GUIDED BY : PRESENTED BY :

DR.P.KARUNAKAR DR.M.RASAGNA
DR.UMRANA FAIZUDDIN
DR.ASHISH JAIN
CONTENTS
• introduction
• Embryology
• Nuclei of origin
• Functional components
• Course of facial nerve
• Branches and distribution
• Surface marking of facial nerve
• Ganglion associated with facial nerve
• Blood supply
• Age changes
• Variations of facial nerve
• Applied anatomy
• Face nerve considerations in endodontics
• Conclusion
• References
INTRODUCTION :

• Seventh cranial nerve.

Motor root
• Mixed nerve
Sensory root

7000 Motor
• 10,000 Neurons

3000 Sensory and

Secretomotor
EMBRYOLOGY
• Developmentally derived from

• Motor division of facial nerve is derived from

• Sensory division originates from the cranial neural crest.

3 rd week Facioacoustic primordium or crest develops
1st distinguishable feature of facial nerve

4th week Facial and acoustic portions are more distinct

5th week Apperance of Geniculate ganglion which

separates into 2 branches-main trunk of facial
nerve and chorda tymphani
6th week Facial motor nucleus is recognizable

7th week Nervus intermedius arises from the

ganglion,formation of peripheral branches
 8th week Formation of fallopian canal
10-15 Peripheral branches are completely
weeks developed
• course ,branching,anatomic relations are established during the first three
months of prenatal life.
• Important steps in facial nerve development occurs throughout gestation and
the nerve is not fully developed until 4yrs after birth.
NUCLEI OF FACIAL NERVE
The fibres of the nerve arise from four nuclei
situated in the lower pons.
1. Motor nucleus of brachiomotor
2.superior salivatory nucleus –parasympathetic
3.lacrimatory nucleus-parasympathetic
4.Nucleus tractus solitarus which is gustatory
and also receives afferent fibres from the gland.
FUNCTIONAL COMPONENTS
• Special Visceral Efferent — Motor to striated muscles derived from the 2nd
branchial arch i.e, muscles responsinble for facial expression and elevation of
hyoid bone.
• General Visceral efferent — these are secretomotor to submandibular,
sublingual, lacrimal and glands of nose, palate and pharynx.
• General visceral afferent — carries afferent impulses from the above mentioned
glands.
• special Visceral Afferent — carries taste sensation from the palate and from
anterior two-thirds of the tongue except from vallate papillae.
• General Somatic Afferent — innervate a part of skin of ear and carries
the impulses of touch and temperature, carries proprioceptive impulses from
muscles of face.
COURSE OF FACIAL NERVE

• The course of facial nerve is divided by stylomastoid foramen into

Intracranial (intrapterous)part Extracranial part

INTRACRANIAL PART :
2 roots attached to the lateral part of the lower border of pons,medial to CNVIII

Both reach the internal acoustic meatus

In the Meatus motor root lies in a groove on CNVIII(accompained by

labrythine vessels)

Two roots fuse in the bottom of the meatus to form a single trunk

Single trunk lies in the pterous part of the temporal bone and enters the facial canal
• Within the canal,the course of the nerve can be divided into three parts by 2
bends.
• First part :directed laterally above the vestibule.
• Second part :runs backwards into relation to the medial wall of the middle ear
above promontory.
• Third part:directed downwards behind the promontory.
• First bend :also called genu,lies anteriosuperior to promontory.
• Second bend: is between promontory and mastoid antrum.
The facial nerve exits the posterior cranial fossa at the internal acoustic meatus
Within the internal acoustic meatus ,facial nerve enters the facial canal
The first branch –the greater superficial petrosal nerve branches from the geniculate ganglion within the genu
of the facial canal and enters the middle cranial fossa by way of hiatus of the canal for the GSPN
EXTRACRANIAL PART:
• As it exits from the stylomandibular foramen,it gives rise to
.posterior auricular
.digastric
.stylohyoid
 Lateral side of base of
styloid process

Then enters the parotid

gland through
posterolateral surface

Behind the neck of the

mandible ,it divides into 5
terminal branches

Emerges out through

anteriomedial surface
 Branches

Branches of Branches of
communication distrubution
BRANCHES OF COMMUNICATION
Internal acoustic meatus VIII cranial nerve
Geniculate ganglion a.greater petrosal nerve
b.lesser petrosal nerve
C.External petrosal nerve
Facial canal Vagus nerve
Stylomastoid foramen IX & X cranial nerves
Greater auricular nerve
Auriculotemporal nerve
Behind ear Lesser occipital nerve
Face V cranial nerve
Neck Transverse cutaneous nerve
 BRANCHES OF DISTRUBUTION

