2. Facial nerve is a mixed nerve (10,000 fibres)
motor root sensory root
(7000) (3000)
N. itermedius
Intracranial part (24mm)
Intratemporal part (28-30mm)
Extracranial part
3. Main Motor Nucleus
lies deep in the reticular formation of the lower part of the
pons.
The part of the nucleus that supplies the muscles of the
upper part of the face receives corticonuclear fibers from both
cerebral hemispheres.
The part of the nucleus that supplies the muscles of the
lower part of the face receives only corticonuclear fibers from
the opposite cerebral hemisphere.
4. • Motor Nuclei:
– Efferent fibers surround
nuclei of CN VI & form
small mounds on floor of 4th
ventricle
(facial colliculi)
• Exits at cerebellopontine angle
(CPA) Facial colliculus
5. Lie posterolateral to the main motor nucleus.
They are :
Superior salivatory nuclei: receives afferent
fibres from the hypothalamus through the
descending autonomic pathways. Information
concerning taste from the oral cavity received
from the nucleus of the solitary tract.
Lacrimal nuclei: receives afferent fibres from
the hypothalamus for emotional responses
and from the sensory nuclei of the trigeminal
nerve for reflex lacrimation secondary to
irritation of the cornea or conjunctiva.
6. It is the upper part of the nucleus of the tractus
solitarius and lies close to the motor nucleus
Sensations of taste travel through the peripheral
axons of nerve cells situated in the geniculate
ganglion on the seventh cranial nerve. The central
processes of these cells synapse on nerve cells in
the nucleus. Efferent fibres cross the median plane
and ascend to opposite thalamus and to a number
of hypothalamic nuclei. From the thalamus, the
axons of the thalamic cells pass through the
internal capsule and corona radiata to end in the
taste area of the cortex in the lower part of the
postcentral gyrus
7.
8.
9. Exits IAC via Fallopian canal
The facial nerve enters the
labyrinthine segment of its fallopian
canal through the meatal foramen,
which is the narrowest portion of
the entire canal and measures
approx. 0.68 mm in diameter.
The labyrinthine segment (4 mm in
length) makes up the first segment
of the bony fallopian canal and is
the narrowest and shortest portion
of the canal.
The labyrinthine segment is
posterocephalad to the cochlea,
anteromedial to the ampulla of the
superior semicircular canal, and
posterior to the vestibule.
Felt to be culprit in facial nerve
compression in Bell’s palsy & other
causes of nerve swelling
Fallopian Canal
10.
11. Progress to
geniculate ganglion
First genu
Start of tympanic
segment
◦ Gives rise to greater
superficial petrosal
nerve
Geniculate ganglion
12.
13. Fibers then course posteriorly under lateral semicircular canal in
middle ear (tympanic portion)
The prominence of the facial canal, lying above the posterior edge
of the promontory and the oval window, immediately below and
parallel to the prominence of the lateral semicircular canal. It runs
almost horizontally across the posterior half of the medial wall, then
turns to enter the posterior wall. The facial nerve courses through
the canal.
Tympanic Portion
14. MASTOID SEGMENT
Behind the base of the pyramidal
eminence the canal makes a broad
turn (second genu) to descend
vertically and somewhat laterally
through the mastoid process. In this
descending or vertical portion the
nerve may have a slight anterior
concavity. The canal normally lies
deep to the sutural groove between
the tympanic and mastoid portions
of the temporal bone.
Here last somatic & parasympathetic
fibers separate from facial nerve via
the chorda tympani nerve
The nerve exits through the
sytlomastoid foramen
Mastoid segment
15. Middle Ear and Mastoid Surgery:
◦ Processus cochleariformis
◦ Oval window and horizontal canal
◦ Short process of the incus
◦ Pyramid
16. Nerve exits stylomastoid foramen:
Facial nerve angles superiorly & anteriorly behind posterior
margin of vertical mandibular ramus
Postauricular nerve - external auricular and occipitofrontalis
muscles
Branches to the posterior belly of the digastric and stylohyoid
muscles
Enters parotid gland splitting it into a superficial and deep lobe
PES ANSERINUS
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
17.
