course of facial nerve, causes of palsy, management and description of few causes, facial nerve decompression and animation techniques

1. DR PRIYANKA SHASTRI
FACIAL NERVE PALSY

2. ORIGIN AND COURSE OF FACIAL
NERVE

7. Histology of facial nerve
 Each nerve fibre :
nerve cell body, axon :
surrounded by myelin
secreted by schwann
cells
 Endoneurium : to form
tubule
 Multiple tubules :
perineurium
 Epineurium : nerve
sheath

8.  The facial nerve gets it’s blood supply from 4 vessels:
 Anterior inferior cerebellar artery – at the
cerebellopontine angle
 Labyrinthine artery (branch of anterior inferior
cerebellar artery) – within internal acoustic meatus
 Superficial petrosal artery (branch of middle
meningeal artery) – geniculate ganglion and nearby
parts

9.  Stylomastoid artery
(branch of posterior auricular artery) –
mastoid segment
 Posterior auricular artery supplies the facial
nerve at & distal to stylomastoid foramen
 Venous drainage parallels the arterial blood
supply

10. Degrees of nerve injury
 Neuropraxia : no
wallerian degenration
 Axonotmesis : distal
wallerian degenration
occurs, intact
perineurium, total
paralysis
 Neurotmesis :
wallerian degenration
occurs

11. Sunderland classification
 1°: Partial block: Neuropraxia
 2°: Loss of axons, endoneurial tubes remain intact:
axonotmesis
 3°: Injury to the endoneurium: neurotemesis
 4°: Injury to the perineurium in addition to above: partial
transection
 5°: Injury to the epineurium in addition to above:
complete transection
 The first three degrees are seen in viral and
inflammatory disorders while 4th and 5th are seen in
surgical or accidental trauma

13. CAUSES OF FACIAL PARALYSIS
CENTRAL
Brain
abcess
Pontine
Gliomas
Poliomyeliti
s
Multiple
sclerosis
GB
syndrome
INTRACRA
NIAL
Acoustic
neuroma
meningioma
congenital
cholesteato
ma
metastatic
carcinoma
meningitis.
INTRATEMPORAL
A. Idiopathic Bell’s palsy
Melkersson’s syndrome
B. Infections
ASOM,CSOM, Herpes
zoster oticus, malignant
otitis externa
C. Trauma –
Mastoidectomy,
Stapedectomy, #
temporal bone
D. NEOPLASMS
Malignancies of external
and middle ear
glomus jugulare tumour
facial nerve neuroma
metastasis to temporal
bone, cholesteatoma, VII
nerve tumour,
meningioma,
schwannoma
EXTRACRAN
IAL
Malignancy
of parotid, sx
of parotid,
accidental
injury in
parotid
region.
Neonatal
facial injury
SYSTEMIC
DISEASES
DM,
Hypothyroidism
, uraemia,PAN,
wegener’s
granulomatosis
,
sarcoidosis,lepr
osy, leukemia,
demyelinating
disease.

14. Altered function of facial nerve following
injury
 SYNKINESIS- Abnormal synchronization movement
occuring with voluntary and reflex activity of muscle
which normally do not contract together.
 CROCODILE TEARS- Increased unilateral
lacrimation on involved side associated with eating.
 STAPEDIUS TENDON CONTRACTION –
Hyperkinetic syndrome with faulty facial regeneration
causes fullness and roaring in ear.
 FACIAL MYOKYNIA – Continuous fine fibrillary
movement of facial muscles giving “bag of worms”
facial appearance.