IN FACE
FACIAL CANAL STYLOMASTOID FORAMEN a.temporal
Greater petrosal a.posterior auricular b.zygomatic
nerve b.nerve to stylohyoid c.buccal
Nerve to stapedius c.nerve to d.marginal mandibular
Chorda tympani digastric(posterior belly) e.cervical
SURFACE MARKING
• Marked by a short horizontal line which joins the following two
points:
1) A point at the middle of the anterior border of the mastoid process.
2)Behind the neck of the mandible.
GANGLIA ASSOCIATED WITH FACIAL NERVE
GANGLION NATURE FUNCTION

Geniculate sensory Taste fibers from

anterior 2/3rds of
the tongue
submandibular parasympathetic Secretomotor fibres
to submandibular
and sublingual
salivary glands
pterygopalatine parasympathetic Secretomotor fibres
to lacrimal gland
VARIATIONS OF FACIAL NERVE

1. Buccal branch usually single, two branches in 15% cases

2. Marginal mandibular branch – pass bellow the lower border of
mandible, incidence varying between 20-50%
3. Cervical branch – 20% cases, two branches
4.Baker and Conley reported trifurcation, quadrifurcation, or even a
plexiform branching pattern of the trunk of the facial nerve
DISORDERS OF FACIAL NERVE
• Facial nerve lesions:
1)supranuclear type
2)nuclear type
3)peripherial lesions
Injury at the internal acoustic meatus
Injury distal to geniculate ganglion
Injury at stylomastoid foramen
SUPRANUCLEAR TYPE:
• Features:
• Paralysis of lower part of the face(opposite side)
• Partial parlysis of upper part of the face
• Normal taste and saliva secretion
• Stapedius not paralysed
NUCLEAR TYPE
• Features:
• Paralyses of the facial muscle of the same side

• PERIPHERAL:
A)Injury at the level of internal acoustic meatus:
Features:
• Paralysis of secretomotor fibres.
• Hyper acusis
• Loss of corneal reflex
• Taste fibres unaffected
• Facial expression and movements paralysed
B)injury distal to geniculate ganglion
• Features:
• Complete motor paralysis(same side)
• Loss of corneal reflex
• No hyper acusis
• Taste fibers affected
• Facial expression and movements paralysed
• C)injury at stylomastoid foramen:
• Condition known as Bell's palsy
CAUSES FOR FACIAL PALSY
• Birth
• Trauma
• Infections
• Toxic
• Metabolic causes
• Neoplastic
• Iatrogenic
• Idiopathic
BIRTH:
• Forceps delivery.
• Dystrophia myotonica.
• Moebius syndrome.
TRAUMA
• Basal skull fracture.
• Facial injuries.
• Penerating injury to middle ear.
• Altitude paralysis(barotrauma).
INFECTIONS
• Malignant otitis Externa(skull base osteomyelitis)
• Acute or chronic otitis media
• Varicella zoster infection
• Herpes zoster infection(Ramsey hunt syndrome)
• Hiv infection
• Parotitis
• Mumps
• Meningitis
TOXIC
• Thalidomide
• Tetanus
• Diphtheria
• Carbon monoxide
METOBOLIC CAUSES
• Diabetes mellitus
• Hyperthyroidism
• Pregnancy
• Hypertension
• Acute porphyria
NEOPLASTIC
• Facial nerve tumor
• Leukaemia
• Meningioma
• Haemangioblastoma
• Sarcoma
• Carcinoma(invading or metastatic)
IATROGENIC
• Mandibular block anesthesia
• Head and neck surgery
IDIOPATHIC
• Myasthenia gravis
• Guillian-barre syndrome
• Sarcodiosis
• Familial bell's palsy
EVALUATION OF FACIAL PARALYSIS
• Clinical features
Central VS peripheral lesion
Complete head and neck examination
Cranial nerve evaluation
• Electrodiagnostic testing
• Tophographic diagnosis
TOPHODIANOSTIC TESTS
• Schirmer test for lacrimation (GSPN)
• Stapedial reflex test (Stapedial branch)
• Taste testing (Chorda tympani nerve)
• Salivary flow rates & pH (Chorda tympani)
ELECTROPHYSIOLOGIC TESTS
• Nerve excitability test(NET)
• Electromyography(EMG)
• Maximal stimulation test(MST)
• Electroneuronography(ENoG)
IMAGING
• 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.
• Computed tomography (CT) is valuable for surgical
planning in cholesteatomas and temporal bone trauma
involving facial nerve paralysis.
HOUSE BRACKMANN FACIAL NERVE GRADING SYSTEM
GRADING DEGREE OF INJURY FEATURES
GRADE 1 NORMAL normal functions
At rest: normal symmetry & tone

