facial palsy

2. FACIAL PALSY
PRESENTED BY
E. DIVYA JYOTHI
POST GRADUATE

3. CONTENTS
• Introduction
• Facial palsy
• Definition
• Etiology
• Diagnosis, Prognosis
• Medical management
• Surgical management
• Indications & Goals
• Direct nerve repair

4. • Regional muscle transposition
• Free muscle grafts, micro neurovascular muscle transfer
• Facial & dermal transplants
• Treatment of paralyzed eyelid
• Bell’s palsy
• Conclusion
• References.

6. INTRODUCTION
• Facial nerve is the seventh cranial nerve
• Nerve of facial expression
• Facial function plays an integral part in our everyday lives
• Smile, nonverbal communication, etc.
• When a facial nerve is either non-functioning or missing, the
muscles in the face do not receive the necessary signals in order
to function properly.
• The term facial palsy generally refers to weakness of the facial
muscles, mainly resulting from temporary or permanent damage to
the facial nerve

7. • Facial palsy not only cause a paresis of the target muscles, but as the
nerve is responsible for a range of facial expressions, it causes serious
disturbances in social life, facial expression being so important in
transferring emotion.

8. THE FACIAL NERVE IS RESPONSIBLE FOR:
I. Contraction of the muscles of the face
II. Production of tears from a gland (lacrimal gland)
III. Conveying the sense of taste from the front part of the tongue (via the
chorda tympani nerve)
IV. The sense of touch at auricular conchae

9. FACIAL PALSY
• Facial paralysis represents the end result of a wide array of disorders and
heterogeneous etiologies, including congenital, traumatic, infectious, neoplastic,
and metabolic causes. Thus, facial palsy has a diverse range of presentations,
from transient unilateral paresis to devastating permanent bilateral paralysis.
although not life-threatening, facial paralysis remains relatively common and
can have truly severe effects on one's quality of life, with important
ramifications in terms of psychological impact and physiologic burden.
• It is important, however, for any practioner to have a sophisticated
understanding of the common etiologies and initial management of facial
paralysis.

10. WHAT CAUSES FACIAL PALSY ?
Birth
Moulding
Forcep delivery
Dystrophic myotonia
Trauma
Base of skull fracture
Facial fractures
Penetrating injuries
to middle ear
Neurological
Opercular syndrome
Millard Gublar
syndrome
Infections
Otitis media
Chicken pox
Mastoiditis
Ramsay Hunt
syndrome
Encephalitis
Mumps
Tuberculosis

11. Iatrogenic
Mandibular surgery
Parotid surgery
Mastoid surgery
Post tonsillectomy
Metabolic
Diabetis mellitus
Hyperthyroidism
Neoplasm
Cholesteroma
Seventh nerve tumour
Glomus jugulare tumor
Leukemia
Meningioma
Sarcoma
Metastatic carcinoma
Idiopathic
Bell’s palsy
Merkerson
Rosenthal
syndrome
Auto immune
diseases
Temporal arteritis
Sarcodiasis

12. • Classification of facial nerve injuries
• There are three different kinds of facial nerve injury:
• First degree injury – when the facial nerve is just concussed or bruised and
recovers within eight weeks.

13. • Second degree injury – where the facial nerve is more severely damaged but still
retains its outer layer. The nerve begins to show the first signs of recovery at
about four months as it slowly repairs itself at the rate of around one millimetre
per day.

14. • Third degree injury – when the facial nerve is more severely damaged, any
recovery is much slower and always incomplete. sometimes the nerve is
completely severed and surgical repair is needed to restore facial function

15. CENTRAL FACIAL NERVE INJURY
• Also known as cerebral facial nerve injury .
• From injury to the brain, the fibers pass from the cortex through the internal
capsule to the facial nucleus .
• Or from the injury of the motor cortex itself .
• Usually a part of hemiplegia-lower part of the face is affected
• Upper part remains unaffected –frontalis and orbicularis oculi