15. APPROACH
HISTORY
onset
duration
Progression
h/o head injury
Recurrence
PHYSICAL FINDINGS
U/l or b/l
pain over mastoid /
preauricular area
vesicles on the pinna /
EAC
s/s/o ASOM / CSOM
Head & neck examn
Showing mass or
involvement of CN
INVESTIGATIONS
Topodiagnostic
tests
Electrodiagnostic
Imaging

17. FACIAL NERVE PALSY

18. TOPOGNOSTIC TESTING

19.  SCHIRMER TEST- decrease in lacrimation of 75%
or more as compared to normal side. Or < 10mm for
both sides at 5 min.
 STAPEDIAL REFLEX TESTING - if absent , site of
lesion between geniculate ganglion and stapedius
muscle. If present then site of lesion is distal to
stapedius muscle.
 TASTE TESTING – conc. Sweet, salt, sour and bitter
solution tested along lateral margin of anterior 2/3 of
tongue towards tip / electrogustometry ( EGM )
 SUBMANDIBULAR GLAND FLOW- compared by
sialometry using 6% citric acid.
 TESTING FACIAL MOVEMENT

21. ELECTRICAL TESTING
 Nerve Excitability Test - minimal current necessary to
stimulate muscle movement when applied to a branch of
facial nerve. A difference of 3.5mA or greater between
two sides is thought to be significant.
 Maximum Stimulation Test – strength and duration of
stimulation is gradually increased from 1mA to 5mA.
Useless <72 hrs.
 ELECTRONEURONOGRAPHY - action potentials
developed in the muscles by stimulation of the nerve is
measured and expressed as % of degeneration
compared to normal side. Surgical intervention in case of
immediate paralysis with> 90% degeneration.No use <
72 hrs.

22. NERVE EXCITABILITY TEST (NET)
 Compares
transcutaneous current
threshold required to
elicit minimal muscle
contraction between two
sides
 A difference of 3.5
milliamperes (mA) or
more in thresholds
between the two sides a
reliable indicator of
progressive
degeneration :indicator
for surgical
decompression
 If the paralysis becomes
total, the test can
determine whether a
pure conduction block
exists or whether
degeneration is
occurring, as indicated
by progressive loss of
excitability.

23. MAXIMAL STIMULATION TEST (MST)
 Instead of measuring
threshold, however,
maximal stimuli (current
levels at which the
greatest amplitude of
facial movement is seen)
is employed.
 degree of facial
contraction is subjectively
assessed as either equal,
mildly decreased,
markedly decreased, or
without response
compared with that on the
normal side.
 Movements on the
paralyzed side are
subjectively expressed as
a percentage (0%, 25%,
50%, 75%, 100%) of the
movement on the normal
side.
 Symmetric response
within first ten days –
complete recovery in >
90%
 No response within first
ten days – incomplete
recovery with significant
sequelae

24. ELECTROMYOGRAPHY
 The recording of
spontaneous and voluntary
muscle potentials by needles
introduced into the muscle is
called electromyography
(EMG).
 Records motor unit
potentials of the orbicularis
oculi & orbicularis oris
muscle during rest &
voluntary contraction
 In a normal resting muscle
biphasic / triphasic potentials
are seen every 30-50msec.

25.  EMG can be used to determine:-
1.If a nerve in question is in fact in
continuity(volitional activity recorded)
2.Evidence of degenration ( fibrillation after 10-14
days)
3.If there are early sign of reinnervation
(polyphasic innervation potentials after 4-6 weeks)

26.  Fibrillation potentials typically arises 2-3 weeks
following injury
 With regeneration of nerve after injury, polyphasic
reinnervation potential replaces fibrillation
potential
 Reinnervation potentials may precede clinical
signs of recovery by 6-12 weeks

27.  Polyphasic potential indicate regenrative process &
surgical intervention is therefore not indicated
 Fibrillation indicate lower motor neuron denervation
but viable motor end plates, so surgical intervention
needed(to achieve nerve continuity)
 Electrical silence indicates atrophy of motor end
plates & need for muscle transfer procedure

28. EVOKED ELECTROMYOGRAPHY
(EEMG) OR EVOKED
ELECTRONEURONOGRAPHY (EnoG)
 Records compound
muscle action potential
(CMAP) with surface
electrodes placed
transcutaneously in the
nasolabial fold
(response) and
stylomastoid foramen
(stimulus)

29. EVOKED ELECTROMYOGRAPHY
(EEMG) OR EVOKED
ELECTRONEURONOGRAPHY (EnoG)
 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.
 Most valuable prognostic indicator---Its main indicaion
acute onset complete facial paralysis
 This method offers the potential advantage of an
objective registration of electrically evoked responses,
and the amplitude of response of the paralyzed side (in
mV) can be expressed as a precise percentage of the
normal side's response.