18. Parotid Surgery:
◦ Cartilaginous pointer
◦ Styloid process
◦ Posterior belly of digastric muscle
19. Small arteries derived from the
anteroinferior cerebellar branch of the
basilar artery,
The stylomastoid or occipital branches of
the external carotid, and
The petrosal arteries.
Insufficiency of the vascular supply to the
facial nerve, from whatever cause, is
regarded by some as one of the primary
causes of bell's palsy.
20. SVE (Special Visceral Efferent) — Motor to
striated muscles derived from the 2nd brachial
arch.
GVA (General Visceral Afferent) — Sensory
from visceral touch, temperature, and pain.
SVA (Special Visceral Afferent) — Taste
GVE (General Visceral Efferent) — Autonomic
innervation to mucosal, lacrimal, and salivary
glands.
GSA (General Somatic Afferent) — Sensory
from somatic touch, temperature, and pain.
21. Greater Superficial Petrosal Nerve (GSPN)
◦ GVA, GVE, SVA
Stapedial Nerve
◦ SVE
Chorda Tympani Nerve
◦ GVE, SVA
Posterior Auricular Nerve
◦ SVE, GSA
Facial Nerve (terminal branch)
◦ SVE
22. • Emerges from the geniculate
ganglion at the facial hiatus
and courses along the floor
of the middle cranial fossa
between layers of dura to
reach the foramen lacerum,
where it joins with the
carotid sympathetic nerves
to form the vidian nerve in
the vidian canal.
• After leaving the vidian
canal, they synapse with
postganglionic neurons in
the sphenopalatine ganglion
that innervate the lacrimal
gland and secretory glands
of the nose.
25. Innervation to muscles derived from the 2nd
branchial arch:
1. Stapedius muscle -- dampens movement of
the ossicles (inserts on stapes of middle ear)
2. Posterior auricular muscle -- posterior
movement of pinna
3. Stylohyoid muscle -- elevates hyoid bone
4. Posterior belly of digastric -- elevates hyoid
bone, depresses mandible
5. Muscles of facial expression -- blinking,
smiling, frowning, facial movements
26. Stapedius muscle dampens
movement of the ossicles
protecting the inner ear from
damage from loud noises
SVE
1. The Stapedius muscle dampens movement of the ossicles
27. The chorda tympani branch of the
facial nerve enters the middle ear
through the iter chordae posterius.
Passes forward and down between
the manubrium malleus and the long
process of the incus, then leaves the
cavity by passing through the
petrotympanic suture.
The chorda tympani has no function
in the middle ear. It contains both
parasympathetic fibres supplying the
submandibular and lingual glands
and taste fibres for the anterior two
third of the tongue.
After leaving the middle ear it joins
the lingual branch of V3 to be
distributed with that nerve.
28. Taste from the anterior
2/3 of the tongue
SVA
Chorda
tympani
32. Stylohyoid
muscle elevates
the hyoid bone.
Through the internal
Acoustic meatus
Through the
stylomastoid
foramen
The Stylohyoid muscle elevates the hyoid bone
Stylohyoid branch of
facial nerve
innervates stylohyoid
muscle
SVE
33. Through the
stylomastoid
foramen
The Posterior belly of digastric muscle elevates the hyoid bone
Posterior belly of
digastric branch of
facial nerve
innervates posterior
belly of digastric
muscle.
Posterior belly of
digastric muscle
elevates the
hyoid bone
SVE
Through the internal
acoustic meatus
34. A. Temporal branch (with zygomatic
branch) innervates orbicularis
oculi--closes eyelids
B. Zygomatic branch (with buccal
branch) innervates zygomaticus
major--smiling
C. Buccal branch innervates
buccinator--tenses cheek
D. Mandibular branch innervates
depressor angularis oris--
frowning
E. Cervical branch innervates
platysma -- lowers mandible,
tenses skin of anterior neck
*These are key innervations to the
muscles of facial expression.
However, each nerve branch
innervates multiple muscles and each
muscle receives multiple nerve
branches.
SVE
37. Buccal branch of
facial nerve innervates
Buccinator muscle.
SVE Contraction of the buccinator muscle
causes tensing of the cheek which
helps position food within the occusal plane
for chewing
39. Platysma muscle
Cervical branch of
facial nerve innervates
Platysma muscle.
Contraction of platysma
Muscle results in depression
of mandible.