At motion: slight weakness

GRADE II SLIGHT DYSFUNCTION
Complete closure of eye with mini
mum effort

Slight asymmetry of mouth

At rest- normal symmetry & tone

At motion: obvious dysfunction but

not disfiguring difference between
GRADE III MODERATE DYSFUNCTION two sides

complete closure of eye with effort

Hemi facial spasm

 At rest: normal symmetry & t
one

At motion: obvious weakness

MODERATE SEVERE DYSFUNC
GRADE IV
TION Disfiguring asymmetry

Incomplete closure of eye

Mouth- asymmetric
At rest: asymmetry
At motion: barely perceptible
motion
GRADE V SEVERE DYSFUNCTION
Eye- incomplete closure

Mouth- slight movement

BELLS PALSY
• Bell's palsy is an idiopathic, acute, unilateral paresis or
paralysis of the face in a pattern consistent with
peripheral facial nerve dysfunction, and may be partial
or complete, occurring with equal frequency on the right
and left sides of the face.
• Named after Sir Charles Bell (1774-1842), who first
described the syndrome along with the anatomy and
function of the facial nerve.
• Bell palsy is certainly the most common cause of facial
paralysis worldwide
DEMOGRAPHICS OF BELL'S PALSY
• Race:slightly higher in persons of japanese descent.
• Sex:no diference exists.
• Age: it is more common in persons aged 15-45 years.
• Bell's palsy is less common in those younger than 15 years and in
those older than 60 years.
PATHOPHYSIOLOGY OF BELL'S PALSY
• Two most common proposed theories are:
1.) infection with virus.(HSV1, Herpes zoster)
2.) Compression of the nerve.
1.)Reactivated herpes viruses from the geniculate ganglion of the facial nerve
may play a key role in the development of this condition.

Primary viral infection (herpes) sometime in the past.

The virus lives in the nerve (geniculate ganglion) from months to years.

The virus becomes reactivated at a later date

The virus reproduces and travels along the nerve.

 The virus infects the cells surrounding the nerve resulting in inflammation.

The immune system responds to the damaged Schwann cells, which causes
inflammation of the nerve and subsequent weakness or paralysis of the face.

The course of the paralysis and the recovery will depend upon the degree
and amount of damage to the nerve.
 2.)Compression of the nerve:

• Edema and ischemia result in compression of the facial nerve

within fallopian or facial canal.

• The first portion of the facial canal, the labyrinthine segment,

is the narrowest.

