Facial nerve


ANATOMY AND PHYSIOLOGY
 It is a MIXED nerve, predominantly motor.
 Supplies muscles of
 Facial expression
 Scalp
 Ear
 Buccinator
 Stylohoid
 Posterior belly of digastric
 Platysma
 Stapedius
 Parasympathetic secretory fibres to
 Submandibular, sublingual glands, lacrimal gland, mucous membranes of oral and
nasal cavities


 Sensory function
 Taste from anterior 2/3rd
of tongue
 Exteroceptive sensation from the eardrum and external auditory canal
 Proprioceptive from muscles it supplies
 General visceral sensation from salivary glands and mucosa of the nose and
pharynx


Segments
 Brain stem / intramedullary segment
 Brainstem nuclei to the exit point
 Cisternal segment
 Exit point to the entrance into the IAC
 Meatal / canal segment
 Course thru the IAC


 Labyrinthine segment
 To the geniculate ganglion
 Short horizontal segment
 To the pyramidal eminence of the posterior wall of the
tympanic cavity
 Mastoid segment
 To the stylomastoid foramen
 Extratemporal / peripheral segment
 To the pes anserinus


MOTOR PORTION
L/3rd
contralateral precentral gyrus, facial area,
motor homonculus
Corticobulbar tract thru corona radiata
Genu of internal capsule
Medial portion of cerebral peduncles
Pons – decussate
Facial nuclei


 This scheme applies to voluntary facial movements
 Unconscious, emotional, involuntary supranuclear control follows different
pathway and may have different degrees of involvement.


Aberrant pyramidal tract
 Some fibres descent in the aberrant pyramidal
tract to medullary levels
 Decussate there
 Ascent contralaterally in the dorsolateral medulla
to reach the facial nucleus.
 Yamashita and Yamamoto, showed that it is a
normal descending fibre tract in the medial
lemniscus in the upper medulla.


Corticofacial fibres
 Majority – fibres travel in the base of the pons, cross at the
level of facial nucleus
 In some – they form an “aberrant bundle” in a
paralemniscal position at the dorsal edge of the pontine
base
 In some – they loop down to the upper ventral medulla,
cross the midline and ascent in the dorsolatral medulla,
ipsilateral to the facial nucleus


 These suggest that facial paresis due to brainstem lesion
may be a contralateral supranuclear facial paresis by a lesion
in
 Cerebral peduncle
 Pontine base
 Aberrant bundle
 Ventral medulla
 Supranuclear facial paresis ipsilateral to the lesion side may
result from a lesion in the
 Lateral medulla
 Supranuclear type maybe imitated by a lesion of the
peripheral nerve in



FACIAL NUCLEUS
 It is special visceral efferent or branchiomotor.
 It lies in the tegmentum of the caudal pons
 Related as : anteromedial to nucleus of spinal tract of
CN V
 Anterolateral to the nucleus of CN VI
 Posterior to the superior olivary nucleus
 It has medial, lateral and dorsal subnuclei, arranged in
columns.
 Lateral subnucleus – lower fafcial muscles, buccinator
 Medial – posterior auricular, platysma, occipital,
stapedius
 Dorsal – upper facial muscles


INTRAMEDULLARY SEGMENT
 Arises from the dorsal surface of the nucleus, encircles
around the abducens nucleus
 Forms an INTERNAL GENU.
 Forma facial colliculus
 Relations with
 Fibres and nucleus of CN VI, pontine paramedian reticular
formation, CN V, CN VIII, long tracts thru pons.
 Two components – motor root (70% fibres) and sensory
(30%)
 Sensory root forms the NERVUS INTERMEDIUS (NI) OF
WRISBERG
 Contains both sensory and autonomic fibres,
 Intramedullary segment contains all three types of axons


CISTERNAL SEGMENT
 Nerve exits the pons laterally at the pontomedullary
junction, just caudal to the roots of CN V between
the olive and the inferior cerebellar peduncle
 The NI is a small bundle that usually leaves the pons
closer to CN VIII than CN VII and runs between the
larger trunks across the cerebellopontine angle
(CPA).
 In about 20% of specimens, the NI is not identifi able
as a separate structure in the CPA.
 At the entrance to the IAC, the facial nerve motor
root lies in a groove on the anterosuperior surface of
the vestibulocochlear nerve, with the NI in between.
 The facial nerve at this point lies in close proximity to
the anterior inferior cerebellar artery (AICA).
 the subarachnoid space extends along the facial
nerve to the geniculate ganglion.