SVE
40. Congenital bony dehiscences
may involve any part of the canal
most often found in the surroundings of the oval window,
located above and posterior to the oval window. During surgery
they should always be anticipated.
“As a rule they are less numerous and smaller in a well-
pneumatized temporal bone”.
The tiny shell of the facial canal can adhere to the jugular
dome, especially when the jugular bulb rises into the tympanic
cavity.
The facial canal may be dehiscent on its route to the
stylomastoid foramen.
41. Anomalies of the route of the facial
nerve
Classified under topographical aspects.
Frequently observed in cases of malformation and
are often associated with other abnormalities of the
external, middle, and inner ear.
An overhanging facial nerve might obstruct the
footplate.
The chorda tympani nerve origin may vary from1 to
11mm from the foramen, and in some cases the
origin is extratemporal.
Anomalous branching pattern of extratemporal
branches
42. • Endonerium
– Surrounds each nerve fiber
– Provides endoneural tube for regeneration
– Much poorer prognosis if disrupted
• Perinerium
– Surrounds a group of nerve fibers
– Provides tensile strength
– Protects nerve from infection
– Pressure regulation
• Epinerium
– Surrounds the entire nerve
– Provides nutrition to nerve
43.
44. – Class I (Neuropraxia)
• Conduction block caused by cessation of axoplasmic flow
• What one experiences when their leg “falls asleep”
• Full recovery
– Class II (Axonotmesis)
• Axons are disrupted
• Wallerian degeneration occurs distal to the site of injury
• Endoneural tube still intact
• Full recovery expected
– Class III (Neurotmesis)
• Neural tube is disrupted
• Poor prognosis
• If regeneration occurs, high incidence of synkinesis
(abnormal mass movement of muscles which do not
normally contract together)
45. ◦ Class IV
Epineurium remains intact
Perineurium, endoneurium, and axon disrupted
Poor functional outcome with higher risk for synkinesis
◦ Class V
Complete disruption
Little chance of regeneration
Risk of neuroma formation
46.
47. The facial nerve may be injured or become
dysfunctional anywhere along its course from
the brainstem to the face.
The paralysis may be supranuclear or
infranuclear.
48. Involves the upper motor neuron pathway
Usually a part of hemiplegia
Paralysis of lower part of face on contralateral side
Stroke, Lacunar infarcts
Brain abscess
Pontine glioma
Poliomyelitis
Multiple sclerosis
Progressive supranuclear palsy: Steele-Richardson-
Oleszewski syndrome
49. Lesion from facial nucleus to anywhere along the course of
facial nerve upto face
The disorder may even involve multiple segments of the
nerve.
The paralysis can be
Idiopathic
Trauma,
Systemic infection,
Acute or chronic otitis media,
Metabolic disorders,
Toxins,
Vasculitides,
Neurologic disorders,
Neoplasms (both benign and malignant),
Radiation therapy, and
Numerous other causes
50. Abrupt, unilateral, peripheral facial paresis or paralysis
without a detectable cause.
First described by Sir Charles Bell
60-70% cases
Pathophysiology – Impaired “axoplasmic” flow from
edema of facial nerve within fallopian canal
Other theories: viral infection, ischaemia, autoimmune
disorder
Rapid onset and evolution < 48 hours
May be associated with acute neuropathies of cranial
nerves V- X
Pain or numbness affecting ear, mid-face, tongue and
taste disturbances
Recurrences are more likely (2.5x) in patients with family
history, immunodeficiency or diabetes
51. 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.
52. 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
53. 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.
54. Bell's phenomenon—upward diversion of the
eye on attempted closure of the lid—is seen
when eye closure is incomplete.
55. Bell palsy is a diagnosis of exclusion.
Other disease states or conditions that
present with facial palsies are often
misdiagnosed as idiopathic.
80-90% recover completely
◦ Over age 60, only 40% recover completely
56. Imaging in typical Bell’s palsy is not usually
necessary
◦ When necessary, MRI is best
Normal facial nerve distal to geniculate ganglion
may enhance
◦ Facial nerve proximal to geniculate ganglion does not
normally enhance
In patients with Bell’s palsy, enhancement of facial
nerve in fallopian & ICA is typical
57.
58. Clinical features
◦ Slower onset of symptoms
◦ Bilateral
◦ Recurrence
Numbness is not unusual
Progression beyond seven days
suggests another cause
59.
