facial nerve disorders, investigations, tests & management facial paralysis, bells palsy

1. FACIAL NERVE PARALYSIS
Dr. Vikas

2. NERVE FIBER COMPONENTS
 Axon
 Myelin sheath
 Endoneurium
 Perineurium
 Epineurium
It has no perineurium from brainstem to IAC

3. NERVE FIBER COMPONENTS
 Endoneurium
 Surrounds each axon
 Adherent to Schwann cell
layer
 Vital for regeneration
 Perineurium
 Encases endoneural
tubules
 Tensile strength
 Barrier to infection
 Epineurium (nerve
sheath)
 Outermost layer
 Houses vasa nervorum for
nutrition

4. NEUROPATHOPHYSIOLOGY OF NERVE INJURY
SEDDON CLASSIFICATION(1943)
 Neuropraxia –
 A low severity injury that typically leads to
complete recovery. The structure of the nerve
remains intact but electrical conduction down the
axon is interrupted, typically by ischemia or
compression injury, additionally secondary
injuries can be caused by vascular damage
leading to intrafascicular edema.
 Complete recovery of function with no distal
Wallerian degeneration

5.  Axonotmesis
 Disruption of the neuronal axon takes place but the
myelin sheath is still intact.
 Endoneural tubules are preserved but Wallerian
degeneration occurs
 Typically this is caused by a crush based injury.
 Depending on the severity of the injury, regeneration
may occur over the timescale of weeks to years.
 Neurotmesis –
 Complete nerve transsection occurs
 Commonly a neuroma forms over the proximal
stump of the nerve, preventing normal continued
regeneration to occur.

6. SEDDON CLASSIFICATION

7. 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

8. HOUSE-BRACKMANN FACIAL NERVE
GRADING SYSTEM

9. HOUSE-BRACKMANN FACIAL NERVE
GRADING SYSTEM
Not a perfect Grading system because of –
1. the problems of inter & intraobserver
variations
2. applicable only to disorders of nerve
proximal to pes anserinus
3. not appropriate for single branch injuries

10. EVALUATION OF FACIAL PARALYSIS
 Clinical feature
 Central v/s Peripheral facial paralysis
 Complete head and neck examination
 Cranial nerve evaluation
 Topographic diagnosis
 Electro-diagnostic testing

11. Central v/s Peripheral facial paralysis
UMN LESIONS LMN LESIONS
 Paralysis of inferior ¼ of
the face Contralateral to the
lesion
 Upper part of face is
innervated bilaterally by the
UMN
 Inferior half have only
contralateral innervation
 Seen mostly in intracranial
lesions (stroke)
 Paralysis of the lateral half
of the face Ipsilateral to the
lesion
 The fibers carrying LMN
(that are supplying the
entire lateral half of face)
are all within within the
fascial nerve
 Seen in Fascial nerve
lesions(Bell’s Palsy)

13. PERIPHERAL PARALYSIS
Lower motor neuron lesion -
 At rest –
 less prominent wrinkles on forehead of affected side,
 eyebrow drop,
 flattened nasolabial fold,
 corner of mouth turned down
 Unable to –
 wrinkle forehead,
 raise eyebrow,
 wrinkle nasolabial fold,
 purse lips,
 show teeth,
 completely close eye

14. 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)

15. SCHIRMER TEST
 Greater superficial petrosal nerve,Geniculate
ganglion
 Filter paper strip is placed in the lower conjunctival fornix bilaterally
 Rate of tear production of the two side is compared after ~5 minutes
 Normally the portion of the filter paper in contact with the conjunctiva
acts as an irritant, stimulating an increased flow of tears, which are then
wicked along the filter paper strip by capillary action

16. SCHIRMER TEST

17. 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)

18. 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.
 Fisch (1977) pointed out that tearing is often inexplicably reduced
bilaterally in Bell's palsy, and this bilateral reduction even persists after
unilateral resection of the geniculate ganglion.
 Thus, judging not only the symmetry of the response but also its
absolute magnitude is important: a total response (sum of the lengths of
wetter filter paper for both eyes) of less than 25 mm is considered
abnormal.