30. ELECTRONEURONOGRAPHY (EnoG)
• )
 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
 Not useful until 4th day of paralysis as it takes about 3 days
for degeneration to reach completion
 Also of less value after three weeks bcoz of nerve fibre
desynchronization
 Advantages: Reliable
 Disadvantages:
 Uncomfortable
 Cost
 Test-retest variability due to position of electrodes

31. Limitation of electophysiological
testing
 Electric impulse can stimulate only normal/
neuropraxic fibres and can’t distinguish b/w
axonotemesis or neurotemesis
 Provides no useful information in cases of
incomplete facial paralysis
 It fails to provide information on the immediate
post paralysis period( first 72 hours)

32. Imaging
 Magnetic resonance imaging (MRI) with intravenous
gadolinium contrast has revolutionized tumor detection in
the cerebellopontine angle and temporal bone and is
currently the study of choice when a facial nerve tumor is
suspected (e.g., in a case of slowly progressive or
longstanding weakness)
 However, enhancement also occurs in most cases of
Bell’s palsy and herpes zoster opticus, usually in the
perigeniculate portions of the nerve. This enhancement
may persist for more than 1 year after clinical recovery;
can be distinguished from neoplasm by its linear,
unenlarged appearance; and has no apparent prognostic
significance.

33.  Computed tomography (CT) is valuable for surgical
planning in cholesteatomas and temporal bone
trauma involving facial nerve paralysis but probably
is less useful than MRI in the investigation of
atypical idiopathic paralysis.
 Unfortunately, even MRI fails to detect a substantial
number of malignant parotid tumors.
 MRI shows the greatest utility in predicting location
and depth of parotid gland tumors, but even in this
capacity it is no better than simple manual
palpation alone.

34. SIGN DIFFERENTIATING SUPRANUCLEAR
FROM INFRANUCLEAR LESIONS
SUPRANUCLEAR INFRANUCLEAR
 Forehead intact bilaterally
 FND, Hemiplegia on side
of facial palsy
 Ataxia
 Reflexes intact
 Tone maintained
 Drooping corner of mouth
 Slight flattening of
nasolabial fold.
 No muscle atrophy/
fasciculation
 Total facial palsy
 No FND
 No hemiplegia
 No ataxia
 No reflexes
 Flaccid
 Not an isolated finding
 Not an isolated finding
 Muscle atrophy /
fasciculations present.

36. BELL’S PALSY
First described more than a
century ago by Sir Charles Bell
Bell palsy is certainly the most
common cause of facial paralysis
worldwide

37.  U/l spontaneous idiopathic lower motor neuron facial
palsy
 Incidence of Bell’s palsy is 20 to 30 patients per 100,000
population
 The incidence is greater in patients
 older than 65 years and lower in children younger than
age 13.
 The male-to-female ratio for Bell’s palsy is approximately
equal,
 except for a predominance in women younger than 20
years of age and a slight predominance in men older
than 40
 The left and right sides of the face are equally involved

38.  Diagnosis by exclusion
 Criteria
 Paralysis or paresis of all muscle groups of one side
of the face
 Sudden onset
 Absence of signs of CNS disease
 Absence of signs of Ear disease

39.  30% of patients will have incomplete paralysis on
presentation
 70% will have a complete paralysis.
 Bilateral paralysis occurs in 0.3%
 Have a history of previous paralysis.
 A family history of Bell’s palsy can be elicited in
8% of patients

40. 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
 Edema of nerve within
inelastic fallopian
canal
 Recovery begins by 3
weeks, full recovery
by 6months
 70 % : 15 % : 15%

41.  most important prognostic factor is whether the paralysis
is incomplete or complete.
 The prognosis for affected persons in whom complete
facial paralysis never develops is excellent: 95% to 100%
 factors associated with poor outcome include
hyperacusis; decreased hearing; age older than 60
years; diabetes mellitus; hypertension;and severe aural,
anterior facial, or radicular pain