60. 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.
61. Usual regimen is 1mg/kg/day for 1 week.
To be tapered in the 2nd week.
62. 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.
63. 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.
Usual regimen is 4000mg/24hrs divided into
5 doses for 7 to 10 days
64. Eye protection –artificial tears
Follow progression with serial examination
Facial nerve decompression
Progression to > 90% degeneration on ENoG
Performed before irreversible injury to the endoneural
tubules occurs (two weeks), will allow for axonal
regeneration to occur
65. Peripheral facial paralysis with erythematous vesicular rash in
the EAC, pinna or mouth
Caused by reactivation of varicella zoster virus (herpes virus
type 3)
◦ Herpes zoster oticus
Other cranial nerves, particularly trigeminal nerves (5th CN)
often involved
Rising titres of antibodies to VZV
Worse prognosis than Bell’s (complete recovery: 50%)
Important cause of facial paralysis in children 6-15 years old
67. Triad
◦ Recurrent orofacial
edema
◦ Recurrent facial palsy
(50-90%)
◦ Lingua plicata (fissure
tongue) – 25%
Lips become chapped,
fissured and red-brown
in appearance
Biopies identify
granulomatous changes
Facial nerve
decompression may be
indicated if facial
paralysis is severe and
recurrent
68. -Second most common cause of FN
paralysis behind Bell’s Palsy
-Represents 15% of all cases of FN
paralysis
-Most common cause of traumatic facial
nerve injury is temporal bone fracture
-Maxillofacial trauma
-Iatrogenic
69. 5% of trauma patients sustain a temporal bone fracture
– Three types
» LONGITUDINAL
Most common type – 70-80%
Fracture line parallel to long axis of petrous pyramid
Secondary to temporoparietal blunt force
Results in facial nerve paralysis in 25% of cases
» TRANSVERSE
10-20% of fractures
Fracture line perpendicular to long axis of petrous pyramid
Secondary to frontal or occipital blow
Results in facial nerve paralysis in 50% of cases
» MIXED
10% of temporal bone fractures
70. • Chang and Cass (1999) reviewed facial nerve
pathology of 67 longitudinal fractures and 11
transverse fractures where facial nerve paralysis
was known
– Longitudinal findings
• Perigeniculate region, tympanic segment
• 76% of cases showed bony impingement or intraneural
hematoma
• 15% showed a transected nerve
• 9% either had no pathologic findings or just neural edema
– Transverse findings
• Labyrinthine or mastoid segment
• 92% of cases showed transection
• 8% showed bony impingement or hematoma
71. -Typically results in FN injury in the extratemporal
segments
-Gun shot wounds cause both intratemporal and
extratemporal injuries
MC site- mastoid segment
GS wounds to temporal bone result in FN paralysis
in 50% of cases
Mixture of avulsion and blunt trauma to different
portions of the nerve
Much worse outcome when comparing GS related
paralysis to TB fracture related paralysis
72. – 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%
– Exostoses removal – 14%
– Stapedectomy
– Mechanism - direct mechanical injury or heat generated from
drilling
– Most common area of injury - tympanic portion due to its high
incidence of dehiscence in this area, and its relation to the
surgical field
• Unrecognized injury during surgery in nearly 80% of cases
74. 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
Immuno-compromised patients are at
risk for pseudomonas infection
Mastoiditis
Parotid & peri-parotid disease
HIV
Lyme disease
Meningitis
Chickenpox
Encephalitis
Poliomyelitis
Mumps
Mononucleosis
Leprosy
Influenza
Coxsackie virus
Malaria
Syphilis
Botulism
Mucormycosis
76. Neurogenic causes
Millard-Gubler syndrome
(abducens palsy with
contralateral hemiplegia
owing to lesion in base of
pons involving corticospinal
tract)
Opercular syndrome
(cortical lesion in facial
motor area)
Toxic
•Thalidomide (cranial nerves VI
and VII with atretic external
ears [Miehlke syndrome])
•Tetanus
•Diphtheria
•Carbon monoxide
•Lead intoxication
77. About 5% of cases of facial nerve paralysis
are caused by tumors
Characteristics of facial nerve palsy
Slow developing
Additional cranial nerve deficits
Recurrent ipsilateral involvement
Adenopathy
Palpable neck or parotid mass
78. 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
Other neoplasms can also involve the facial
nerve
◦ Adults: metatstatic disease, glomus tumors,
vestibular schwannomas & meningiomas
◦ Children: eosinophilic granuloma & sarcomas
79.
