About facial neve

1. Disorders of facial nerve
Dr vivek malpani
Nims medical college
Jaipur

6. SADDONS CLASSIFICATION

7. Sunderland classification

8. • 🞤 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

9. HOUSE-BRACKMANN FACIAL NERVE
GRADING SYSTEM

10. • Audio visual on facial nerve grading…..

11. LMN vs UMN

12. What is UMN
. The motor neurons that reside in cerebral cortex above the nuclei of
cranial nerves or the anterior horn cells of the spinal cord.
. Upper motor neurons relay information from the brain to the
spinal cord and brainstem.
. Lesion in these neurons or in their axons is known as UMN or
SUPRANUCLEAR lesion.

13. What is LMN
• Lower motor neurons directly innervate skeletal
muscle.
• They have cell bodies in cranial nerve nuclei in brain
stem or in the anterior horn of the spinal cord (ventral
horn).
• . The motor nucleus that belongs to the facial nerve, is a
collection of neurons in the brainstem.
• . This is the lower motor neuron that innervate the
muscles of facial expression and the stapedius.

14. LMN LESION OF FACIAL NERVE
• If the lesion occurs anywhere from the facial nucleus along the nerve
course, it will result in LMN deficits. (Bell's palsy.)
• the facial nerve can get damaged at :
1. Internal acoustic meatus
2. Middle ear
3. Facial nerve canal/fallopian canal
4. In the parotid gland

15. • Lower motor neurone (LMN) facial palsy is characterized by ipsilateral
paralysis of all the upper and lower muscles of facial expression.
• Because the forehead is involved, the affected individual will be
unable to wrinkle their forehead and not able to lift their eye brow.
• The patient is unable to close the eye on that side.
• The corner of the mouth droops.
• The nasolabial fold is obliterated.
• Saliva may dribble from the angle of mouth.
• Food collects in the vestibule on the affected side.

16. Why there is sparing of the forehead muscles
in UMN lesion?
• If any part of the corticobulbar tract from the motor cortex to the facial
nerve nucleus is damaged, it will result in UMN deficits.
• This will result in contralateral facial paralysis involving the lower muscles
of facial expression.
• The neurons supplying the lower face receive upper motor neurons (UMN)
from the contralateral motor cortex only.
• Whereas the neurons to the upper face receive bilateral UMN innervation.
An UMN lesion, therefore, causes unilateral facial palsy with sparing of the
frontalis and orbicularis oculi muscles because of the bilateral cortical
representation of forehead muscles.

18. Tests for facial nerve
• T
opographic diagnosis
• Electro-diagnostic testing

19. TOPOGNOSTIC TESTING
1. Schirmer test for lacrimation (Geniculate ganglion)
2. Stapedial reflex test (stapedial branch)
3. Taste testing (chorda tympani nerve)
4. Salivary flow rates and pH (chorda tympani)

22. SCHIRMER TEST
🞭 The reflex is consensual; that is, the irritating stimulus
in either eye causes tearing in both eyes, and a
unilateral sensory (trigeminal) deficit will reduce tearing
bilaterally. However, unilateral corneal anesthesia
reduces tearing asymmetrically, with a greater
reduction on the anesthetized side. (Crabtree and
Dobie, 1989);
🞭 when a sensory deficit is present, one should consider
bilateral corneal anesthesia and stimulation of
lacrimation by other noxious stimuli (for example,
inhalation of ammonia)

23. SCHIRMER TEST
🞭 Schirmer's test is usually considered positive if
🞭 the affected side shows less than half the amount of lacrimation seen on
the normal side.
🞭 a total response (sum of the lengths of wetter filter paper for both
eyes) of less than 25 mm is considered abnormal.

25. • It is absent in 69% of cases of Bell's palsy (84% when the
paralysis is complete) at the time of presentation (Koike et al,
1977);
• It can be elicited by either ipsilateral or contralateral
acoustic stimulation, or in cases of bilateral severe hearing
loss, by tactile or electrical stimulation.

26. TASTE TESTING (ELECTROGUSTOMETRY)
🞭 Psychophysical assessment can be performed with
natural stimuli, such as aqueous solutions of salt, sugar,
citrate, and quinine, or with electrical stimulation of the
tongue.
🞭 Electrical stimulation (electrogustometry), has the
advantages of speed and ease of quantification
🞭The tongue is stimulated electrically to produce a metallic
taste & Threshold of the test is compared between two
sides.

