The facial nerve is a mixed nerve that arises from nuclei in the brainstem and controls muscles of facial expression. It has both motor and sensory functions. Clinically, facial nerve disorders can result in facial paralysis and loss of taste sensation on the anterior tongue. Evaluation involves physical examination and electrodiagnostic testing to localize the lesion. Bell's palsy is the most common cause of acute facial paralysis and typically resolves on its own, while Ramsay Hunt syndrome causes paralysis along with ear symptoms from varicella zoster virus reactivation.

1. FACIAL NERVE
Presenter: Dr N. Brojendro Singh
Moderator: Prof Y.Nandabir Singh
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2.  Facial nerve is the 7th cranial nerve
 Mixed nerve
 Arises from brain stem between pons and medulla
 Controls muscles of facial expression
 Carry taste sensations from anterior 2/3rd of tongue and oral cavity
 Supplies preganglionic parasympathetic fibres to head and neck
ganglia
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3. DEVELOPMENT
 Facial nerve derived from the hyoid arch (second branchial arch)
 Motor division derived from the basal plate of the embryonic pons
 Sensory division originates from the cranial neural crest
 Nerve is not fully developed until about 4 years of age
 First identifiable Facial Nerve tissue seen at the 3rd wk of gestation
facioacoustic primordium or crest
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4. NUCLEI OF ORIGIN
• Arises from 4 nuclei
1. Motor nucleus of facial nerve (SVE):
 It lies in the lower part of the pons
2. Superior salivatory nucleus (GVE):
 Lies in the pons lateral to the main motor nucleus of VII
 Gives rise to secretomotor parasympathetic fibers that pass in
greater superficial petrosal nerve and chorda tympani
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5. 3. Nucleus of tractus solitarus (SVA):
- lies in the medulla
- receives taste sensation from anterior 2/3 of tongue via
geniculate ganglion of the facial nerve
4. Lacrimal nucleus
- lies in the pons lateral to the main motor nucleus of VII
- gives rise to secretomotor parasympathetic fibers
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6. NUCLEUS OF ORIGIN
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7. Course of Facial Nerve
 Intracranial portion (23-24 mm)
 Intratemporal portion (28-30 mm)
a. Meatal segment (8-11)
b. Labyrinthine segment (3-5 mm)
c. Tympanic segment (8-11 mm)
d. Mastoid segment (10-14 mm)
 Extratemporal portion
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8. Intracranial Segment
 Portion of the nerve from the
brainstem to internal auditory
canal (IAC)
 Made up of two components
1. Motor root
2. Nervus intermedius
 Both join at internal auditory
canal to form common facial
nerve
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9. Intratemporal Segments
• From IAC to stylomastoid
foramen
• Length – 28 to 30 mm
• Longest bony canal
• Three segments by 2 genus
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10. • Meatal Segment
– Lies in IAC
– Enters in ant. sup. segment of IAC with VIII CN
– Length 5 – 12 mm
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11.  Labyrinthine(3-5mm)
–From fundus to the geniculate ganglion
–Runs in the narrowest portion
–Greater superficial petrosal nerve comes off at this point
 Posterolateral to the ampullated ends of the horizontal and superior
semicircular canals and rests on the anterior part of the vestibule
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12.  Tympanic (8-11mm)
 Extends from the geniculate ganglion to the horizontal
semicircular canal
At geniculate ganglion the nerve turns posteriorly across tympanic
cavity to pyramidal eminence making second genu
 Then it emerges from middle ear between the posterior wall of
external auditory canal and horizontal semicircular canal
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13.  Mastoid Segment (10-14mm)
 Second genu marks the beginning of the mastoid segment
 Located lateral and posterior to the pyramidal process
 Continues vertically down the anterior wall of the mastoid
process to the stylomastoid foramen
 Gives branch to stapedius muscle and chorda tympani
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14. Extratemporal Segments
• From stylomastoid foramen to Terminal branches
• Runs in substance of parotid
• Main trunk divides forming “pes anserinus” superficial to
Retromandibular vein & Ext. carotid artery
• upper temperofacial
• lower cervicofacial
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15. Functional Components
 Special Visceral Efferent/Branchial Motor
 General Visceral Efferent/Parasympathetic
 General Sensory Afferent/Sensory
 Special Visceral Afferent/Taste
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16. 23/7/2016 16

17. Branches
 Within the facial canal:
-Greater petrosal nerve
-Nerve to Stapedius
- Chorda tympani
 At the exit from the stylomastoid foramen:
- Posterior auricular
-Digastric
-Stylohyoid
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18.  Terminal branches within the
parotid gland
a. Temporal
b. Zygomatic
c. Buccal
d. Marginal mandibular
e. Cervical
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19. Temporal
– Comes out through the upper pole of parotid gland
– Cross zygomatic arch
– Muscles supplied
• Auricularis anterior & superior
• Frontalis
• Corrugator supercilii
• Procerus
• Upper orbicularis oculi
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20.  Zygomatic :
– Cross zygomatic bone
– Muscles supplied
Lower Orbicularis oculi
Action – Tight shutting of eye
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21. • Buccal
– below zygomatic arch
– upper deep buccal & lower deep buccal
– runs along parotid duct
– Muscles supplied
• Risorius
• Buccinator
• Levator Labii Superioris Alaque Nasi
• Levator Anguli Oris
• Nasalis
• Upper Orbicularis Oris23/7/2016 21