16.  Upper motor neuron lesions- usually
a part of hemiplegia, only the lower
part of the face is paralysed. The
upper part (frontalis and part of
orbicularis oculi)escapes due to
bilateral representation in the
cerebral cortex.
 Lower motor neuron lesions- Entire
face is paralysed, as seen in bell’s
palsy

17. Upper motor neuron Lower motor neuron
Upper face is unaffected Both upper and lower face is affected
Emotional movements are not affected in
unilateral cases .The whole half of the face
is paralyzed affecting the emotional
movements in bilateral cases
Emotional movements are lost .
Bells phenomenon is absent Present
No atrophy of the facial muscles Atrophy of the affected side is seen
Taste sensation is retained Taste sensation is lost.
Corneal reflex is not affected Absent
Hemiplegia is ipsilateral Hemiplegia is always crossed
DIFFERENCES BETWEEN UMN AND LMN TYPE OF FACIAL PALSY

19. • Lesions of facial nerve at various levels.
• Can be classified as,
• 1) Supranuclear lesions of the facial n.
• a) Corticospinal lesion above pons
• b) Mimic paralysis
• 2) Nuclear lesions of facial n. at the pons
• 3) Infra-nuclear lesions of the facial n.
• a) Cerebellopontine angle
• b) Near geniculate ganglia
• c) Between geniculate ganglion & nerve to stapedius.
• d) Between nerve to stapedius and chorda tympani
• e) Between chorda tympani & stylomastoid foramen
• f) Extra-cranial
.
4) Bilateral infra-nuclear facial palsy.
a) Bilateral infra-nuclear lesions
b) Muscle diseases

20. features resulting from lesions of the facial nerve at various levels
• 1) Supranuclear lesions of the facial nerve
a) Corticospinal lesion above pons
Causes: cerebrovascular accidents, cerebral tumors, infections like meningitis,
haemorrhage.
Features: Ipsilateral hemiplegia
b) Mimic paralysis
Causes: same as above.
Features : There is weakness of the emotional movements with normal
voluntary movements of the face.

21. 2) Nuclear lesions of the facial nerve at the pons
Causes :brainstem tumours, polioencephalitis, vascular lesions of
brainstem,
Features: The earliest sign would be loss of corneal reflex, ipsilateral
loss of sensation over the face, paralysis of the muscles of mastication

22. 3) Infra-nuclear lesions of the facial nerve
a) Cerebellopontine angle
Causes : Tumors like meningioma
Features :Hemiplegia, Deafness, Vertigo.
b)Lesions near geniculate ganglia, between geniculate ganglion &
nerve to stapedius and between the stapedius and chorda
tympani are caused by herpes zoster infection, spread of infection
from the middle ear or by trauma.
And the features are defective lacrimal secretion, impaired
salivary secretions, hyperacousis, loss of taste, deafness, vertigo.

23. c)The lesions between the chorda
tympani and the stylomastoid foramen
are caused due to bell’s palsy, tetanus,
infective polyneuritis, otitis media
leading to facial paralysis.
4) Bilateral infra-nuclear facial palsy.
causes:Acute infective polynueritis,
leprosy, leukemia, meningitis, otitis
media, rheumatic diseases, bell’s
palsy.

24. SINGS AND SYMPTOMS OF FACIAL PALSY
• Forehead
• Loss of forehead wrinkles and inability to frown
• Eye :
• Droopy eyebrow and inability to raise eyebrow
• Inability to close the eye fully or blink
• Watery eye or dry eye
• Inability to squint
• Drooping of the lower eyelid which may make the eye appear wide
• Painful eye with symptoms of grittiness or irritation
• Sensitivity to light

25. • Mouth:
• The corner of the mouth pulls down/droops
• Inability to smile on affected side
• Inability to puff up cheeks, whistle or blow
• Altered taste ,tingling of the affected half of the tongue
• Difficulty eating and drinking
• Difficulty brushing teeth and spitting out
• Drooling from the weak corner of mouth
• Excess or reduced salivation (dry mouth)
• Inability to pout
• Difficulty speaking because of weakness in the lips and cheek