27. ELECTROGUSTOMETER

28. TASTE TESTING (ELECTROGUSTOMETRY)
🞭 In normal subjects, the two sides of the tongue have similar thresholds for
electrical stimulation, rarely differing by more than 25%
🞭 thresholds difference of more than 25% is abnormal
🞭 Taste function apparently recovers before visible movement in some
cases, so if the results of electrogustometry are normal in the second week
or later, clinical recovery is imminent.
🞭 Total lack of Chorda tympani : No response at 300 uAmp
🞭 Disadvantage : False +ve in acute phase of Bell’s palsy

29. SALIVARY FLOW TESTING
🞭 For Chorda tympani
🞭 The patient is advised to refrain from intake of any food or beverage (water
exempted) one hour before the test session. Smoking, chewing gum and
intake of coffee also are prohibited during this hour. The subject is advised to
rinse his or her mouth several times with deionized (distilled) water.
🞭 Cannulation of Wharton's ducts bilaterally
🞭 Gustatory stimulus – 6% citric acid on anterior Part of tongue
🞭 Output is measured after 5 minutes.
🞭 Significant if 25% reduction in flow of the involved side as compared to the
normal side
🞭 Salivary pH  Flow Rate
🞭 Submandibular salivary pH of 6.1 or less predicts incomplete recovery in
cases of Bell's palsy.

30. SALIVARY FLOW TESTING

31. ELECTRO-PHYSIOLOGICAL TESTS
🞤 Nerve excitability test (NET)
🞤 Maximal stimulation test (MST)
🞤 Electromyography (EMG)
🞤 Electroneuronography (evoked
electromyography) (ENoG)

32. NERVE EXCITABILITY TEST (NET)
🞭 Compares transcutaneous current threshold required to
elicit minimal muscle contraction between two sides
🞭 The stimulating electrode is placed on the skin over the
stylomastoid foramen with a return electrode taped to the
forearm.
🞭 Beginning with the normal side, electrical pulses (0.3 msec
in duration) are delivered until a facial twitch is just
noticeable.
🞭 The lowest current eliciting a twitch is the threshold of
excitation.

33. NERVE EXCITABILITY TEST (NET)
🞭 Next, the process is repeated on the paralyzed side, and the
difference in thresholds between the two sides is calculated.
🞭 After a more severe injury (Sunderland class II to V), in
which distal axonal degeneration occurs, electrical
excitability is gradually lost.
🞭 A difference of 3.5 milliamperes (mA) or more in thresholds
between the two sides is a reliable indicator of progressive
degeneration and has been used as an indicator for surgical
decompression
🞭 The NET is useful only during the first 2 to 3 weeks of
complete paralysis before complete degeneration has
occurred.
🞭 It is unnecessary in cases of incomplete paralysis, in which
the prognosis is always excellent

34. NERVE EXCITABILITY TEST (NET)
🞭 Once excitability is lost and that result is confirmed by
repeat testing, further excitability tests are pointless
because clinically evident recovery always begins before
any apparent electrical excitability returns.
🞭 Electrical stimulation is generally relatively ineffective in
eliciting a synchronous and thus observable twitch in the
early stages of regeneration. Similarly, if a paralysis that has
become complete begins to recover clinically before any
degeneration is noted, continuing stimulation is unnecessary
because recovery will be rapid and complete.

35. 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.
🞭 The electrode type and placement and the nerve-stimulating
equipment are the same as in the NET.
🞭 Increasing current levels are used until maximal movement
is seen, and the paralyzed side is compared to the normal
side (maximal nevre stimulation(~5mA)
🞭 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

36. 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.

38. 🞭Polyphasic potential indicate regenerative
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

39. 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)
🞭 Responses to maximal electrical stimulation of the two
sides are compared
🞭 Responses are recorded electrically by a bipolar
electrode pair placed in the nasolabial groove.

40. EVOKED ELECTROMYOGRAPHY
(EEMG) OR EVOKED
ELECTRONEURONOGRAPHY
(ENOG)
🞭 Most valuable prognostic indicator---Its main indication
is in 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.

42. EVOKED ELECTROMYOGRAPHY
(EEMG) OR EVOKED
ELECTRONEURONOGRAPHY (ENOG)

43. ◾ )
🞭 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 because of nerve
fibre desynchronization
🞭 Advantages: Reliable
🞭 Disadvantages:
🞤 Uncomfortable
🞤 Cost
🞤 Test-retest variability due to position of electrodes

44. LIMIT
A
TIONOFELECTROPHYSIOLOGICAL
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)

45. DISORDERS
• FACIALPARALYSIS

47. BELL
’SPALSY
🞭 Bell palsy is the most common cause
of facial paralysis worldwide.
🞭 Paralysis of all muscle groups on one
side of the face, sudden onset,with
absence of signs of CNS disease;
absence of signs of ear or cerebello-
pontine angle disease.
🞭 first described by Sir Charles Bell

