimental effects of chronic
exposure:
 Eye glasses or contact lenses
 Artificial tears and ophthalmic ointments
 Lid taping
 Occlusive moisture chambers
 Scleral shells
 When lagophthalmos is permanent, seek surgical
treatment
 If the orbicularis oculi muscle is not yet atrophied, cross-
facial nerve grafting or direct neurotization of the muscle can
relieve the lagophthalmos.
 Tarsorrhaphy
 Lateral overlapping tarsorrhaphy tightens and
shortens the upper and lower eyelids
 adequate functional results, but cosmetic results are
unsatisfactory
 The lateral tarsal strip procedure can be used as an
alternative
 No lid notching is required, baseline tear production is
preserved, tarsal plate is not sacrificed; less morbidity than
the classic technique
 Neither provides equally sized eyes or coordinated
movement; they limit vision, provide poor corneal
protection.
 Eye Spring
 For patients w/o normal blink reflex or those with
intact corenal reflex and trigeminal nerve.
 Inserted through two or three small incisions between
the skin and tarsal plate
 Complications: spring breakage and extrusion through
the skin, uncommon
 Reduction in tension is a more common complication,
can be corrected under sedation.
 If lower eyelid drooping also present - specialized
upper and lower eyelid springs
 Lid Loading
 Lagophthalmos - Gold weight
 Choose gold weights pre-op in upright position
 At insertion, pocket must be large enough to anchor
to the tarsal plate
 Complications: displacement, implant infection,
entropion, inflammatory reaction to gold, poor eyelid
contour, corneal ulceration and scarring,
asYmmetrical closure, residual lagophthalmos, and
thickening of eyelid tissue over the prosthesis
 If complication encountered, remove implant, consider
alternative reconstructive method.
 Minitendon Graft for Lower Eyelid
 Treatment of choice for paralytic ectropion
 Helps decrease lagophthalmos
 it raises the lower eyelid
 A palmaris longus tendon graft (from the nondominant
hand)
 Longitudinal split of the tendon is performed before it
is transferred to the eye
 Punctum is canalized to prevent injury
 Retighten if the lower lid is still lax, symmetry with the
normal eye is insufficient, and tearing cannot be
controlled.
 Physiological methods of eye reanimation
 Eye sphincter substitution in patients with
unilateral, long-duration paralysis
 Transplantation of free platysma muscle
 Transfer of pedicled contralateral frontalis m.
 Both muscles have thin flat bellies and have
comparable density of innervation to that of
orbicularis oculi.
 Physiological Methods of eye
reanimation
 Harvest the platysma muscle - through a
submandibular incision
 Isolation of the frontalis is carried out through
a bicoronal incision
 Risk: webbing at the medial canthus level
 invariably requires Z-plasty revision
 Mild weakness may develop during the immediate
postoperative period, but this weakness resolves typically
in 3 months
 Postoperative care is very important:
 limit motions of the mouth and jaw to protect the coaptation sites.
 A fluffy cotton roll dressing and elastic bandages is placed
around the patient's head to protect the repairs.
 During the first 24 hours, a plaster of Paris wrap is also utilized
and subsequently removed.
 Antiemetics are given to prevent vomiting in the early
postoperative period.
 Diet - fluids or a soft diet and speaks only through the teeth for 2
to 3 weeks.
 6 weeks post-op –
 Start massage and ultrasound treatments over the
coaptation sites to prevent formation of scars around
the nerves and adhesions with overlapping cheek skin
flap.
 Start intensive slow-pulse stimulation of the
denervated muscles to prevent further atrophy while
the facial fibers are elongating across the face.
 Facial exercises, biofeedback, and physical therapy
are important in restoring coordinated facial
movements bilaterally.
Terzia, JK & Mersa, B. Facial Reanimation. 2001. In The Unfavorable Result in Plastic Surgery, Avoidance and Treatment.
Goldwyn R.M. & Cohen, M.N., Lippincott, Williams & Wilkins; pp. 597-610.
PRACTICE USING FACIAL
MUSCLES SELECTIVELY IN
FRONT OF MIRROR
 Bell’s Palsy
 Background:
 one of the most common neurologic
disorders affecting the cranial nerves.
 abrupt, unilateral, peripheral facial paresis
or paralysis without a detectable cause.
 Background:
 first described more than a
century ago by Sir Charles Bell,
 yet much controversy still
surrounds its etiology and
management.
 Bell palsy is certainly the most
common cause of facial
paralysis worldwide.
 Incidence:
 The incidence of Bell palsy is
approximately 23 cases per 100,000
persons.
 Demographics:
 Race: slightly higher in persons of
Japanese descent.
 Sex: No difference exists
 Age: highest in persons aged 15-45 years.
Bell palsy is less common in those
younger than 15 years and in those older
than 60 years.
 ETIOLOGY
 HYPOTHESIS-
1. RHEUMATIC HYPOTHESIS- Berard (1936) rheumatic
swellings may press the nerve (obsolete)
2. COLD HYPOTHESIS – Charles bell. Exposure to
extreme cold or cold draught
3. ISCHAEMIC HYPOTHESIS – factors like cold, CO2
excess, vasomotor instability, injury toxic allergic
hormonal influence
4. IMMUNOLOGICAL HYPOTHESIS -
sensitization of lymphocytes to the peripheral mylin
gives rise to cell mediated autoimmune response
5. VIRAL HYPOTHESIS – viral infections such as herpes
zoster or herpes simplex
 Pathophysiology:
 Main cause of Bell's palsy is latent herpes
viruses (herpes simplex virus type 1 and
herpes zoster virus), which are reactivated
from cranial nerve ganglia.
 Polymerase chain reaction techniques
have isolated herpes virus DNA from the
facial nerve during acute palsy.
 Pathophysiology:
 Inflammation of the nerve initially results in
a reversible neurapraxia,
 Herpes zoster virus shows more
aggressive biological behaviour than
herpes simplex virus type 1
 History:
 The most alarming symptom of Bell's
palsy is paresis
 Up to three quarters of affected patients
think they have had a stroke or have an
intracranial tumour.
 History:
 The palsy is often sudden in onset and
evolves rapidly, with maximal facial
weakness developing within two days.
 Associated symptoms may be
hyperacusis, decreased production of
tears, and altered taste.
 History:
 Patients may also mention otalgia or aural
fullness and facial or retroauricular pain,
which is typically mild and may precede
the palsy.
 A slow onset progressive palsy with other
cranial nerve deficits or headache raises
the possibility of a neoplasm
 Physical exam:
 Bell's palsy causes a peripheral lower
motor neurone palsy,
 which manifests as the unilateral
impairment of movement in the facial and
platysma muscles, drooping of the brow
and corner of the mouth, and impaired
closure of the eye and mouth.
 Physical exam:
 Bell's phenomenon—upward diversion of
the eye on attempted closure of the lid—is
seen when eye closure is incomplete.
 Physical exam:
 Polyposis or granulations in the ear canal
may suggest cholesteatoma or malignant
otitis externa.
 Vesicles in the conchal bowl, soft palate,
or tongue suggest Ramsay Hunt
syndrome
 Physical exam:
 The examination should exclude masses
in the head and neck.
 A deep lobe parotid tumour may only be
identified clinically by careful examination
of the oropharynx and ipsilateral tonsil to
rule out asymmetry.
 Investigations:
 Serum testing for rising antibody titres to
herpes virus is not a reliable diagnostic
tool for Bell's palsy.
 Salivary PCR for herpes simplex virus type
1 or herpes zoster virus is more likely to
confirm virus during the replicating phase,
but these tests remain research tools.
 Investigations:
 MRI has revolutionised the detection of
tumours.
 Investigations:
 Topognostic tests and electroneurography
may give useful prognostic information but
remain research tools.
 Diagnosis:
 Bell palsy is a diagnosis of exclusion.
 Other disease states or conditions that
present with facial palsies are often
misdiagnosed as idiopathic.
 Management:
 The main aims of treatment in the acute phase
of Bell's palsy are to speed recovery and to
prevent corneal complications.
 Treatment should begin immediately to inhibit
viral replication and the effect on subsequent
pathophysiological processes that affect the
facial nerve.
 Psychological support is also essential, and for
this reason patients may require regular follow
up.
 Management, Eye care
 It focuses on protecting the cornea from drying
and abrasion due to problems with lid closure
and the tearing mechanism.
 The patient is educated to report new findings
such as pain, discharge, or change in vision.
 Lubricating drops should be applied hourly
during the day and a simple eye ointment should
be used at night.
 Management, Steroid
 Two systematic reviews concluded that
Bell's palsy could be effectively treated
with corticosteroids in the first seven days,
providing up to a further 17% of patients
with a good outcome in addition to the
80% that spontaneously improve.
 Management, Steroid
 Usual regimen is 1mg/kg/day for 1 week.
 Management, Steroid
 Cochrane review*:
“There is insufficient evidence about the effects of corticosteroids
for people with Bell's palsy, although their anti-inflammatory
effect might prevent nerve damage.”

*Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial
paralysis). Cochrane Database of Systematic Reviews 2004, Issue 4. Art. No.:
CD001942.
 Management, Antivirals
 It seems logical in Bell's palsy because of
the probable involvement of herpes
viruses.
 Acyclovir, a nucleotide analogue,
interferes with herpes virus DNA
polymerase and inhibits DNA replication.
 Management, Antivirals
 Usual regimen is 400mg/24hrs divided into
5 doses for 7 to 10 days
 Bell’s palsy:
Antivirals:
 Cochrane review*:
“More evidence is needed to show whether the antiviral drugs
acyclovir or valacyclovir are effective in aiding recovery from
Bell's palsy.”

* Allen D, Dunn L. Acyclovir or valaciclovir for Bell's palsy (idiopathic facial paralysis).
Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD001869.
 Bad Prognostic Factor:
 Complete facial palsy
 No recovery by three weeks
 Age over 60 years
 Severe pain
 Ramsay Hunt syndrome (herpes zoster virus)
 Associated conditions—hypertension, diabetes,
pregnancy
 Severe degeneration of the facial nerve shown
by electrophysiological testing
 References
 Gray’s anatomy
 Anatomy: B.D Chaurasia
 Maxillofacial surgery: Peter Ward Booth

(Vol I, II)
 Maxillofacial surgery:Mc carthy
 Internet sources
Thank you!