43. Ramsay Hunt Syndrome
 Caused by reactivation varicella zoster virus (herpes
virus type 3)
 Facial paralysis + hearing loss +/- vertigo
 Herpes zoster oticus
 Two-thirds of patients have rash around ear
 Other cranial nerves, particularly trigeminal nerves (5th
CN) often involved
 Worse prognosis than Bell’s (complete recovery: 50%)
 Important cause of facial paralysis in children
6-15 years old

44.  The timing of the appearance of the vestibular eruption
may have prognostic significance. In most cases, eruption
and paralysis occur simultaneously.
 In approximately 25% of cases, the eruption precedes the
paralysis; these patients have a higher likelihood of
recovery.
 Patients with Ramsay Hunt syndrome also are more likely
than patients with Bell’s palsy to have associated cranial
nerve symptoms, including hyperacusis, hearing loss, and
pain.
 In approximately 10% of patients, the vesicular rash
appears well after the initial facial paralysis,
many patients demonstrate a rise in antibody to VZV
without ever exhibiting cutaneous or mucous membrane
vesicles—so-called Ramsay Hunt sine herpete.

46.  Severe ocular complications can occur with
herpes zoster ophthalmicus.
 These complications include uveitis,
keratoconjunctivitis, optic neuritis, and glaucoma
and are almost always associated with
involvement of the ophthalmic division of the
trigeminal nerve

47.  Management of patients with herpes zoster, including
cephalic zoster, consists of systemic corticosteroids.
 A specific benefit of corticosteroid therapy is a
reduction in postherpetic neuralgia. The usefulness of
corticosteroids in fostering recovery from the facial
paralysis is controversial; however, early institution of
corticosteroids seems to
 relieve acute pain, reduce vertigo, and decrease the
incidence of postherpetic neuralgia
 The antiviral agent acyclovir also is recommended to
treat herpes zoster facial

48. Congenital Facial Paralysis
 The incidence of facial paralysis in newborns has been
estimated at 0.23% of live births.
 Birth trauma usually causes isolated facial paralysis and
other signs of injury, including facial swelling,
ecchymosis, and hemotympanum. Abnormalities of other
cranial nerves or abnormalities on brainstem audiometry
(prolongation of the I to III or I to V interval) suggest that
the facial paralysis is congenital and not traumatic.
 Of facial paralysis cases in infants, 78% are related to
birth trauma.
 These cases are equally divided between forceps
deliveries and vaginal deliveries plus cesarean sections,
suggesting that intrauterine facial nerve injury can occur
from pressure on the infant’s face by the sacral
prominence during birth

49.  Möbius’ syndrome represents a broad spectrum of
clinical and pathologic findings ranging from isolated
unilateral facial paralysis (usually associated with
sixth cranial nerve paralysis) to bilateral absence of
facial and abducens nerve function.
 Multiple other cranial nerves,including the
glossopharyngeal, vagus, hypoglossal, and other
extraocular motor nerves, also may be affected

50. Infectious causes
 Acute facial paralysis may result from bacterial or
tuberculous infection of middle ear, mastoid &
necrotizing otitis externa
 Incidence of facial paralysis with otitis media:
0.16%
◦ Infection extends via bone dehiscences to nerve in
fallopian canal leading to swelling, compression &
eventually vascular compromise & ischemia
 Immune compromised patients are at risk for
pseudomona infection
 Poor prognosis (complete recovery is < 50%)

51. Neoplasms
 27% of patients with tumors involving the facial
nerve develop acute facial paralysis
 Most common causes: schwannomas,
hemangiomas (usually near geniculate ganglion)
& perineural spread such as with head and neck
carcinoma, lymphoma & leukemia, congenital
cholesteatoma
 Other neoplasms can also involve the facial
nerve
◦ Adults: metatstatic disease, glomus tumors,
vestibular schwannomas & meningiomas
◦ Children: eosinophilic granuloma & sarcomas

52.  Slowly progressive facial paralysis
 Early diagnosis : high degree of suspicion
 h/o recurrent palsy, involvement of other cranial
nerves.
 CT and MRI
 Tumout resection with grafting