MEATAL SEGMENT
 At the bottom or lateral end of the IAC, the nerve
pierces the meninges and enters the facial canal,
or fallopian aqueduct.
 The point of entry is the narrowest portion of the
canal.
 The facial nerve and the NI merge as the nerve
enters the canal.
 In traversing the facial canal, the nerve makes
two abrupt, tortuous turns, creating two external
genus.
 In its course through the petrous bone, from its
entrance into the facial canal until its exit from the
stylomastoid foramen, the nerve has three
segments: labyrinthine, horizontal or tympanic,
and mastoid or vertical.


LABYRINTHINE SEGMENT
 The labyrinthine segment lies laterally between the cochlea and vestibule,
toward the medial wall of the tympanic cavity, running perpendicularly to
the long axis of the petrous pyramid.
 The labyrinthine segment ends at the first external genu where the
geniculate ganglion lies.


HORIZONTAL / TYMPANIC SEGMENT
 the nerve turns abruptly and runs horizontally for about 1 cm (the horizontal or
tympanic segment), then turns backward and arches downward behind the tympanic
cavity (mastoid or vertical) segment.
 The branch to the stapedius muscle arises from the distal tympanic or upper end of
the mastoid segment.
 At the end of the tympanic segment, the nerve encounters the second external genu
as it makes a 90-degree turn to enter the mastoid segment.


MASTOID SEGMENT
 The mastoid segment then descends toward the stylomastoid foramen,
gives off the chorda tympani about 6 mm before its exit, and emerges
from the stylomastoid foramen.
 The tight confi nes of the bony canal may make the nerve particularly
vulnerable to damage from infl ammation and edema, a point of possible
signifi cance in some CN VII neuropathies


VARIATIONS
 It may split into two or three strands at or distal to the geniculate ganglion.
 The more proximal the division into strands, the more bizarre the
subsequent course.
 Facial motor fi bers may run in an enlarged chorda tympani, diminishing
the distal facial nerve into a tenuous strand exiting through a narrowed
stylomastoid foramen.
 CN VII runs along with the labyrinthine branch of the AICA, but there is
evidence to suggest it is less well vascularized in its intrapetrous segment,
particularly in the labyrinthine segment, than elsewhere along its course.
 In patients with Bell’s palsy, the involved side usually correlates with the
side of the narrower facial canal as determined by high-resolution
computed tomography (CT).


EXTRATEMPORAL SEGMENT
 Just after exit, the posterior auricular, digastric, and
stylohyoid branches arise.
 The posterior auricular branch supplies the
occipitalis, posterior auricular, and transverse and
oblique auricular muscles.
 The digastric and stylohyoid branches supply
respectively the posterior belly of the digastric and
the stylohyoid.
 The nerve turns forward and passes into the parotid
gland.
 Within the substance of the parotid, it divides into
temporofacial and cervicofacial divisions at the pes
anserinus (intraparotid plexus) in the cleft between
the superficial and deep lobes of the gland
 The temporofacial branch crosses the zygoma about
1 cm anterior to the ear, where it is vulnerable to
injury.


NERVUS INTERMEDIUS
 The NI is the sensory and autonomic component of the facial nerve.
 It runs in a position intermediate between CNs VII and VIII across the
CPA, moving ever closer to the main facial nerve trunk as it enters the
facial canal.
 At the external first external genu, the NI fuses with the geniculate
ganglion.
 The sensory cells located in the geniculate ganglion are general
somatic afferent (GSA) and special visceral afferent (SVA).
 The GSA fibers carry exteroceptive impulses from the region of the
external auditory canal and tympanic membrane.
 The SVA fibers convey taste from the anterior two-thirds of the tongue.
 The autonomic component of the NI consists of preganglionic general
visceral efferent parasympathetic fibers from the superior salivatory
and lacrimal nuclei, which consist of scattered cells in the reticular
formation near the caudal end of the motor nucleus.
 Their axons are bound for the submandibular gland enroute to the
sublingual and submaxillary glands, the lacrimal glands, and glands in
the nasal mucosa.