48. DEMOGRAPHICS:
🞭Race: more in Japanese descent.
🞭 Sex: No difference exists
🞭 Age: can occur at any age, but more in 5th and
6th decade of life(poor recovery in older pt.)
🞭 Recurrence rate 7-12%
🞭 Familial incidence is about 10%
🞭 pregnancy and eclampsia increases the risk
of developing acute facial palsy

49. 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.
🞭 Herpes zoster virus shows more aggressive
biological behaviour than herpes simplex virus
type 1
🞭 PCR techniques have isolated herpes virus DNA
from the facial nerve during acute palsy.
🞭 Inflammation of the nerve initially results in a
reversible neurapraxia,
The facial paralysis in Bell's palsy may be abrupt in
onset and can progress to complete paralysis over
1 to 7 days.

50. PATIENT‘SHISTORY:
🞭 Sudden in onset and evolves rapidly, with
maximal facial weakness developing within two
days.
🞭 A slow onset progressive palsy with other cranial
nerve deficits or headache raises the possibility
of a neoplasm
🞭 Associated symptoms may be hyperacusis,
decreased production of tears, and altered taste.
🞭 otalgia or aural fullness and facial or
retroauricular pain, which is typically mild and
may precede the palsy.

52. PHYSICALEXAM:
🞭Bell's palsy causes a peripheral LMN
palsy,
🞭U/L impairment of movement in the
facial & platysma muscles, drooping of
the eye brow & corner of the mouth, &
impaired closure of the eye and mouth.
🞭Bell's phenomenon—upward &
outwards diversion of the eye on
attempted closure of the lid—is seen
when eye closure is incomplete.

53. PHYSICALEXAM:
🞭Polyposis or granulations in EAC
suggest cholesteatoma or malignant
otitis externa.
🞭 Vesicles in the conchal bowl, soft
palate, or tongue suggest Ramsay Hunt
syndrome
🞭 A deep lobe parotid tumour may only be
identified clinically by careful
examination of the oropharynx and
ipsilateral tonsil to rule out asymmetry.

54. MANAGEMENT, STEROID
🞭 Usual regimen is 1mg/kg/day for 1 week.
🞭 To be tapered in the 2nd week.
🞭 ANTIVIRALS , Usual regimen 200 mg – 400 mg,
5 times a day for 10 days

56. OUTCOMES:
🞭 In patients who recover without treatment,
major improvement occurs within three weeks
in most.
🞭 If recovery does not occur within this time, then
it is unlikely to be seen until four to six months,
when nerve regrowth and reinnervation have
occurred.
🞭 Patients with a partial palsy fair better, with
94% making a full recovery.
🞭 The outcome is worse when herpes zoster
virus infection is involved

57. BADPROGNOSTICF
ACTOR:
🞭 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

58. MELKERSSON-ROSENTHAL SYNDROME
🞭 u/l facial paralysis
🞤 Facial swelling
🞤 Fissured tongue
🞭 Very rare
🞭 Familial but sporadic
🞤 Usually begins in
adolescence
🞭 Leads to facial disfigurement
🞭 No definite therapy

59. RAMSAY HUNT SYNDROME
🞤 Herpes zoster oticus
🞭 Caused by reactivation varicella zoster virus (herpes
virus type 3)
🞭 Facial paralysis + hearing loss +/- vertigo
🞭 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

60. 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.

62. 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
pseudomonas infection
⚫ Poor prognosis (complete recovery is < 50%)
Necrotizing otitis externa (NOE) classically occurs in
elderly patients wlith poorly controlled diabetes mellitus or in
patients who are immunosuppressed

63. LYME DISEASE
🞭 aka borreliosis., caused by spirochete
borelia burgdorferi.
🞤 Endemic areas (Northeast USA, central Europe,
Scandinavia, Canada)
🞤 Consider in children w/atypical facial palsy
🞭Imaging: small white matter lesions similar to
multiple sclerosis, enhancement of facial &
other cranial nerves
🞭 Bilateral facial paralysis: 25%
🞭Important to make diagnosis early because it
is curable early with antibiotics

64. 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
⚫ Other neoplasms can also involve the facial
nerve
◦ Adults: metatstatic disease, glomus tumors,
vestibular schwannomas & meningiomas
◦ Children: eosinophilic granuloma & sarcomas

65. GLOMUS TUMOR
⚫ Glomus tumors arising from jugular bulb (jugulare)
and/or middle ear (tympanicum) may involve the
facial nerve
VESTIBULAR SCHWANNOMA
Common tumor
🞭However, facial nerve is resistant to
compression,therefore, tends to produce facial
paralysis mostly when they attain a large size.