26. • Ear:
• Pain in or near the affected ear
• Loss of hearing
• Increased sensitivity to high pitched noise
• Nose:
• Nose runs or feels stuffy
• Inability to flare nostril

27. • History:
• A detailed and careful history
• The onset of symptoms , duration, rate of progress, chronology of events and
associated features.
• History of prior episodes, family history, medical history, history of trauma , and
surgical history .
• Physical examination :
• Head and neck examination
• Detailed examination of ears, eyes, precise palpation of parotid gland
• Complete neurological examination
DIAGNOSTIC EVALUATION OF FACIAL PALSY

28. House-Brackmann Grading System
House JW and Brackmann DE facial nerve grading system, oryntolaryngology, head and neck surgery, 93, 1985

29. SPECIAL DIAGNOSTIC TESTS FOR FACIAL PALSY
Topognostic
tests
• Schirmer test,
• Stapedial reflex test,
• Taste testing
• Salivary flow rates and pH
Electrical
tests
• Maximum stimulation tests
• Evoked electromyograpthy
• Electromyography
Radiographic
tests
• CT Scans of temporal bone
• MRI
• Chest X ray

30. • Topognostic testing
• The principle behind topognostic testing is that lesions distal to the site of a
particular branch of the facial nerve will spare the function of that branch
• Schirmer test :
 Evaluates the function of the greater superficial petrosal nerve .
Filter paper is placed in the lower conjunctival fornix bilaterally.
After 3 - 5 minutes, the length of the strip that is moist is compared to the
normal side.
 A value of 25% or less on the involved side or total lacrimation less than 25 mm
is considered abnormal. An abnormal result can indicate injury to the GSPN or to
the facial nerve proximal to the geniculate ganglion and may predict patients at
risk for exposure keratitis.

32. • Stapedial reflex:
This test evaluates the stapedius branch of the facial nerve .
One is the most objective and reproducible.
A loud tone is presented to either the ipsilateral or contralateral ear which
should evoke a reflex movement of the stapedius muscle.
An absent reflex or reflex that is less than one half the amplitude of the
contralateral side is considered as abnormal

33. • Taste testing: This test is extremely subjective.
Can be done by placing a small amount of salt, sugar, or lemon juice, quinine
and on the tongue.
The patient is asked to indicate that he perceives the taste before he withdraws
the tongue
 Loss of taste may indicate interruption of the ipsilateral chorda tympani nerve.

34. • Taste testing (electrogustometry):
• 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
• In normal subjects, the two sides of the tongue have similar thresholds for
electrical stimulation.
• Thresholds difference of more than 25% is abnormal

35. • Salivary flow test:
 To evaluate functional integrity of the chorda tympani nerve.
Involves cannulation of Wharton's ducts bilaterally with measurement of output after
five minutes.
 A 25% reduction in flow of the involved side as compared to the normal side is
considered significant.
Salivary pH may be examined as an indirect measure of flow. As the rate of flow
increases, the pH increases. therefore, a pH of less than 6.1 may predict loss of function
of the chorda tympani.
 Disadvantages :
Time consuming
Unpleasant.
 Cannot perform repeatedly

36. • ELECTROPHYSIOLOGIC TESTS
• These tests are useful for patients with complete paralysis for determining
prognosis for return of facial function and the endpoint of degeneration by
serial testing.
• The nerve excitability test (NET)
Is the most commonly used.
This test involves placement of a stimulating electrode over the stylomastoid
foramen.
The lowest current necessary to produce a twitch on the paralyzed side of the
face (threshold) is compared with the contralateral side.
 A difference of greater than 3.5 milliamps indicates a poor prognosis for return
of facial function.