19. STAPEDIAL REFLEX
 Stapedius branch of the facial nerve
 A loud (supra threshold) tone is presented to either the
ipsilateral or contralateral ear 
 evokes a reflex movement of the stapedius muscle 
 changes the tension on the Tympanic Membrane (which must be
intact for a valid test) resulting in a change in the impedance of
the ossicular chain.
 An absent reflex or a reflex that is less than half the
amplitude of the contralateral side is considered
abnormal

20. STAPEDIAL REFLEX
 The reflex can be elicited by either ipsilateral or
contralateral acoustic stimulation, or in cases of
bilateral severe hearing loss, by tactile or
electrical stimulation.
 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);
 the reflex recovers at about the same time as
clinically observed movements do. The
prognostic value of this test therefore seems
limited.

21. 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.
 Electirical 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

22. ELECTROGUSTOMETER

23. 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
 The major problem with taste testing is that the results of
this test will be abnormal in almost all patients who are in
the acute phase of Bell's palsy (Tomita et al, 1972); thus
this test cannot be used to select patients with a poor
prognosis.

24. 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 antr. 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 (Saito et al,
1977)

25. SALIVARY FLOW TESTING

26. ELECTRO-PHYSIOLOGICAL TESTING
 When a conduction block exists, the patient is unable
to move his face voluntarily, but a facial twitch can
still be elicited by percutaneous electrical stimulation
of the nerve distal to the lesion.
 The electrical response of the facial muscles to
voluntary, mechanical, or electrical activation of the
nerve may also be recorded. Tests based on these
two principles –
 electrical stimulation and
 recording of the electromyographic (EMG) response
 are useful in prognosis and in the selection of
patients for different treatments.

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

28. 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, steadily increasing current levels
until a facial twitch is just noticeable.
 The lowest current eliciting a twitch is the threshold of
excitation.

29. NERVE EXCITABILITY TEST (NET)
 Next, the process is repeated on the paralyzed side, and the
difference in thresholds between the two sides is calculated.
 In a simple conduction block, such as occurs after infiltration
of the perineural tissues with lidocaine (Xylocaine), no
difference exists between the two sides; the paralyzed nerve
is as easy to stimulate (distal to the point of the conduction
block) as is the normal nerve.
 After a more severe injury (Sunderland class II to V), in
which distal axonal degeneration occurs, electrical
excitability is gradually lost
 this takes 3 to 4 days, even after a total section of the nerve.
This means that the findings of the NET always lag several
days behind the biologic events themselves

30. NERVE EXCITABILITY TEST (NET)
 A difference of 3.5 milliamperes (mA) or more in thresholds
between the two sides has been proposed as 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 .
 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.

31. 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.

32. 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)

33. 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

34. 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.

35.  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)

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

38.  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

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)
 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.

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

43. 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

44. 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 pariod( first 72
hours)

45. FACIAL PARALYSIS

46. CAUSES:
 Central:
 Intacranial part:
 Intratemporal part:
 Extracranial part:
 Systemic:

47. CAUSES:
 Central:
 Brain abscess
 Pontine glioma
 Poliomyelitis
 Multiple sclerosis
 Intacranial part:
 Acoustic neuroma
 Meningioma, congenital cholesteatoma
 Metastatic CA
 Meningitis

48. CAUSES:
 Intratemporal part:
 Idiopathic:
 Bell’s palsy
 Melkersson’s syndrome
 Infections:
 ASOM,CSOM
 Herpes Zoster Oticus
 Trauma:
 Surgical: Mastoidectomy, Stapedectomy
 Accidental:# temporal bone
 Neoplasms:
 Glomus jugulare tumour,Facial nerve
neuroma,Metastatic CA

49. CAUSES:
 Extracranial part:
1.Malignancy of parotid
2.Surgery of parotid
3.Accidental injury in parotid region
4.Neonatal facial injury(forceps delivery)
Systemic diseases:
diabetes,
uraemia,
hypothyroidism,
leprosy,sarcoidosis,
demyelinating disease

50. BELL’S PALSY
 Bell palsy is certainly the most common
cause of facial paralysis worldwide.
 Paralysis of all muscle groups on one
side of the face, sudden onset,absence of
signs of CNS disease; absence of signs
of ear or cerebello-pontine angle disease.
 first described by Sir Charles Bell,
 controversy still surrounds its etiology and
management.

51. 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.
 Recurrence rate 4-15%
 Familial incidence 4.1%
 Less comman in pregnancy but prognosis is
significantly worse in pregnant women

52. 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,

53. HISTORY:
 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.

54. PHYSICAL EXAM:
 Bell's palsy causes a peripheral LMN
palsy,
 U/L impairment of movement in the
facial & platysma muscles, drooping of
the 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.

