facial nerve, its disorders, investigations and management

1. FACIAL
NERVE AND
ITS
DISORDERS
Submitted by
Manjari Reshikesh
IV BDS II
DEPARTMENT OF ORAL AND MAXILLOFACIAL
SURGERY

2. FACIAL NERVE
• Facial nerve is the seventh cranial nerve
• Known as “QUEEN OF FACE”
• Also known as “ Nervus facialis ”
• Mixed nerve- both motor & sensory
• Nerve of second branchial arch
• It controls muscles of facial expressions
• controls Taste sensations

3. EMBRYOLOGY
• Develops from 2nd pharyngeal arch (hyoid)
• Formation of facial nerve begins at 3rd week of
emryonic life
• Course,branching,anatomic relations
completed at the end of 3rd month of prenatal
life
• Not fully developed till 4yrs

4. ANATOMY
NUCLEI OF FACIAL NERVE
1. Motor nucleus or branchiomotor
2. Superior salivatory nuclus or parasympathetic
3. Lacrimatory
4. Nucleus tractus solitarius (NTS)

5. FUNCTIONAL COMPONENTS
1. Special visceral or branchial efferent (SVE)
to muscles of facial expression and elevation
of hyoid bone
2. General visceral efferent or parasympathetic
scretomotor(GVE) to
• submandibular &sublingual gland
• Lacrimal gland
• Glands of Nose, palate & pharynx
3. General visceral afferent(GVA)- carries
impulses from above glands
4. Special visceral afferent – carry taste
sensations from palate and anterior 2/3rd
tongue
5. General somatic afferent- a part of skin of ear

6. GSA

7. COURSE OF FACIAL NERVE

12. BRANCHES AND DISTRIBUTION
1.Within the facial canal:
• Greater petrosal nerve
• Nerve to stapedius
• Chorda tympani
2. As it exits from stylohyoid
foramen
• Posterior auricular
• Digastric
• Stylohyoid

13. 3.Terminal branches
• Temporal
• Zygomatic
• Buccal
• Marginal mandibular
• Cervical
4. Communicating
branches with adj spinal
&cranial nerves

14. FACIAL NERVE DISTURBANCE
• Weakness of facial muscles to
perform motor functions –
paresis(partial)
• Total flaccidity - paralysis
• Dreaded functional & esthetic
complication
• Loss of control of lips&cheeks-
affect drinking& mastication
• cornea- pain, visual acuity
• Facial assymetry

15. • Unilateral facial weakness
• Loss of taste
• Hyper acusis
• Vesicles in the ear(shingles)
• Facial pain]
• decreased salivation
• Decreased tear secretion

16. FACIAL NERVE PARALYSIS
 Facial nerve paralysis is a common problem that
involves paralysis of any structures innervated by
facial nerve.
 Pathway of facial nerve is long and convoluted,
so there are a number of causes that result in
facial paralysis.
 facial nerve paralysis classified as
1. Supranuclear lesions(UMN lesion)
2. Infranuclear lesions(LMN lesion)

17. UMN LESION VS LMN LESION

19. Central Vs peripheral palsy

20. CLASSIFICATION OF FACIAL PALSY
House- Brackmann (1985)classification
Grade I: normal function without weakness
Grade II: Mild dysfunction with slight facial assymetry with
minor degree of synkinesis
Grade III: Moderate dysfunctions-obvious assymetricwith
contracture &/hemifacial spasm,but residual forehead
movement
Grade IV: moderately sever dysfunction-obvious disfiguring
assymetry with lack of forhead motion and incomplete eye
closure
Grade V: severe dysfunction-assymetry at rest and only
slight movement
Grade VI: Totalparalysis: complete absence of tone/motion

22. Rainer schmelzein et al (1999)based on
causes
1.Congenital
 Rare- congenital aplasia- moebius syndrome
 Myotonic dystrophy
 Melkersson-rosenthal syndrome
 Congenital cholesteatoma/facial palsy
2.Neurologic:
 Myasthenia gravis
 Multiple sclerosis
 Gullain barre syndrome
3. Neoplastic
 Tumors-schwannoma,neuro fibroma,neurogenic
sarcoma
 Glomus tumor,,parotid tumors,temporal tumors