66. OTHER CAUSES
🞭 Guillain-Barre Syndrome
🞤 Ascending paralysis
🞭 Iatrogenic
🞤 T
emporal bone surgery
🞫Excision of vestibular schwannoma has <10%
chance of paralysis
🞫Middle ear surgeries
🞤 Babies who required forceps delivery
🞫>90% recovery

67. 🞭 Rcurrent facial palsy is
seen in
🞤 Bell’s palsy,
🞤 Melkersson’s syndrome,
🞤 diabetes,
🞤 sarcoidosis
🞤 tumuors

68. TRAUMATIC FACIAL PARALYSIS
- 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

69. TEMPORALBONEFRACTURE
– 5% of trauma patients sustain a temporal bone fracture
– 3 types
» Longitudinal
🞤 Most common type – 70-80%
🞤 Fracture line parallel to long axis of petrous pyramid
🞤 Secondary to temporopartietal blunt force
🞤 facial nerve paralysis in 25% of cases(delayed)
🞤 Hemotymoanum, ,ossicular chain disruption
» Transverse
🞤 10-20% of fractures
🞤 Fracture line perpendicular to long axis of petrous
pyramid
🞤 Secondary to occipital blow
🞤 facial N. paralysis in 50% of cases(immediate)
🞤» Mixed
🞤 10% of temporal bone fractures
🞤 Snhl, vestibular dysfn

71. IA
TROGENICTRAUMA
– 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

72. SURGICALTREA
TMENT FORF
ACIALNERVE
INJURY
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
For parotid surgery
 Cartilaginous tragal pointer
of conley
 Tympanomastoid
suture
 Posterior belly of
digastric
 Styloid process

73. A. Facial nerve decompression
B. Neurorrhaphy(nerve repair)
1.direct end to end anastomosis
2. interposition cable grafting: sural / great auricular
C. Facial reanimation

74. FACIAL NERVE DECOMPRESSION
• Performed in severe cases when the facial nerve is seriously
deteriorating
• Patient are at high risk of permanent paralysis and have a poor
prognosis without aggressive intervention
• To be effective , surgery must be performed within 2 weeks of the
onset of symptoms after doing detailed clinical work up and
investigations

75. PREOPERATIVE PLANNING
• ENoG :10% or less muscle function on affected side
(degneration of >90% nerve fibers indicates poor
recovery).
• EMG : fibrillations or complete silence on the graph
• HRCT : trauma ,fallopian canal involvement in CSOM
or temporal bone malignancies
• MRI: suspicion of underlying tumor (schwannomas,
neuromas,hemangiomas)
• Audiometric tests : associated hearing loss , surgical

76. Site to be explored -
Based on causes of facial paralysis and suspected site of
injury
• Bells palsy : the labyrinthine segment and perigeniculate
region are decompressed via a middle fossa approach.
• Acute or chronic otitis media : the mastoid and tympanic
segments are explored via transmastoid approach .
• Canal wall down mastoidectomy :cholesteatoma involving
facial nerve
• Intraoperative injury :directed to the site of injury

77. SURGICAL APPROACHES
Selection of the surgical approach is determined by the
location of the facial nerve injury and hearing status in the
affected ear
• Trans-mastoid approach
• Middle cranial fossa approach
• Translabyrinthine approach

78. 1. TRANSMASTOID APPROACH
Indication
• Tumors and cholesteatomas limited to mastoid and tympanic
segment
• Longitudinal fracture limited to mastoid segment
• AOM,COM involving tympanic segment and mastoid segment of
facial nerve.
Limitations
• Limited access to geniculate ganglion
• No access to labyrinthine segment

79. Steps -
• Post. Auricular incision is made in the hairline (2-
3cm ).
• Complete mastoidectomy is performed .
• The landmarks for vertical segment of facial
nerve are –
horizontal SCC, fossa incudis, incus, chorda
tympani nerve and digastric ridge.
 Facial recess is opened , giving access to
tympanic segment.
 Diamond bur is used to delinate the course of
the nerve.

80. • Once the fallopian canal in the tympanic and mastoid
segments has been exposed,any residual impinging
bony spicule is removed.
• The circumference of the facial nerve should be
exposed for 180 degrees .
• The nerve sheath is opened at the site of injury and
for a short distance proximal and distal to the site of
injury to assess the severity of injury tothe fascicles.
• If the fascicles are intact, the decompression
procedure is complete.
• If more than 50% of the nerve fascicles have
been violated or the nerve is completely
transected, primary neurorrhaphy or cable
grafting is indicated.