53.  Recurrent facial palsy: seen in
 Bell’s palsy,
 Melkersson’s syndrome,
 diabetes,
 sarcoidosis
 tumuors

54. Melkersson-Rosenthal Syndrome
 Acute episodes of facial paralysis
 Facial swelling
 Fissured tongue
 Very rare
 Familial but sporadic
 Usually begins in adolescence
 Leads to facial disfigurement
 No definite therapy

55. Bilateral simultaneous facial palsy
 Moebius syndrome
 GB Syndrome
 Sarcoidosis
 Myotonic dystrophy
 Skull trauma
 Infectious mononucleosis
 CMV
 Acute porphyria
 Botulism
 Lyme disease
 Bell’s herpes simplex

56. Traumatic facial nerve palsy
 Second most common cause of FN
paralysis
 - Represents 15% of all cases of FN
paralysis
 - Most common cause of traumatic facial
nerve injury is temporal bone fracture

57. Temporal bone fractures
Longitudinal Transverse
 70-90%
 Parietal , temporal
trauma
 Hemotymoanum,
ossicular chain disruption
 Facial nerve paralysis :
10-20 %: horizontal
segment
 10-30%
 Occipital
 Snhl, vestibular dysfn
 Facial nerve palsy :
50%: labyrinthine
segment
 Can be from iac to
horizontal segment

59. Iatrogenic
– Surgical
• Most common overall surgery with FN injury is parotidectomy
• Most common otologic procedures with FN paralysis
– Mastoidectomy – 55% of surgical related FN
paralysis
– Tympanoplasty – 14%
– Mechanism - direct mechanical injury or heat
generated from drilling
– Most common area of injury – distal tympanic
segment including the 2nd genu, followed by
mastoid segment
• Unrecognized injury during surgery in nearly 80% of cases

60. SURGICAL LANDMARKS OF FACIAL
NERVE
FOR MIDDLE EAR AND MASTOID SURGERY
 Processus cochleariformis
 Oval window and horizontal canal
 Short process of incus
 Pyramid
 Tympanomastoid suture
 Digastric ridge

61. For parotid surgery
 Cartilaginous pointer
of conley
 Tympanomastoid
suture
 Posterior belly of
digastric
 Styloid process

63. Surgical management
A. Facial nerve decompression
B. Neurorrhaphy(nerve repair)
1.direct end to end anastomosis
2. interposition cable grafting
C. Nerve transposition: hypoglossal-facial
D. Muscle transposition: temporalis, masseter
E. Micro-neuro-vascular muscle flap
F. Static procedure: eyelid implant, facial sling

64. Intratemporal Approaches to
Decompression
• Nerve may be injured along multiple segments
– localize injured site pre-operatively
– Full exposure of the nerve from IAC to the stylomastoid
foramen if can’t localize
• Approach to full exposure is based on patient’s auditory
and vestibular status
– Intact - Transmastoid/Middle cranial fossa approach
– Absent – Transmastoid/Translabyrinthine approach

65.  General principles
 Monitoring of facial nerve
 Instrumentation
 Sharp dissection

66. Retrolabyrinthine and retrosigmoid
approach
Advantages Complications
 Access to FN in CP
angle without sacrificing
the inner ear function
 No cerebellar
compression
 AICA and other vessels
easily manipulated
 Visualization of nerve
hampered by location
of 8th nerve
 Increased risk of
hearing loss during
separation from 8th
nerve
 Csf leak
 Vascular
complications

68. Middle cranial fossa approach

69. Advantages Complications
 the only method that
exposes the entire
internal auditory canal
and labyrinthine
segment with
preservation of hearing
 most commonly used
for decompression of
the facial nerve in Bell’s
palsy and with
longitudinal temporal
bone fractures.
 Dural elevation can be
difficult
 Persistent CSF leakage
 Conductive and
sensorineural hearing
losses can result

70. Transmastoid approach
Advantages Complications
 excellent exposure of the
mastoid and tympanic
segments of the facial
nerve
 used in conjunction with
middle fossa and
retrolabyrinthine
approaches if total facial
nerve exposure is
required and inner ear
function is to be
preserved
 limited access to the
geniculate ganglion and
the inability to reach the
labyrinthine segment.
 Conductive or
sensorineural hearing
loss also can be a
complication if the incus
is removed or touched
by a rotating burr during
the procedure.