23. 4. Infection
 Otitis media,mastoditis
 Bacterial cause(diphtheria,TB)
 Viral causes(herpes zoster,lyme
disease, mumps, IMN)
5. Other causes- Toxic,
metabolic(DM), idiopathic(bells)
6. Iatrogenic- parotidectomy,
rhytidectomy,lat. skull base
surgery
7. Traumatic
temporal bone #,penetrating
trauma(gunshot)
Facial lacerations,high altitude
palsy

24. As a complication of IANB – into parotid
gland

25. Systemic causes
▫ Diabetes Mellitus
▫ Hypothyroidism
▫ Uremia
▫ Polyarteritis Nodosa
▫ Wegener’s granulomatosis
▫ Sarcoidosis
▫ Leprosy- ALL
▫ Leukemia

26. NERVE INJURIES
1. Seddons classification
• Neuropraxia
• Axonotmesis
• neurotmesis
2.Sunderland classification
• 1st degree( type I ,II,III)
• 2nd degree
• 3rd degree
• 4th degree
• 5th degree

27. NERVE INJURIES
Neuropraxia: (Rev. conduction block)
▀ Epineurium& endoneurium intact but nerve is just
compressed
▀ No axonal degeneration distal to site
▀ Temporary conduction block
▀ No surgical intervention
Axonotmesis: (prolonged conduction block)
 Loss of continuity of some axons(axonal degeneration)
 Distal to site, WALLERIAN DEGENERATION occurs
 After 3 months, initial signs of recovery

28. Neurotmesis; (total permanent conduction block)
 Complete severence of all layers of nerve
 Distal to injury wallerian degeneration occurs
 Space between proximal & distal filled by scar
tissue
 Surgical intervention must
Wallerian degeneration

30. SUNDERLAND CLASSIFICATION
 1st degree (neuropraxia(seddon)
no axon degeneration, only compression
rapid and complete return of sensation
3 types based on mechanism of injury:
Type 1: mild compression anoxia. No axon degeneration
Return to normal within 24 hrs
Type 2: moderate compression injure capilaries
conduction block intrafascicular edema
Recovery- 1 week

31.  Type 3 : severe compression
segmental demyelination
Recovery- 1-2 months
Surgery not indicated
2nd degree: Axonal injury with degeneration &
regeneration.
Compression ischemia edema/ demyelination
Epineurium, perineurium and endoneurium intact
2-4 months- signs of sensation
Complete recovery by 1 year
Unless an extraneurial irritant inhibits recovery, no
surgery

32.  3rd degree: severe compression
not only axon, endoneurium damaged
Sensation within 2- 5 months.
Recovery never complete
Endoneurial fibrosis prevent axon regenration
leading to neuroma
 4th degree:
1. traction
2. Compression
3. Injection injury
4. Chemical injury
Axon, endoneurium and perineurium damaged
Epineurium intact
Poor prognosis

33.  5th degree:
Severe disruption
Tissue loss also
Laceration & avulsion
All layers of nerve disrupted
Amputation neuroma may occur
Poor prognosis
Microconstructive surgery indicated

35. BELL’S PALSY
HISTORY
• from Sir Charles Bell (1774-1842)
• Studied facial anatomy extensively
• Concluded that facial nerve controlled
facial expression
• “Respiratory nerve of Face”
• Demonstrated separation of the motor
and sensory innervation of face

36. • DEFINITION : an idiopathic paresis or paralysis
of facial nerve of sudden onset.
• Most common cause of facial paralysis
• 15-40 cases per 1 lakh
• Both sexes equally affected
• Seen more in middle aged
• Diabetics r more prone
• Family history
• Mostly unilateral. Only 1% bilateral

37. Etiology
• Idiopathic
• autoimmune response
• Viral hypothesis
• Ischemic hypothesis: factors producing
vasospasm
1. cold
2. anoxia
3.Injury
4.Toxicity
5.Allergic