22. • Mandibular
Comes out through the ant. border of parotid gland
– Runs below the ramus of mandible inferiorly
– Supplies muscles of lower lip & chin
• Lower Orbicularis Oris
• Deperessor anguli oris
• Depressor labii inferioris
• Mentalis
Action– Whistle & Puckering of Lips
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23. • Cervical
– Comes out from lower pole of parotid gland
– Muscle Supplied – Platysma
– Action – Contraction of Platysma
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24. Facial Nerve blood supply
 Facial nerve get blood supply from 4 vessels
 Anterior inferior cerebellar artery – at the cerebellopontine angle
 Labyrinthine artery – within internal acoustic meatus
 Superficial petrosal artery – geniculate ganglion and nearby parts
 Stylomastoid artery – mastoid segment
 Posterior auricular artery - distal to stylomastoid foramen
 Venous drainage parallels arterial blood supply23/7/2016 24

25. Central Connections of FN Nucleus
• Upper part of Nucleus – B/L
supranuclear innervation
• Lower part of Nucleus– C/L
supranuclear innervation
• Function of forehead preserved in
supranuclear lesions
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26. Clinical Correlations
 Flaccid paralysis of muscles of
facial expression
 Loss of the corneal reflex which
lead to corneal ulceration
 Loss of taste from the anterior two
thirds of the tongue
 Hyperacusis
 Lack of salivation
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27. Central facial paralysis
• Upper motor neurone lesion
• Movements of the frontal and
upper orbicularis oculi spared
• Because of uncrossed
contributions from ipsilateral
supranuclear area
• Involvement of tongue
• Involvement of lacrimation
and salivation
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28. Peripheral paralysis
• Lower motor neurone lesion
• At rest
– less 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
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29. CONDITIONS RESULTING IN FACIAL
NERVE WEAKNESS
 Bell’s Palsy
 Ramsay Hunt Syndrome
 Melkersson Rosenthal syndrome
 Traumatic causes-
 Endocrine causes-DM, Hyperthyroidism, HTN
 Tumours
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30. Bell’s palsy
 Unilateral
 Peripheral
 Acute onset
 No apparent cause
 Does not involve any other cranial nerves
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31. Etiology
 Exposure to air
 Neurotropic virus
 May be autoimmune
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32. SIGNS AND SYMPTOMS
• No systemic manifestations
• Hyperacusis
• Initial symptom is
retroauricular pain.
• Dysgeusia
• Decreased lacrimation
• Complete paralysis of the
facial muscles on the affected
side of LMN nature within 72
hours
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33. COMPLICATIONS
 Synkinesis.
 Chronic loss of taste
 chronic facial spasm
 facial pain
 corneal infections.
 contracture
 tinnitus or hearing loss during facial movement
 crocodile tear syndrome.
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34. TREATMENT
 Corticostroid
 Anti- viral agents
 Corneal protection
 Physical therary
 Facial nerve decompression
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35. RAMSAY HUNT SYNDROME
 Caused by varicella zoster virus
 Virus resides on the nerve tissue in dormant state on the nerve ganglia
after the initial infectious stage
 When virus is reactivated the resulting blisters are called “Shingles”
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36. SYMPTOMS
 Facial paralysis
 Ear pain
 Vesicles
 Sensorineural hearing loss
 Vertigo
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37. MELKERSSON – ROSENTHAL SYNDROME
 It is a rare neurological disorder characterized by
– Recurring facial paralysis
– Swelling of the face and lips (usually the upper lip)
– The development of folds and furrows in the tongue
– Cause is unknown
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38. EVALUATION OF FACIAL NERVE
DISORDERS
 Muscles of facial expression
- Central vs Peripheral facial paralysis
 Complete head and neck examination
 Topographic diagnosis
 Electrodiagnostic testing
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39. TOPOGNOSTIC TESTING
• Taste sensation
• Lacrimation (Schirmer's Test )
• Stapedius(Acoustic Reflex Testing)
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40. ELECTROPHYSIOLOGIC TESTS
• Nerve conduction test
• Electromyography(EMG)
• Maximal stimulation test (MST)
• Electroneuronography (ENoG
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41. NERVE EXCITABILITY TEST
• Compares transcutaneous current threshold required to elicit minimal
muscle contraction between two sides
• Difference of 3.5 milliamperes (mA) or more in thresholds between
the two sides a reliable indicator of progressive degeneration
• If the paralysis becomes total, test can determine a pure conduction
block exists or degeneration is occurring, as indicated by progressive
loss of excitability
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42. MAXIMAL STIMULATION TEST
• Instead of measuring threshold, however, maximal stimuli is employed.
• Degree of facial contraction is subjectively assessed as either equal, mildly
decreased, markedly decreased, or without response compared with that 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
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43. ELECTROMYOGRAPHY
Indication
 Acute paralysis less than 1 week
or chronic paralysis longer than 2
weeks
Interpretation
• Active MUAP- intact motor axons
• MU fibrillation potentials- partial
degeneration
• Polyphasic - regenerating nerve
• Cannot assess degree of
degeneration or prognosis for
recovery
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44. ELECTRONEURONOGRAPHY
 Records compound muscle action potential (CMAP)
 surface electrodes placed transcutaneously in the nasolabial fold
(response)
 stylomastoid foramen (stimulus)
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45.  Indication- complete paralysis<3wks
 Response <10% of normal in first 3 weeks-poor prognosis
 Response >90% of normal within 3 weeks of onset-
 80-100% probability of recovery
 Not useful until 4th day of paralysis as it takes about 3 days for
degeneration to reach completion
 Less value after three weeks due to nerve fibre desynchronization
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46. THANK YOU
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