80.
81.
82. Glomus tumors arising
from jugular bulb
(jugulare) and/or middle
ear (tympanicum) may
involve the facial nerve
83. Common tumor
However, tends to produce facial paralysis
mostly when they attain a large size
84. Second most common
primary tumor of
cerebellopontine angle
Rarely results in facial
paralysis
86. History
Onset: Sudden vs. Gradual
Duration:
Rate of progression:– progressive loss of function or sudden
loss
○ Transected nerve -> sudden loss
○ Intraneural hematoma or impingement -> progressive loss
(better prognosis)
Recurrent or familial
recent surgery, facial/head trauma
Associated symptoms – hearing loss or vertigo (hint more toward a
temporal bone injury)
Medical history
87. Perform a full head and neck examination
Complete vs. incomplete
Segmental vs. uniform involvement
Unilateral vs. bilateral
Facial asymmetry
– Signs of facial injury (lacerations, hematomas, bruising)
– Exam head/scalp for signs of injury to help guide you to vector of force if head
trauma is involved
Otoscopic examination is a must
• Canal lacerations or step-offs
• Hemotympanum, TM perforation, drainage of blood or clear fluid from middle ear
• Polyposis or granulations in the ear canal may suggest cholesteatoma or
malignant otitis externa.
Tuning fork tests (Weber/Rinne) with a 512 Hz fork can help
determine if there is a conductive hearing loss
Cranial nerves assessment
Neurologic evaluation
Cerebellar signs
88. Localization of facial nerve lesion:
Central vs. Peripheral.
Peripheral
◦ Level of nucleus
◦ CPA level:
◦ Bony canal level: Topodiagnostics
◦ Outside the Temporal bone
89. Grade Characteristics
I. Normal facial function in all areas
II. Mild dysfunction •Slight weakness noticeable on close inspection
•Forehead - Moderate-to-good function
•Eye - Complete closure with minimal effort
•Mouth - Slight asymmetry
III. Moderate dysfunction
-First time you can notice a difference at rest
•Obvious but not disfiguring difference between the two sides
• Forehead - Slight-to-moderate movement
•Eye - Complete closure with maximum effort
•Mouth - Slightly weak with maximum effort
IV. Moderately severe dysfunction
-First time you have incomplete eye closure
-No forehead movement
•Obvious weakness and/or disfiguring asymmetry
• Forehead – No motion
•Eye - Incomplete closure
•Mouth - Asymmetric with maximum effort
V. Severe dysfunction •Only barely perceptible motion
•At rest, asymmetry
•Forehead – No movement
•Eye - Incomplete closure
•Mouth - Slight movement
VI. Total paralysis No movement
90. • Degree of electrical dysfunction
• Site of injury
• Helps determine treatment
• Can predict recovery of function – partial
paralysis is a much better prognosis than total
paralysis
• Divided into two categories
– Topographic tests
• Tests function of specific facial nerve branches
• Do not predict potential recovery of function
• Rarely utilized today
– Electro diagnostic tests
• Utilize electrical stimulation to assess function
• Most commonly used today
91. Intended to determine the level of facial nerve injury by
testing peripheral facial nerve function.
The underlying hypothesis is that injury to the facial nerve at
a particular location will affect all branches proximal to the
lesion, yet leave distal branches with normal function.
Schirmer test: if tearing is diminished the lesion is assumed
to be proximal to the point at which the greater superficial
petrosal nerve branches from the geniculate ganglion.
Immittance testing (abnormal stapedial muscle function
reflecting nerve impairment above the stapedial motor
branch),
Salivary secretion and taste testing (chorda tympani nerve
function).