38. Signs and symptoms
• Sudden onset
• Unable to close eyes
• Bells phenomenon( eyeball rolls up
and out on attempting to close the
eye & white sclera visible)
• Dribbling of saliva
• Epiphora
• Assymetrical face
• Noise intolerance
• Loss of taste
• Unable to smile on affected side
• Drooping corners of mouth

40. *
*James Ramsay hunt (1907)
*Caused by varicella zoster
*Infection along facial nerve near inner ear
*Syndrome occurs when geniculate ganglion is involved due to
reactivation
*Classical triad:
1. Ipsilateral facial paralysis
2. Ear pain/hearingloss
3. Vesicles in pinna,
* Sensation of spinning
* tinnitus

42. *
*Also known as orofacial granulomatosis
*Idiopathic Neurological disorder
*Non tender persistent swelling of one or both lip
*Facial paralysis
*Lingua plicata(fissured tongue)

43. MOEBIUS SYNDROME
• Described by Moebius(1888)
• Rare neurological disorder
• Congenital oculofacial paralysis
• Congenital defect -Paralysis of
VII and VI neves
• Mask like face –expressionless
• Unable to close eyes-corneal
ulcerations
• strabismus

44. GUILLAIN BARRE SYNDROME
• first Described by Jean landry
(1800s)
• Discovered by jean barre and
georges guillain(1916)
• Inflammatory demyelinating
poly neuropathy affecting
peripheral nerves including
VII nerve causng facial palsy
• Treated by IVIG&
• Plasma exchange

45. TRANSIENT FACIAL PALSY
• Encountered during IANB
• Due to injection of LA into parotid gland ifneedle
injected too backwards
• Temporary paralysis of facial nerve
• Effect wears off over a period of time(<3Hrs) during
which eye needs to be protected(eye patch)

46. Hyperkinetic disorders
• Involuntary twitching of facial
muscles on one or both sides
1. Hemifacial spasm- on one
side
due to irritation of nerve @
cerebellopontine angle
( microvascular decompression,
botulinum toxin)
2. Blepharospasm- limited to
orbicularis oculi on both sides
(bot toxin into periorbital
muscles

47. 1.Facial nerve evaluation
 careful case history for onset,duration and
degree of recovery
 Acute onset in morning- bell’s palsy
 Sudden onset –infectious/inflamatory
 Neoplasm-paresis over long period of time
 Trauma-definite history
 Delayed onset- better prognosis
 Full otologic investigation needed
2. Examination of face at rest & motion to
differentiate paresis & paralysis

48. Raise eyebrows
Close eyes against resistance
Forced smile- buccal & marginal mandibular
Depth of nasolabial fold
Puff out cheeks

49. Schirmer’s test
• Measurement of wetting of filer paper (41
whatman)(35x5mm)
• Folded and placed @ juntion of middle and outer third of
lower lid
• Asked to keep eyes closed
• After 5 mins,measured
• If +ve,lesion @ geniculate
ganglion

50. Stapedius reflex test
• Stapedius reflex – involuntary muscle contracion that occurs
in middle ear in response to high intensity sound stimuli
• Absent reflex or reflex less than1 /2 of amplitude of
contralateral abnormal
• Acoustic reflex equipment
• 69% facial palsy- absent

51. Electro gustometry
• Simplest regional evaluation of taste
• EGM delivers taste sstimuli in controlled manner
• To dtermine gustatorythresholds by electric stimulus on L/R or
A/P tongue
• Stimulated chordatympani
• electrode atached to tongue
• Current passed till patient
feels metallic/sour taste

52. Submandbular Salivary flow
test
• Cannulate wharton duct on each side with no. 50
polyethylene tube
• Stimulate saliva with lemon juice
• Output measured
• 25%reduction significant

53. Electromyography
• Recording of spontaneous or voluntary muscle potenitials by
needle electrodes introduced to muscles is EMG
• Records potential of muscles at function and rest
• In early stage, use is limited (10-14 days post onset)
Useful in assesing reinnervation after 2 weeks

54. ElectroNeurography(ENoG)
• Most accurate prognostic test
• Objective,qualitative measurement of neural degeneration
• Nerve stimulated with impulse TC at using bipolar electrodes
• Place electrodes one each on either sides of nose &forehead
• Electrical stimulator used & placed in front of ear
• Recordings obtained in computer
• Peak to peak amplitude- intact axons
• Two sides compared.
• Reduction in amplitude <10 %- poor prognosis