72. Translabyrinthine approach
Advantages Complications
 The translabyrinthine
exposure of the facial nerve
is used primarily when the
cochlear and vestibular
functions have been lost
preoperatively.
 The greatest advantage with
this technique of facial nerve
exposure is the ability to
access the entire nerve
using one approach
 Hearing and balance
function must be
sacrificed for total
exposure of the nerve
 CSF leakage and
infection are the greatest
risks

74. Facial Reanimation
 Facial reanimation is a family of different
surgical techniques to make one's
paralyzed face move more normally.
74

75. Assessment and Planning
 Cause of facial paralysis
 Functional deficit/extent of paralysis
 Time course/duration of paralysis
 Likelihood of recovery
 Other cranial nerve deficits
 Patient’s life expectancy
 Patient’s needs/expectations

76. Primary Nerve Repair
 End-to-end
anastomosis
preferred
 Can be performed
with defect < 17 mm
 Extratemporal repair
performed < 72 hrs of
injury
 Most common
methods
 Group fascicular
repair
 Epineural repair
Group fascicular repair

77. Primary Nerve Repair
 Severed ends of nerve
exposed
 Devitalized tissue/debris
removed with fine scalpel
 Small bites of epineurium
 Epineural sheath
approximated with 9-0
nonabsorbable suture
 Epineural repair
recommended for injury
proximal to pes anserinus
and intratemporal
 Horizontal segment rarely
accessible to suture repair Epineural repair technique

78. Nerve Repair
• Recovery of function begins around 4-6 months and
can last up to 2 years following repair
• Nerve regrowth occurs at 1mm/day
• Goal is tension free, healthy anastomosis
• Rule is to repair earlier than later -
– After 12-18 months, muscle reinnervation becomes less
efficient even with good neural anastomosis
– Some authors have reported improvement with repairs as
far out as 18-36 months
• 2 weeks following injury -> collagen and scar tissue
replace axons and myelin
– Nerve endings must be excised prior to anastomosis for
this reason if this far out

79.  The clinical uses of interposition grafts
 (1) radical parotidectomy with nerve sacrifice;
 (2) temporal bone resection;
 (3) traumatic avulsions;
 (4) cerebellopontine angle tumor resection;
 (5) any other clinical situation in which viable
proximal nerve can be sutured and distal
elements of facial nerve can be identified

80. Interposition Grafting
 Cable grafts
 Used when defect > 17mm; nerve cannot be
reapproximated w/o tension
 Most common
 Greater Auricular Nerve
 Sensory nerves from superficial cervical plexus
 Sural nerve
 Medial antebrachial cutaneous nerve

81.  Useful features
 Proximity to facial
nerve
 Cross-sectional
area (~equal)
 Limited morbidity
 Limitations
 Reconstruction of
long defects and/or
branching nerve
gaps
 maximum of 10 cm

82.  Pros:
 Length (70cm)
 Accessibility
 Low morbidity
associated with
sacrifice
 Two team approach
 Reduced surgical time
 Cons:
 Variable caliber
 Often too large
 Difficult to make
graft approximation
 Unsightly scar

83. MBCN
 Important landmarks:
 Medial epicondyle of
humerus
 Biceps tendon
 Basilic and medial
cubital veins
 Fascial plane
separating bicep from
tricep
 Upper extremity can be
prepped from axilla to
wrist or continuous with
the head/neck.
 Nerve diameter and
branching pattern are
 similar to those of the
facial nerve, and donor
site morbidity is minimal
 with nerve harvest

84. Surgical Technique
 For the surgical technique of neurorrhaphy, interrupted sutures using
 9-0 or 10-0 monofilament nylon are preferred.
 Both ends of the nerve graft and the proximal and distal stumps should be
transected cleanly with a fresh sterile blade.
 Epineural sutures
 Approximation of the nerve ends using an acrylic glue has been
 described : Histacryl or cyano-butyl-acrylate
 The nerve graft should lie in the healthiest possible bed of supporting tissue
 Suction drainage systems should be placed away from any portions of the
nerve graft.