37. • The maximum stimulation test (MST)
Is a modified version of the NET.
Instead of measuring threshold, however, maximal stimuli (current levels at
which the greatest amplitude of facial movement is seen) is employed.
Increasing current levels are used until maximal movement is seen, and the
paralyzed side is compared to the normal side
 Maximal nerve 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 > 90%
• No response within first ten days – incomplete recovery with significant
sequelae

38. • 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.
Electromyography:

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

41. • 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
Evoked Electromyography
(EEMG) or Evoked Electroneuronography (ENOG)

42. • Waveform responses are analyzed to compare peak-to-peak amplitudes
between normal and involved sides where the peak amplitude is proportional to
the number of intact axons.
• Response <10% of normal in first 3 weeks-poor prognosis
• Response >90% of normal within 3 weeks of onset-
80-100% probability of recovery

43. • Computed tomography (CT) is valuable for surgical planning in cholesteatomas
and temporal bone trauma involving facial nerve paralysis but probably is less
useful than MRI in the investigation of atypical idiopathic paralysis.
• Magnetic resonance imaging (MRI) with intravenous gadolinium contrast has
revolutionized tumor detection in the cerebellopontine angle and temporal
bone and is currently the study of choice when a facial nerve tumor is suspected
(e.g., in a case of slowly progressive or longstanding weakness)
Imaging

45. MANAGEMENT OF FACIAL PALSY
Medical
management
Steroids
Boutulinum toxin
Vasodilator therapy
Physiotherapy
Eye care
Reassurance
Surgical
management
Decompression
Micro surgery
Implants

46. CORTICOSTEROIDS
• Prednisolone 1mg/kg. body wt. in divided doses .
• Then tapered dependent on whether the paresis progresses to paralysis or
remains stable
• If the palsy remains stable, we either stop steroids without tapering or rapidly
taper the dose for the next 5 days .
• If the patient presents with paralysis or progresses to complete paralysis, the
dose is proceeded for the next 15 days and tapered in 5 days
Ramsey et al. Corticosteroid Treatment for Idiopathic Facial Nerve Paralysis: A Meta-analysis Laryngoscope 110: March 2000

47. BOUTULINUM TOXIN
• Clostridium botulinum toxin (BOTAX)
• Neurotoxin
• Temporarily interfere with the acetylcholine release from the motor nerve end
plates causing skeletal muscle paralysis .
• 4 to 6 months
• Used to weaken the contralateral side to allow centering of the mouth , more
symmetry on smiling and treatment of hypertrophic platysmal bands
Use of Botulinum Toxin A in the Rehabilitation of Facial Nerve Paralysis: A Cases Series. Susana
Moraleda,MD (Hospital La Paz,Madrid, Spain); Sandra Espinosa, MD; Mercedes Martinez, MD

48. vasodialators
• Stennert’s protocol: In 1979, Stennert devised an infusion therapy
• Low molecular wt Dextran I.V infusion 1000cc/day for 3 days over 16 hour
period ; reduced to 500 cc/day for 8 days .
• Cortisone 200mg/day for 2 days, reduce to 50mg/day in 10 days and stop
between 11 & 12 days
• Pentoxyphilline 10 mg per day IV
• Acyclovir 200 to 400 mg 5 times daily for 10 days

49. A. Acute (< 3 wks)
1. Nerve exploration/decompression
2. Nerve repair
a. Primary anastomosis
b. Cable grafting
i. Great auricular nerve
ii. Sural nerve
B. Intermediate (3 wks- 2 yrs)
1. Nerve transfer
a. Hypoglossal-facial
b. Spinal accessory-facial
c. Masseteric-facial
2. Cross face nerve grafting using sural nerve
C. Chronic (>2 yrs)
1. Muscle transfers
a. Temporalis
b. Masseter
c. Digastrics
2. Free muscle flaps/
microneurovascular transfer
a. Gracilis
b. Latissimus dorsi
c. Serratus anterior
d. Pectoralis minor
D. Static procedures/ancillary procedures
(can be performed at any time period
listed above)
1. Gold weight/spring implants
2. Slings
3. Lid procedures
Ryan Ridley. Facial Reanimation .Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
SURGICAL TREATMENT MODALITIES