55. PHYSICAL EXAM:
 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.

56. MANAGEMENT, STEROID
 Usual regimen is 1mg/kg/day for 1 week.
 To be tapered in the 2nd week.
 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.”

57. 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.
 Usual regimen 200 mg – 400 mg,5 times a
day for 10 days
 Cochrane review*:
“More evidence is needed to show whether the antiviral drugs
acyclovir or valacyclovir are effective in aiding recovery from
Bell's palsy.”
.

58. WHEN TO DO DECOMPRESSION
 If the pt either progresses to complete paralysis or
present with complete paralysis, an ENOG is
obtained 3 days after occurance of complete
paralysis
 If degeneration <90% -conservative
 Repeat ENOG every 1-3 day
 If degeneration >90% -surgical decompression is
an option
 However, if >90% degeneration occur after the 2-
week, surgical decompresion does not alter
outcome

59. OUTCOMES:
 It has a fair prognosis without treatment, with
almost 3/4 of patients recovering normal
mimetical function and just over a tenth
having minor sequelae.
 A sixth of patients are left with either
moderate to severe weakness, contracture,
hemifacial spasm, or synkinesis.

60. 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

61. 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

62. MELKERSSON-ROSENTHAL SYNDROME
 Acute episodes of facial paralysis
 Facial swelling
 Fissured tongue
 “Scrotal” tongue
 Very rare
 Familial but sporadic
 Usually begins in
adolescence
 Leads to facial disfigurement
 No definite therapy

63. ALTERNATIVE CAUSES OF ACUTE FACIAL
NERVE PARALYSIS
 Atypical signs & symptoms which suggest
etiology other than Bell’s palsy require
imaging
 Clinical history is crucial in distinguishing
etiologies
 Choice of imaging technique depends on
clinical suspicion

64. LYME DISEASE
 Lyme disease (borreliosis)
 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 w/antibiotics

65. 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

66. 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%)

67. 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

68. GLOMUS TUMOR
 Glomus tumors
arising from jugular
bulb (jugulare) and/or
middle ear
(tympanicum) may
involve the facial
nerve

69. VESTIBULAR SCHWANNOMA
 Common tumor
 However, facial nerve is resistant to
compression
 Therefore, tends to produce facial paralysis
mostly when they attain a large size

70. OTHER CAUSES
 Guillain-Barre Syndrome
 Ascending paralysis
 Iatrogenic
 Temporal bone surgery
Excision of vestibular schwannoma has <10%
chance of paralysis
Middle ear surgeries
 Babies who required forceps delivery
>90% recovery

71.  Rcurrent facial palsy: seen in
 Bell’s palsy,
 Melkersson’s syndrome,
 diabetes,
 sarcoidosis
 tumuors

72.  Bilateral facial paralysis: simultaneous
bilateral facial paralysis may be seen in
 GBS,
 sarcoidosis,
 sickle cell anaemia,
 acute leukemia,
 bulbar palsy
 leprosy

73. FACIAL NERVE TRAUMA - OVERVIEW
- 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

74. TEMPORAL BONE FRACTURE
– 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)
» 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

75. IATROGENIC TRAUMA
– 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

76. SURGICAL TREATMENT FOR FACIAL NERVE
INJURY

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

78. TREATMENT PROTOCOL
A.Upto 3 weeks:
 nerve decompression or nerve repair
B. 3 weeks- 2 years:
 nerve repair or nerve transposition
C. >2yrs with fibrillation in EMG
 nerve repair or nerve transposition
D. >2yrs with electrical silence in EMG
 muscle transposition/ eyelid implant/ facial sling

79. APPROACH TO TREATMENT AND
TREATMENT OPTIONS - IATROGENIC INJURY
• 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
exploration is warranted
• If loss of function is noted following surgery,
wait 4 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

80. APPROACH TO TREATMENT AND
TREATMENT OPTIONS - IATROGENIC INJURY
• Integrity of nerve known to be intact
– High dose steroids – prednisolone 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
If more than 50% of the circumferance has been
disrupted it should be repaired with either
direct epineural suture or inlay graft

81. 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
• 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 debateable
– Recommended to drain hematoma if identified