81. 2. MIDDLE CRAINAL FOSSA APPROACH
Exposure from IAC to tympanic segment (for intracanalicuar and
labyrinthine segments)
Indication:
A) Bells palsy
B) Temporal bone fractures
Advantages:
A) MCF approach can gain the necessary exposure of the labyrinthine
segment, IAC, and CPA while preserving hearing
B) Geniculate ganglion and tympanic segment can be decompressed
C) Combined with retrolabyrinthine ,transmastoid for entire facial nerve
exposure

82. • A posteriorly based skin flap (6*8 cm ) is created within the hairline above
the ear.
• a large piece of 4x4 cm temporalis fascia graft harvested for later
use to cover the MCF floor.
• An anteriorly based temporalis muscle flap is elevated. Care is
taken to prevent injury to the frontal branch of the facial nerve, which
lies on the undersurface of the superficial temporalis (
temporoparietal) fascia.
• A 4 x 5-cm craniotomy, located above the zygomatic root is created
with help of burrs.
• The bone flap is dissected from the temporal lobe dura; care is taken
to protect the middle meningeal artery that is sometimes encased
within the bone. Dura is elevated from the MCF floor.
• Petrous ridge is identified, it is the medial limit of dissection.

83. • Locating SCC allows identification of : IAC,
cochlea, GG and tympanic cavity.
•The dura of the internal auditory canal
(IAC) is opened.
• The acousticofacial bundle (AFP) can
be seen within the opened internal
auditory canal.

84. • Once the surgical procedure is completed, the IAC defect is
covered with a temporalis muscle plug; a bone chip
can be used to cover any large MCF floor defects to
prevent postoperative dural herniation or
encephalocele.
• Bone wax is applied to air cells in the petrous apex
prior to closure to prevent postoperative CSF
leakage.
• The bone flap is replaced and the wound is closed in
layers. A bulky mastoid dressing is applied

85. 3.TRANSLABYRINTHINE APPROACH
The translabyrinthine approach can be utilized for decompression of
the entire intratemporal course of the facial nerve in cases where
vestibulocochlear function is already lost
Indication
• Transverse temporal bone fracture,
• Extensive facial neuroma, or a
• Large congenital cholesteatoma that extends into the IAC.
Advantages
• This approach can also allow complete mobilization of the facial
nerve from the brainstem to the stylomastoid foramen. Entire nerve
is exposed using a single approach

86. • Incision is made 3 cm behind the
postauricular crease and carried
inferiorly over the mastoid tip.
• The translabyrinthine approach begins
with the transmastoid exposure,
mastoidectomy is performed
• Labyrinthectomy is done to access the
IAC, labyrinthine segment, and GG.

89. Complications
• Further surgical trauma to the facial nerve
• Hearing loss (either conductive or sensorineural),
• Vertigo
• CSF leak
• Wound infection.
• Edema of the temporal lobe
• Subdural hematoma
• CSF leak
• Meningitis.
• Brainstem and cerebellar infarction

90. Nerve repair and grafting
• Restoration of the continuity of the facial nerve by a primary
neurorrhaphy is always preferred over nerve grafting if it
can be accomplished without tension.
• When a segment of the facial nerve is disrupted (eg, by
tumor or trauma), the best functional results are obtained
with cable grafting.
• Cable grafts is used when defect > 17mm; nerve cannot be
reapproximated w/o tension.
• Most commonly used are greater auricular nerve and sural
nerve.

91. • if defect is less than < 17mm than primary anastomoses is done
with suturing the 2 segments together with three sutures 8-0 to
10-0 monofilament sutures to bring the epineurium or
perineurium together
• It is best to freshen the end of both the nerve & graft by making
an oblique(45 degree) cut, increasing the surface area fotr the
anastomoses.

92. F
ACIALREANIMA
TION
🞭 There are many factors
important in reanimation:
1. cause and degree of paralysis,
2. timing/duration of paralysis,
and
3. Patient factors like age,
general health, patient
expectations, life expectancy,
nerve condition, and healing
capacity.
83
include eye closure, oral
competence,
muscle tone/facial symmetry at
rest, voluntary movement/ minimal
synkinesis, and involuntary
(mimetic) movt.
Goal includes…

93. • Hypoglossal to facial nerve graft is the most common graft used.
◾ 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.

94. Cross facial nerve grafting
• Done in Contralateral CN VII used to reinnervate paralyzed side
using a nerve graft most commonly sural nerve.

96. THANK YOU