50. NERVE DECOMPRESSION
• Can be carried out internally or externally
• Internal decompression- the nerve is exposed in the fallopian canal and
pressure in the canal is relieved by exposing the nerve and the epineural sheath
is opened to visualize the nerve fibers and release adhesions or reestablish
continuity
• External decompression is done by releasing the epineural sheath from
surrounding scar tissue ,bone or foreign body

51. NEURORRHAPY PROCEDURES

52. • DIRECT END TO END ANASTOMOSIS
• Direct nerve repair: Indicated when sharp precise lacerations of facial nerve .
• can be performed with defect < 17 mm.
• can be performed < 72 hrs of injury
• Adequate preparation of nerve ends by resecting devitalized tissue/debris
with fine scalpel.
• Epineural sheath approximated with 9-0/10-0 nonabsorbable suture(nylon
or prolene )
• Avoid tension at suture line

53. MICROSURGICAL SUTURING
Interfascicular
Epineurium
Perineurium

54. • 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

55. NERVE ANASTOMOSIS
• Anastomosis of the central end of the hypoglossal or spinal accessory nerve with
the distal end of the facial nerve is done

56. NERVE GRAFTING
• Nerve grafting- whenever there is evidence of neuroma or loss of portion of the
nerve, nerve grafting can be considered.
• Similar to direct nerve repair except addition anastomosis at each nerve branch.
• Autogenous nerve grafts remains the standard
• Common donor sites
• Greater auricular nerve – up to 10 cm
• Sural nerve –for longer grafts
• Antebrachial cutaneous nerve
56

57. GREATER AURICULAR NERVE GRAFTING
Harvesting;
 Located on lateral surface of SCM at the
midpoint of a line drawn between mastoid tip
and mandibular angle
 Postauricular incision or use separate neck
incision
 Advantages:
 Proximity to facial nerve
 Cross-sectional area
 Limited morbidity
 Limitations:
 Reconstruction of long defects
 Ideal for defects < 6cm in length

58. SURAL NERVE
• Is the branch of tibial nerve in the middle of the popliteal fossa .
Can be identified adjacent to the lesser saphenous vein posterior to the lateral
malleolus
 ADVANTAGES :
 Length : as much as 40 cm
 Accessibility
 Low morbidity .
 DISADVANTAGES:
 Variable caliber
 Often too large
 Difficult to make graft approximation
 Unsightly scar

59. MEDIAN ANTEBRACHIAL CUTANEOUS NERVE
• Can be harvested from the upper extremity .
• Identified adjacent to the basilic vein .
• Divides into anterior and posterior branches near antecubital fossa.
• Incision parallel to the plane formed by the fascial plane separating the biceps
and triceps muscles

60. • Branches from the cervical plexus, from the ipsilateral or contralateral side are
also most frequently used for facial nerve autografting

61. CROSS FACE NERVE GRAFTING
 Contralateral facial nerve is used to reinnervate
paralyzed side using a nerve graft
Sural nerve often employed.
Disadvantages :
• Surgical intrusion on normal side
• Highly specialized technique & longer time
• Longer time required for reinnervation from long
shafts by which time there may be further muscle
atrophy
• Results not free of mass movements, synkinesis

62. FACIAL NERVE TRANSPOSITION
• Reinnervation by connecting an intact proximal facial nerve to the distal
ipsilateral facial nerve.
 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

63. MUSCLE TRANSPOSITION
(“DYNAMIC SLING”)
• It is employed when there has been long standing paralysis and the muscles of
facial expression have atrophied.
• The masseter and temporalis muscles are the two most commonly used.