• The meatal foramen in this segment has a diameter of only

about 0.66 mm. This is the location that is thought to be the
most common site of compression of the facial nerve in Bell
palsy.
FEATURES OF BELL'S PALSY
• Unilateral involvement.
• Loss of nasolabial fold.
• Drooping of the corner of the mouth.
• Slight widening palpebral fissure.
• Inability to close eyelid (bell's sign).
• Mask like appearance of face.
• Inability to smile , close eye or raise eyebrow .
• Whistling impossible.
• Inability to puffing cheeks.
• Inability to wrinkle forehead .
• Slurred speech.
• Loss/alteration of taste.
DIAGNOSIS OF BELL'S PALSY
• By exclusion
• Criteria:
• Paralysis or paresis of all the muscles groups on side of the face.
• Sudden onset.
• Absence of signs of CNS disease.
• Absence of signs of ear disease.
HISTORY
• Patient also mentoin otalgia or aural fullness and facial or
retroauricular pain,which is typically mild and may precede the palsy.
• The palsy is often sudden in onset and evolves rapidly ,with maximal
facial weakness developing within two or three days.
• Associated symptoms may be hyperacusis,decresed production of
tears and altered taste.
• The most alamring symptom of bell's palsy is paresis.
PHYSICAL EXAMINATION
• Bell's phenomenon —upward diversion of the eye on
attempted closure of the lid—is seen when eye
closure is incomplete.
• Careful inspection of the ear canal, tympanic
membrane, and oropharynx.
• Evaluation of peripheral nerves function in the
extremities.
• Palpation of the parotid gland.
COURSE AND PROGNOSIS
• Partial paralysis always resolves completely within a few weeks.
• Recovery from complete paralysis takes longer (months)and is
complete in only about 60-70% cases.
• Approximately 15% of patients are left with troublesome residual
palsy and or synkinesis.
MANAGEMENT
• The main aims of treatment in the acute phase of Bell's palsy are to
speed recovery and to prevent corneal complications.
• Psychological support is also essential, and for this reason patients
may require regular follow up.
• There is general agreement that 70-80% of these patients recover
completely ,while the reminder develop various sequelae within one
to three months
• Eye care:
• It focuses on protecting the cornea from drying
and abrasion due to problems with lid closure and
the tearing mechanism.
• Lubricating drops (carboxy methyl
cellulose)should be applied hourly during the day
and a simple eye ointment should be used at
night.
MEDICAL TREATMENT
• Corticosteroids :
• Prednisolone 1mg/kg/day 7-10 days
• Corticosteroids combine with antiviral drugs is better.
• Acyclovir 400mg 5 times/day.
• Famciclovir and valacyclovir 500mg bid
SURGICAL TREATMENT
• Facial nerve decompression.
• INDICATION:
• Completely paralysis.
• Appropiate time for surgery is 2-3 weeks after paralysis.
SYNDROMES INVOVLING FACIAL NERVE :
HERPES ZOSTER OTICUS SYNDROME
• Symptoms:
• Facial paralysis
• Ear pain
• Vesicles
• Hearing loss
• vertigo
MELKERSSON ROSENTHAL SYNDROME
• Recurrent attacks of facial paralysis.
• Associated with mulitple episodes of non-pitting ,non-inflammatory
painless edema of the face.
• Chelitis granulomatosa.
• Fissured tongue.
TREACHER COLLINS SYNDROME
• Features :
• There is a set of typical symptoms within Treacher Collins Syndrome
• The OMENS classification was developed as a comprehensive and
stage-based approach to differentiate the disease.
• O; orbital asymmetry
• M; mandibular hypoplasia
• E; auricular deformity
• N; Abberent Nerve development and
• S; soft-tissue disease
Facial nerve involvement in treachers collins syndrome
• N0:No facial nerve involvement
• N1: Upper facial nerve involvement (temporal or
zygomatic branches)
• N2: Lower facial nerve involvement (buccal,
mandibular or cervical)
• N3: All branches affected
MOEBIUS SYNDROME(CONGENITAL FACIAL DIPLEGIA)
• Abnormal VI ,VII,XII Nerve nuclei
• Facial Nerve absent / smaller
• Congenital Extra ocular muscle & facial palsy
CROCODILE TEAR SYNDROME
• Due to injury to facial nerve ,proximal to geniculate ganglion,there
may be misdirection of nerve fibers to lacrimal gland instead of going
to submandibular gland,through the greater pterosal nerve.
• As a result ,patient lacrimates is termed as crocodile tear syndrome
and can be treated by dividing the greater petrosal nerve.
AURICULOTEMPORAL NERVE SYNDROME
• Is a complication of paradicetomy .
• Abberant nerve regeneration after injury(a
complication develops between auriculo
temporal and greater auricular nerves such
thst the parasympathetic fibers migrate into
cutaneoussympathetic nerves that supply the
swaet glands .
FACIAL NERVE CONSIDERATIONS IN ENDODONTICS
• Through dental or surgical procedures; dentist may cause the transient or
permanent facial palsy.

• An dentist may treat a patient with FP

or
• The first medical professional to observe FP in a patient

or
• Even induce iatrogenic errors themselves
SUMMARY
• In endodontics facial nerve palsy is caused by :
• Direct anaesthesia to the facial nerve.
• Reflex vasospams of the external carotid artery ischemia of the
facial nerve.
• Direct damage with the irrigants.
• Dental infections may secondarily infect the facial nerve.
CONCLUSION
• The diagnosis,clarification of etiology and treatment of facial paralysis
require a multidisciplinary team with neurosurgeon, otorhinolaryngologist, oral and
maxillofacial surgeon.

• The dentist must evaluate and remove the dental foci.

• The dentist should avoid inducing iatrogenic facial paralysis in the dental office.

• Dentist should have a thorough knowledge of facial nerve, its complications, clinical
findings, diagnosis and should have an essential treatment plan of FNP in dental office

• The dentist can make oral devices to implement multifunctional rehabilition and must
also rehabilitate an asymmetric oral cavity with functional disorders ,in order to improve
the quality of life of patients with facial paralysis.
REFERENCES
• B.D.chausaria 's human anatomy 4th edition.
• Gray's anatomy 2 nd edition.
• The facial nerve –May's 2nd edition.
• Shafers textbook of oral pathology-5th edition.
• Management of patients with facial paralysis in the dental office: A
brief review of the literature and case report:Aranka Ilea,Alxendaru
cristea ,Viorica Tarmure,Veronica E. Trombita,Radu S Campian,Silviu
Albu.