82. ACUTE VS. LATE DECOMPRESSION -
CONTROVERSIAL
 Quaranta et al (2001) examined results of 9 patients undergoing late
nerve decompression (27-90 days post injury) who all had >90%
degeneration
 7 patients achieved HB grade 1-2 after 1 year
 2 achieved HB grade 3
 Concluded that patients may still have a benefit of decompression up to
3 months out
 Shapira et all (2006) performed a retrospective review looking at 33
patients who underwent nerve decompression. They found no significant
difference in overall results between those undergoing early (<30 days
post-injury) vs. late (>30 days post-injury) decompression
 Most studies like these have been very small, and lack control groups.
Some studies have shown improvements with decompression occurring 6-
12 months post-injury, but further evidence is needed

83. FACIAL REANIMATION
 Facial reanimation is a family of different
surgical techniques to make one's paralyzed
face move more normally.
83

84. GENERAL PRINCIPLES
 Reinnervation of facial muscles should occur
ASAP
 Upper and lower face should be reanimated
separately
 Avoids mass movement
 Both static and dynamic procedures can be
employed
 Procedure tailored to patient’s needs

85. 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

86. 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

87. 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

88. NERVE REPAIR - OVERVIEW
• 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
– May and Bienstock 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 for this
reason if this far out

89. NERVE REPAIR - OVERVIEW
Rule is to repair earlier
than later

90. PRIMARY ANASTOMOSIS
• Best overall results of any surgical intervention
• Done if defect is less than < 17mm
– 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 9-0/10-0
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

91. 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

92. 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

93. INTERPOSITION GRAFTING
 Recovery
 Movement first noticed 6 months after surgery
 Tinel’s sign heralds recovery
 Muscle tone preceeds voluntary movement
 Mid 1/3 of face usually recovers first, then spreads
superiorly toward eye
 Expect 12-18 months
 Variable degree of synkinesis
 Majority of cases reach House-Brackmann III

94. INTERPOSITION GRAFTING
GREATER AURICULAR NERVE
 Harvesting
 Located on lateral
surface of SCM at the
midpoint of a line
drawn between
mastoid tip and
mandibular angle
 May extend
postauricular incision
or use separate neck
incision

95. INTERPOSITION GRAFTING
GREATER AURICULAR NERVE
 Useful features
 Proximity to facial nerve
 Cross-sectional area (~equal)
 Limited morbidity
 Limitations
 Reconstruction of long defects and/or branching
nerve gaps
 Ideal for defects < 6cm in length

96. SURAL NERVE
 Anatomy
 Formed by union of medial
sural cutaneous nerve and
lateral sural cutaneous
branch of peroneal nerve.
 Pierces fascia of
gastrocnemius and runs in
lateral compartment in
association w/ saphenous
vein
 Distally, located between
lateral malleolus and
tendon of the calcaneus.

97. SURAL NERVE
 Harvesting
 Multiple transverse
incisions v. longitudinal
incision are made.
 Longitudinal incision
made posterior to the
lateral malleolus and
then extended
upwards depending on
length needed
 Nerve dissected
proximally to desired
length

98. SURAL NERVE
 Pros:
 Length (40cm)
 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

99. MEDIAL ANTEBRACHIAL CUTANEOUS NERVE
(MACN)
 Anatomy
 Arises from medial cord of brachial plexus,
adjacent to ulnar nerve
 Medial to axillary artery
 Anterior and medial to brachial artery
 Distally, it is closely associated with basilic vein

100. MACN
 Harvest
 Important landmarks:
 Medial epicondyle of humerus
 Biceps tendon
 Basilic and medial cubital veins
 Fascial plane separating bicep from tricep
 Tips
 Use of sterile, proximal tourniquet
 Facilitates basilic vein identification
 Upper extremity can be prepped from axilla to wrist or
continuous with the head/neck.
 May employ 2-team approach

101. CROSSOVER TECHNIQUES
 Scenarios for use:
 Irreversible facial nerve injury
 Intact facial musculature/distal facial nerve
 Intact motor endplates
 Intact proximal donor nerve
 Ideal if performed within a year of facial
paralysis
 Prior to distal muscle/facial nerve atrophy

102. CROSSOVER TECHNIQUES
 Pros
 Low level of difficulty
 Time interval until movement
 4-6 months
 Avoid multiple sites of anastomosis
 Mimetic-like function achievable with practice
 Cons
 Donor site morbidity
 Some degree of synkinesis

103. 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

104.  CN XII-CN VII anastomosis contraindicated
with ipsilateral vagal paralysis
 Swallow dysfunction
 Improved facial tone/symmetry in ~ 6
months
 Pt learns to smile by moving the tongue
 Exercise/biofeedback training
 Adjunctive lid procedures usually required

105. 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

106. 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.