64.  Often used for reanimation of the oral commisure.
 Middle 1/3 of muscle is best for transfer
TEMPORALIS

65. TEMPORALIS TRANSFER
Incision in preauricular crease extending to superior
temporal line
Obtain wide exposure of temporalis muscle by dissecting
above the SMAS
Incise down on periosteum to elevate muscle fibers
• -harvest middle 1/3
Large tunnel created over zygomatic arch
Orbicularis oris muscle exposed via vermilion border
incision at oral commissure.
Temporalis flap detached and elevated from its origin and
tunneled to the oral commissure.
3-0 prolene used to suture orbicularis to temporalis at oral
commissure

66. MASSETER TRANSFER
1. Expose muscle with gingival incision along mandibular sulcus
2. Dissection carried out in a plane between mucosa and muscle.
3. Muscle freed off of mandible medially and from the inferiolateral edge
of mandible.
4. Vertical incision made in inferior portion of muscle
5. Anterior half of muscle is split into 2 divisions.
6. The 2 anterior slips of muscle are tunneled anteriorly to reach the oral
commisure via external vermillion border incisions
7. Muscle slips are attached to lips and oral commisure in the deep dermal
layer using suture

67. Microneurovascular transfer free muscle flaps
• They have potential of achieving individual segmental
contractions
• reduction of synkinesis
• Muscle flaps used are:
• Gracilis
• Latissimus dorsi
• Inferior rectus abdominus
 Requires viable muscle and nerve innervation
 Traditionally done in 2 stages
 1st: cross-face nerve graft 1 yr prior to muscle
transfer
 2nd: muscle transfer performed after neural
ingrowth of graft

68. ADDRESSING PARALYTIC EYELIDS
• Complications of orbicularis oculi paresis
 Delayed blinking
 Impairment of nasolacrimal system
 Dry eye
 Risk of exposure keratitis, corneal ulceration and blindness
• Goal of treatment is to maintain cornea
• Treatment options
 Tarsorrhaphy
 Gold weight/spring implants
 Open / endoscopic brow lifts for significant brow ptosis

69. GOLD WEIGHT
IMPLANTATION
1. Small incision made several millimeters
above the upper eyelid margin.
2. Tarsal plate exposed with sharp dissection
3. Gold weight secured to tarsus using 8-0
nylon.
4. Wound closed in 2 layers

70. TARSORRHAPHY
• Tarsorrhaphy is a surgical procedure in which the eyelids
are partially sewn together to narrow the eyelid opening
Horizontal mattress 5-0 nylon
Begin 3mm medial to lateral canthus, 6mm from lid
margin
Stitch travels through gray line to 5mm below lower lid
margin

71. Static procedures
 Indications:
 Debilitated individuals; poor prognosis
 Nerve or muscle not available for dynamic procedures
 Adjuct procedure with dynamic techniques to provide
immediate benefit
 Advantages:
 Immediate restoration of facial symmetry at rest
 No oral commissure ptosis
 Drooling, disarticulation, mastication difficulties
 Relief of nasal obstruction caused by alar collapse
• Static facial suspension is used to lift the corner of the
mouth so that balance is restored to the face and drooling
out of the mouth is helped.

72. 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

74. BELL'S PALSY
• Facial paralysis of acute onset presumed to be due to non-suppurative inflammation (of
unknown aetiology) of the facial nerve
• The name was ascribed to sir charles bell, who in 1821 demonstrated the separation
of motor and sensory innervation of face.
• Site of lesion in bell's palsy is the meatal foramen (junction of the internal auditory
canal portion of the nerve and the labyrinthine segment of the nerve), which is
considered to be the narrowest portion of the fallopian canal.

75. WHAT CAUSES IT ?
The exact reason bell's palsy occurs isn't clear.
Brain tumor, stroke, myasthenia gravis, and lyme disease (infectious disease).
It's often linked to exposure to a viral infection.
Viruses that have been linked to bell's palsy include the virus that causes:
•Chickenpox and shingles (Herpes zoster)
•Respiratory illnesses (Adenovirus)
•German measles (Rubella)
•Mumps (Mumps virus)
•Flu (Influenza B)

76. WHO CAN GET THIS?
• Incidence- 15-40 cases per 1 lakh cases
• Sex predilection- Women more affected than men.
• 3.3 more times common in pregnancy and in the third trimester.
• Age- Can occur at any age, common in middle aged people.
• Side involvement- Can be equally seen, usually unilateral.

77. RISK FACTORS
• Associated known clinical conditions are diabetes,
• Severe hypertension,
• Last trimester of pregnancy,
• Dental anesthesia.
• Exposure to cold.