92. To evaluate for concurrent SNHL or CHL
CHL – middle ear tumors, cholesteatomas,
other processes involving tympanic segment
SNHL – acoustic neuromas, meningiomas,
congenital cholesteatoma, others involving
CPA or IAC
93. • Compares amount of current required to illicit
minimal muscle contraction - normal side vs.
paralyzed side
• How it is performed
• A stimulating electrode is applied over the stylomastoid
foramen
• DC current is applied percutaneously
• Face monitored for movement
• The electrode is then repositioned to the opposite side, and
the test is performed again
• A difference of 3.5 mA or greater between the two
sides is considered significant
• Drawback - relies on a visual end point (subjective)
94. • Similar to the NET, except it utilizes
maximal stimulation rather than minimal
• The paralyzed side is compared to the
contralateral side
• Comparison rated as equal, slightly
decreased, markedly decreased, or absent
– Equal or slightly decreased response = favorable
for complete recovery
– Markedly decreased or absent response =
advanced degeneration with a poor prognosis
• Drawback - Subjective
95. Thought to be the most accurate of the electrodiagnostic
tests
How it works:
◦ Bipolar electrodes deliver an impulse to the FN at the
stylomastoid foramen
◦ Summation potential is recorded by another device
◦ The peak to peak amplitude is proportional to number of
intact axons
◦ The two sides are compared as a percentage of response
90% degeneration – surgical decompression should be
performed
Less than 90% degeneration within 3 weeks predicts 80 -
100% spontaneous recovery
Disadvantages: discomfort, cost, and test-retest variability
96. • Determines the activity of the muscle itself
• How it works
– Needle electrode is inserted into the muscle, and
recordings are made during rest and voluntary
contraction
• Normal = biphasic or triphasic potentials
• 10-21 days post injury - fibrillations
• 6-12 weeks prior to clinical return of facial
function – polyphasic potentials are recordable
– Considered the earliest evidence of nerve recovery
• Does not require comparison with normal side
97. CT scans
◦ Bony evaluation
◦ Locate middle ear, mastoid, and temporal bone pathology
Gadolinium enhanced MRI
◦ Utilized for soft tissue detail and CPA pathology
98. Incomplete recovery
Exposure keratitis
Synkinesis
Tics and spasms
Crocodile tears
Frey’s syndrome “gustatory sweating”
Psychological and social problems
Abnormal facial expressions
Mastication
Speech production
99.
100. • If transected during surgery
– Explore 5-10mm of the involved segment
– Stimulate both proximally and distally
• Response with 0.05mA = good prognosis;
further exploration not required
• If only responds distally = poor prognosis, and
further exposure is warranted
101. • If loss of function is noted following surgery, wait 2-3 hours and
then re-evaluate the patient.
• This should be ample time for an anesthetic to wear off
– Waited time and still paralysis
• Unsure of nerve integrity – re-explore as soon as possible
• Integrity of nerve known to be intact
– High dose steroids – prednisone at 1mg/kg/day x 10 days
and then taper
– 72 hours – ENoG to assess degree of degeneration
» >90% degeneration – re-explore
» <90% degeneration – monitor
if worsening paralysis occurs re-explore
if no regeneration, but no worsening, timing of exploration
or whether to is controversial
102. • Birth trauma and Extratemporal blunt trauma
– Recommend no surgical exploration
– >90% expected to regain normal/near normal recovery
• Complete paralysis following temporal bone fracture
– Likely nerve transection
– Surgical exploration
• Partial or delayed loss of function
– Approach similar to iatrogenic partial or delayed loss
– High dose steroids
– ENoG 72 hours
• >90% degeneration – explore
• < 90% degeneration – can monitor and explore at later date
depending on worsening or failure to regenerate
103. • 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
• Diamond burs and copious irrigation is utilized to prevent
thermal injury
• Thin layer of bone overlying the nerve is bluntly removed
• Whether to perform neurolysis or not to open the nerve
sheath is debatable
– Recommended to drain hematoma if identified
104. Performed in severe cases when the facial nerve
is seriously deteriorating.
Patients are at risk for permanent paralysis and
have a poor prognosis without aggressive
intervention.
Research has shown that this procedure is
effective in improving outcomes in a selected
group of patients.
To be effective, the surgery must be performed
within 2 weeks of the onset of symptoms.