55. Nerve excitability test/ hilgers test
• Commonly used
• Minimum threshold current to elicit twitching/ visible muscle
movement on both affected and unaffected side and compare
• Placement of stimulating electrode at stylomatoid foramen.
• Difference .3.5 mA – poor prognosis
•Maximum stimulation test
• Modified version of NET
• Same equipment
• Maximum stimulus applied on unaffected side until no
Further increase in response obtained. Same stimuli applied on AS.
• If no response, decompression is only option

56. IMAGING
 MRI with IV gadolinium contrast
revolutionised tumor detetction
 In case of tumors, MRI is choice
 CT – valuable in surgical planning of cholesteatoma
and skull base fractures
 Exclusion of other pathologies

57. Complications of facial
paralysis
• Synkinesis/ Mass movement
• Tics & spasms
• Crocodile tears/bogorad’s
syndrome
• uncommon consequence of
regeneration causing
communication between
salivatory nucleus and lacrimal
glands
• unilateral lacrimation with
mastication(faulty regeneration )
• Exposure keratitis

58. TREATMENT
• Based on etiology of nerve damage/
dysfunction treatment is planned.
1. Medical Management
2. Surgical Management

59. Medical Management
• Physiotherapy- in case of bell’s palsy or paralysis,
muscle atrphy may occur. So massage, excercises
indicated
• Within 2- 3weeks of onset, prednisolone 1mg/kg
for 10 -14 days with tapering
• Vitamins B1,B6,B12 administered
• Antivirals like acyclovir 400 mg 5 times a day

60. SURGICAL
MANAGEMENT
• Open injuries of facial nerve
repaired surgically as soon as
possible
• 12 months - limit for successful
repair
• NERVE DECOMPRESSION
• NEURORRHAPHY
• NERVE TRANSFER
• MUSCLE TRANSPOSITION
• TARSORRAPHY
• Static procedure: GOLD
IMPLANTS,

61. Facial Nerve
Decompression
• Compression on facial nerve is
relieved
• 2 approaches
Middle cranial approach is common
• Used to relieve compression of
facial nerve in bell’s palsy and
temporal bone fracture
• The bone fragments are removed
and compression releived

62. Neurorraphy
END TO END ANASTOMOSIS
• Surgical repair of transected facial nerve is done with direct end
to end approximation and suturing(Lacerations, iatrogenic
injuries,benign conditions)
• May be epineural only or along with perineural suture
• 9-0 8-0 nylon monfilament

63. 2. NERVE GRAFTING
If there is gap between proximal &
distal- autogenous grafting done.
And if gap>1cm – cable graft
• The hypoglossal nerve
• Sural nerve - 1cm posterior to
lateral malleolus
• Great auricular nerve
• Branches from cervical plexus

64. *
*Employs a nerve graft typically
sural nerve that acts a
connection for motor axons from
normal to affected facial nerve
*FISCH Technique- on
nonparalysed side intact buccal
branch connected to paralysed
stem of facial nerve by sural
graft

65.  Facial hypoglossal transfer
 When direct and grafting
procedures not possible
 An intact distal segment and
muscles suitable for
reinnervation
 Nearly normal appearence at
rest
 With stump of 12th nerve
hooked to end of 7th nerve,fac
will move when tongue is
moved
Nerve transfers

67. TEMPORALIS MUSCLE
TRANSPOSITION
• Exposure of temporalis
muscle through extended
preauricular incision
• Elevation of temporalis
muscle slings
• Slings brought forward
through tunnel to
commisure
• Tunneling near outer
canthus of eye
• Slings transposed to
upper and lower eyelids

68. Tarsorrhaphy
0 Eyelids are partially sewn together to narrow eyelid
opening
0 Done to protect cornea as in facial palsy
Mc Laughlins tarsorrhaphy
incisons

69. Gold / platinum lid
weights
Before and after placement

70. Facial Reanimation Results
BEFORE AFTER

71. T
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