78. Clinical features:
• There is sudden onset, occurrence after awakening early
morning.
• Unilateral involvement of entire side of the face.
• Abrupt loss of muscular on one side of face.
• Inability to smile, close the eye or raise the eyebrow on
affected side.
• Whistling is not possible.

79. • Inability to wrinkle forehead or elevate upper or
lower lip.
• Obliteration of nasolabial fold.
• Face appears distorted and mask like appearance to
the facial features.
• Speech becomes slurred.
• Occasionally there is loss or alternative of taste.

80. • On closing the eye ,the eyeball moves upwards and inwards.
• This is obvious on the affected side due to ineffective closure of the eyelids.
BELL’S PHENOMENON

81.  Outcome is good!!!
 Total recovery depends on amount of damage to nerve
 Improvement is gradual
 Most people begin recovery in 2 to 3 weeks.70% to 85% of people showing complete
recovery in 2 to 3 months
 In a few cases, the symptoms may never completely disappear.
 In rare cases, the disorder may recur, either on the same or the opposite side of the
face. (10%)

82. MANAGEMENT OF BELLS PALSY
 It focuses on protecting the cornea from drying and
abrasion due to problems with lid closure and the
tearing mechanism.
 Eyes to be protected with dark glasses or eye patch.
 Eyes to be washed with zinc-boric solution to prevent
conjunctivitis.
 Lubricating drops should be applied hourly during the
day and a simple eye ointment should be used at night.
EYE CARE
82

83. • 2.) Local treatment of muscles
• Massage the facial muscles with bland oil twice daily for 5 minutes
• The massaging movements should start from chin and upwards.
• Prevention of facial sagging can be down done by application of strips of
adhesive tape.
• The tape is attached to the temple and extends down in a v shaped fashion to
the upper and lower lips.

84. RECENT ADVANCES
• Surgeons from UC Davis Medical Center have demonstrated
that artificial muscles can restore the ability of patients with
facial paralysis to blink
• Sling that is attached to the electroactive polymer artificial
muscle device (EPAM) after passing through an interpolation
unit that is implanted in the lateral orbital wall (note screw
fixation). The power supply and artificial muscle are
implanted in the temporal fossa. conceptually, when the
normal right eyelid blinks, the electrical sensor (green) sends
a signal to the battery to activate the EPAM
Artificial Muscles Restore Ability to Blink, Save Eyesight; Science Daily (Jan. 18, 2010)

85. CONCLUSION
• The human face signals expressions of happiness, anger, fear, and surprise that
appear to be universal in character. Impairment of the facial nerve interferes
with the transmission of this intimate information that is an essential addition to
the flow of our conversation that significantly supplements the meaning of our
speech.
• Therefore it is highly essential to have a precise diagnosis of the problem and
then the surgeon should use his skill and imagination to bring back the
expressions of the face which will eventually take a long way in improving the
patients functional esthetical and emotional status.

86. REFERENCES
• Gray’s anatomy.
• Textbook of Oral and Maxillofacial Surgery – Neelima Anil Malik
• Textbook of Oral and Maxillofacial Surgery –SM Balaji
• Maxillofacial surgery: Peter ward booth vol 1 & 2
• Maxillofacial trauma and esthetic facial reconstruction - Peter ward booth
• Peterson’s principles of Oral & Maxillofacial Surgery, 2nd edition.
• Hazarika – Text book of Oryntolaryngology.
• Ramsey et al. Corticosteroid treatment for idiopathic facial nerve paralysis: A meta-analysis laryngoscope 110: March
2000
• Use of botulinum toxin a in the rehabilitation of facial nerve paralysis: a cases series. susana moraleda,md (hospital
la paz,madrid, spain); sandra espinosa, md; mercedes martinez, md
• Ryan ridley. Facial reanimation .grand rounds presentation, utmb, dept. of otolaryngology
• Artificial Muscles Restore Ability to Blink, save eyesight; ARCHIVES OF FACIAL PLASTIC SURGERY.