106. • Recovery of function takes around 4-6 months
• Nerve regrowth occurs at 1mm/day
• Goal is tension free, healthy anastomosis
• Rule is to repair earlier than later - controversial
– 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
– Some recommend repair within 30 days, but others have found
superior results if done up to 12 months out
• 2 weeks following injury -> collagen and scar tissue
replace axons and myelin
– Nerve endings must be excised prior to anastomosis
107. • Best overall results of any surgical intervention
• Done if defect is less than < 2cm
– Mobilization of the nerve can give nearly 2cm of length
– With more mobilization comes devascularization
• Endoneurial segments must match - promotes
regeneration
• Ends should be sutured together using three to
four 9-0 or 10-0 monofilament sutures to bring
the epineurium or perineurium together
108. Approach is based on availability of proximal
nerve ending
Performed for defects > 2cm
Results in partial or complete loss of donor
nerve function
109. • Great auricular nerve
– Usually in surgical field
– Located within an incision made from the mastoid tip to the angle
of the mandible
– Can provide only upto 12cm of length
– Loss of sensation to lower auricle
• Sural nerve
– Located 1 cm posterior to the lateral malleolus
– Can provide 35cm of length
– Very useful in cross facial anastomosis
– Loss of sensation to lateral calf and foot
• Ansa Cervicalis
– Only utilized if neck dissection has been performed
• 92-95% of these patients have some return of facial
function
• 72-75% have good results (HB 3 or above)
110. • Requires that the patient have an intact distal nerve segment
and facial musculature suitable for reinnervation
– Determined by EMG and/or muscle biopsy
• Hypoglossal nerve
– Direct hypoglossal-to-facial graft
• Distal branch of facial nerve is attached to hypoglossal nerve
• 42-65% of patient’s expected to experience decent symmetry and
tone
• Complications – atrophy of ipsilateral tongue, difficulties with
chewing, speaking, and swallowing
– Partial hypoglossal-to-facial jump graft
• Uses a nerve cable graft, usually the sural nerve, to connect the
distal end of the facial nerve to a notch in the hypoglossal nerve
• Much fewer complications, but increased time
• May compared the results of direct VII-XII graft to the VII-XII jump
graft
Also known as Nerve transposition
112. • Facial-to-Facial Graft
Nerve Substitution
Is indicated when the nerve cannot be repaired in the
conventional manner.
In this procedure, another cranial nerve involved in
facial movement is connected to the damaged nerve
and takes over its function.
113. 113
– Options
• Single contralateral branch to distal nerve
anastomosis
• Multiple anastomoses from segmental branches to
segmental branches
– Best described is the use of a sural nerve graft to
connect the buccal branch on the contralateral
side to the distal nerve stump
– Most do not recommend this technique
• Weakness caused to the contralateral facial nerve
• Lack of power to control musculature resulting in
poor results
114.
115. Dynamic procedures
◦ Aim to reproduce movement in paralyzed face
◦ Improves symmetry at rest and in motion
Static procedures
◦ Alter the facial posture
◦ Alter the facial symmetry at rest
◦ Improve oral continence
◦ Improve nasal valve collapse
◦ No voluntary facial movement
116. Musculofascial transpositions:
◦ Move new muscles and nerves into the face to
take the place of the injured facial nerve.
Facial plastic procedures.
Prosthetics.
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117. 117
Involves taking a 1-2 cm band of the temporalis
muscle.
Rotating it from the temple region, over the
cheek bone and down, to attach to the corner of
the mouth.
When it is appropriately secured, the act of biting
down will result in elevation of the corner of the
mouth toward the cheekbone, just as in smiling.
121. In a combination muscle and nerve graft, two
procedures are performed several months apart.
Free muscle tissue is grafted from the leg to the
face following a cross-facial nerve graft.
The nerve graft becomes the nerve supply for the
healthy, transplanted muscle.
124. Is accomplished by one of
several techniques
Blepharoplasties: The eyebrow
can be repositioned by
performing a unilateral brow lift,
and matching the brow height
with the other side.
The eyelids can be addressed
using implantable eyelid springs
so that gravity assists with eye
closure.
Using lid gold weights
Canthoplasty
126. The collapse of the nasal sidewall
can be corrected either from the
outside or the inside of the nose.
Outside techniques involve
placing strips of suspension
material from the cheekbone,
under the skin, to the nasal
sidewall, and suspending the
nasal sidewall in its anatomic
position.
127. 12
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To widen the nasal cavity from the
inside, small cartilage grafts can be
inserted into the framework of the nose.