85. Grafting and Nerve Transfer -
Overview
 Approach is based on availability of proximal nerve ending
 Performed for defects > 17mm
 Results in partial or complete loss of donor nerve function
 Best functional results are obtained with cable grafting when a
segment of the facial n. is disrupted
 Also recommended if there is tension at the anastomotic site of
a primary nerve repair
 Graft should be aprox. 25% longer than needed to allow for
a tension free anastomosis

86. Facial nerve transposition
 Reinnervation by
connecting an intact
proximal facial nerve
to the distal ipsilateral
facial nerve

87. Hypoglossal-Facial
 Technique modification aka partial XII-VII transfer
 Donor nerve harvested
 One end of donor nerve is sutured to severed main
trunk of CN VII; other end hooked up to proximal
segment of partially severed CN XII
 The procedure has been modified by only partially
sectioning the hypoglossal nerve and interposing, by
end to-side anastomoses,by a greater auricular nerve
graft between the hypoglossal and facial nerves.
 Since the hypoglossal nerve is transected only
halfway, tongue function can be preserved.
 Limits tongue dysfunction and atrophy

88. Cross-facial Nerve Grafting
 Contralateral CN VII used to reinnervate paralyzed
side using a nerve graft
◦ Sural nerve often employed
◦ ~25-30cm of graft needed
 Restitution of smile and eye blinking when
successful
 Disadvantage
◦ 2nd surgical site
◦ Violation of the normal facial nerve

89. Cross-facial Nerve Grafting
 4 techniques
1. Sural nerve graft routed from
buccal branch of normal CN VII
to stump of paralyzed CN VII
2. Zygomaticus and buccal branch
of normal CN VII used to
reinnervate zygomatic and
marginal mandibular portions
respectively
3. 4 separate grafts from
temporal, zygomatic, buccal
and marginal mandibular
divisions of normal CN VII to
corresponding divisions on
paralyzed side.
4. Entire lower division of normal
side grafted to main trunk on
paralyzed side.

90. Muscle Transposition
(aka “Dynamic Sling”)
 When to use:
 Facial neuromuscular system absent
 Neural techniques unsuitable
 i.e. congenital facial paralysis
 Facial nerve interruption of at least 3 years
 Loss of motor endplates
 Crossover techniques not possible due to donor
nerve sacrifice

92.  Muscle transposition most commonly employs the
temporalis muscle because of its good location,
length,contractility, and vector of pull.
 good for reanimation of the mouth in patients with
long-standing (at least 1 year in length) paralysis.
 Allows patients to have a voluntary smile.
Temporalis

93. Temporalis
 Overcorrection at oral
commissure is critical
 2nd or 3rd molar of upper dental
arch should be exposed when
procedure is finished
 Harvest and placement of
temporoparietal facial flap
recommended to fill donor site
 Oral support possible within 6
weeks
 Movement achieved by clenching
the jaws
 Unnatural contraction requiring
rehabilitation/Physiotherapy

94. Masseter
 Used when temporalis muscle is not available
 May be preferred due to avoidance of large facial
incision
 Disadvantage:
 Less available muscle compared to temporalis
 Vector of pull on oral commisure is more horizontal
than superior/oblique like temporalis

95. Facial Paralysis
(Acute < 3 wks) Intermediate
(3 wks-2 years)
Chronic (>2 years)
CN VII
decompression
Nerve
repair
Primary Cable graft
-G. auricular
-Sural
-MACN
Nerve transfer
-hypoglossal
-masseteric
-spinal acc.
Cross-facial
Graft
Regional
Muscle
Transfer
-Temporalis
-Masseter
-Digastric
Free
Muscle
Transfer
-Gracilis
-serratus
-L. dorsi
-Pec minor
+/-Static Techniques: Slings, Gold weight/Lid procedures, etc
Reanimation
Summary

96. THANK U