107. 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

108. TEMPORALIS
 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.

109. 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

110. 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

111. MICRONEUROVASCULAR TRANSFER
FREE MUSCLE FLAPS
 Created based on the potential of achieving
individual segmental contractions
 Reduction of mass movement/synkinesis
 Numerous muscle flaps used thus far:
 Gracilis
 Latissimus dorsi
 Inferior rectus abdominus

112. ADDRESSING PARALYTIC
EYELIDS
 Pre-op assessment by ophthalmology
 Complete eye exam including:
Visual acuity assessment
Lower lip laxity (snap test)
Tear production (Schirmer test)
 Lacrimal system integrity (Jones test)
Measurement of the distance btwn upper and
lower eyelids upon closure (margin gap)

113. STATIC FACIAL SLING TECHNIQUE
1. Preauricular, temporal or nasolabial
fold incision may be used
2. Additional incisions made adjacent to
oral commisure at vermillion border
of upper and lower lip
3. Subcutaneous tunnel dissected to
connect temporal to oral commisure
incisions
4. Dissection may be carried out in
midface adjacent to nasal ala, if
needed (for alar collapse)
5. Implant strip is split distally to
connect to the upper/lower lips
6. Implant secured to orbicularis
oris/commisure using permanent
suture
7. Implant is suspended and anchored
superiorly to superficial layer of deep
temporal fascia, or zygomatic arch
periosteum, using permanent suture.
8. May also secure to malar eminence
using small miniplate or bone
anchoring screw

114. 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

115. Thanks

116. PROXIMAL AND DISTAL SEGMENTS
AVAILABLE
• Great auricular nerve
– Usually in surgical field
– Located by drawing a line perpendicular to a line drawn b/w
mastoid tip to the angle of the mandible
– Can only harvest 12cm of this nerve
– Loss of sensation to lower auricle with use
• 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)

118. ONLY DISTAL SEGMENT AVAILABLE
• 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 great auricular 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

121. COMPARISON OF DIRECT HYPOGLOSSAL
GRAFTING VS. JUMP GRAFTING
• Jump graft
– 8% of patients experienced permanent
complications
– 41% obtained good movement with less
synkinesis
– Longer recovery time (9-12 months prior to some
function)
• Direct graft
– 100% permanent complications
– Stronger motor function
– Less recovery time

122. MUSCULAR TRANSPOSITION
 If there is no functional neuromuscular
system, surgical reconstruction involve
muscular transposition
 Pedicaled muscle graft: temporalis, masseter
 Free muscle graft: gracillis, rectus abdominis
abductor hallucis, pectoralis minor ,
latissimus dorsi

123.  In adults, the pedicled grafts are most
commonly used
 Free muscle transfer with a neurovascular
anastomosis(using the contralateral facial
nerve for innervation) is the mainstay of
treatmentof children with congenital disorder
( moebius syndrome)
 Free muscle transfer procedure are of limited
effectiveness

124.  Muscle transposition most commonly
employes the temporalis muscle bcoz of its
good location, length & contractility
 It is a proven & useful technique for facial
reanimation in who nerve grafting or cranial
nerve substitution procedure are not
poissible
 Temporalis transposition is a dynamic
technique that allows the patients to have a
voluntary smile

125. COMPLICATION OF FACIAL PARALYSIS
1. incomplete recovery: facial asymmetry persists,
eye can’t be closed resulting in epiphora. A weak
oral sphinctor causes drooling & difficulty in
taking food
2.exposure keratitis: eye can’t be closed,
tear film from the cornea evaporates
causing dryness, exposure keratitis and
corneal ulcer
3. synkinesis(mass movement): when the
pt. wishes to close eye corner of mouth
also twiches or vice versa

126.  4.tics and spasm: result of faulty regeneration of
fibres. Involuntary movements are seen on the
affected side of face
 5. contractures: results from fibrosis of atrophied
or fixed cotraction of a group of muscles
 6. Crocodile tears(gustatory lacrimation):
unilateral lacrimation with mastication. Due to faulty
regeneration of parasympathetic fibres which now
supply lacrimal gland instead of the salivary glands.
It can be treated by section of GSPN or tympanic
neuractomy

127.  7. Frey’ syndrome(gustatory sweating):
there is sweating and flushing of skin over
the parotid during mastication. It results from
parotid surgery
 8. psychological and social problems

128. THANK YOU