COURSE AND BRANCHES
GREATER (SUPERFICIAL) PETROSAL NERVE
 Carries preganglionic parasympathetic fibres,
conveyed by NI to the geniculate ganglion.
 They pass thru the ganglion, without
synapsing into the GPN, which goes forward
thru the hiatus of the facial canal to join the
DEEP PETROSAL NERVE from the carotid
sympathetic plexus to form the VIDIAN
NERVE / NERVE OF THE PTERYGOID
CANAL, which runs to the sphenopalatine
ganglion, from where postganglionic fibers
proceed to thelacrimal gland.


BRANCH TO OTIC GANGLION
 A branch from the geniculate ganglion joins
the lesser petrosal nerve and is then carried
to the otic ganglion
 This conveys secretomotor fibres in the
auriculotemporal nerve to the parotid gland.
 It also carries sympathetics from the carotid
artery to the blood vessels of the gland.


NERVE TO STAPEDIUS
 Arises from the distal tympanic / upper
mastoid segment
 Passes forward through a small canal to
reach the muscle.


CHORDA TYMPANI
 Leaves the main trunk, slightly above the
stylomastoid foramen.
 Carries taste and general visceral afferent
fibres as well as preganglionic
parasympathetics.
 Runs forward and upward in a canal in the
posterior wall of the tympanic cavity, acquires
a mucous membrane investment, enters and
crosses the middle ear.
 Sometimes, visible as a small cord behing
the eardrum, on otoscopy.
 It runs to exit the skull and join the lingual
nerve, branch of CN V3, on its posterior
border.


 Somatosensory afferents in the chorda tympani, have their cell bodies in
the geniculate ganglion.
 They carry sensatiions from the part of EAC, tympanic membrane, lateral
surface of the pinna, small area behind the ear and over the mastoid
process.
 The central processes terminate in the spinal tract and nucleus of the
trigeminal nerve.
 Taste sensations from the anterior 2/3rd
of the tongue is carried through
the lingual nerve to the chorda tympani, then to the geniculate ganglion.
 CN VII carries taste sensation from the mucosa of the soft palate throught
the sphenopalatine gangliion.


 Their central processes carrying taste and GVA sensations, terminate in
the nucleus of the solitary tract.
 The solitary tract sends communications to the superior and inferior
salivatory nuclei, which send parasympathetics to the salivary glands.
 Other fibres synapse in the reticular formation; next order neurons form a
component of the reticulospinal tract bilaterally to synapse with the
sympathetic neurons in the intermediolateral gray column of the uppeer
thoracic cord.
 These send sympathetic innervation via the superior cervical ganglion to
the salivary glands.
 The taste fibres ascent via the contralateral medial lemniscus to the
thalamus.


 The primary gustatory cortex, located in the anterior insula, the frontal
operculum, mediates the perception of taste.
 Taste fibres also communicate with the hypothalamus and the olfactory
system.
 The chorda tympani also carries preganglionic parasympathetic fibres to
the submandibular gland.
 Postganglionic fibres convey secretory and vasodilator impulses the the
submandibular and sublingual glands and mucuous membranes of the
mouth and tongue.
 They also receive sympathetics from the superior cervical ganglion and
the carotid plexus.


TWIGS TO THE VAGUS AND GLOSSOPHARYNGEAL
 At the stylomastoid foramen, small branches join the
above nerves.
POSTERIOR AURICULAR NERVE
 Supplies the muscles of the ear, occipital belly of
occipitofrontalis
BRANCHES TO THE MUSCLES OF FACIAL
EXPRESSION
 They pass through the parotid gland
 They are temporal, zygomatic, buccal, marginal,
mandibular and cervical
CUTANEOOUS BRANCHES distributed with the auricular
branch of vagus, supplying the skin on both the sides
of the auricle and part of EAC and TM.


CLINICALLY IMPORTANT FEATURES
 For clinical purposes, CN VII is purely motor, apart from sensory
component to the EAC, carried in the auricular branch of vagus.
 Taste sensations via chorda tympani, it joins the nerve in middle ear,
theoritically, it has great localising value. But in practice, taste fibres are
often spared in lesions proximal to the middle ear.
 Stapedius with tensor tympani (by CN V), contracts to damp down the
stapes when subjected to high intensity sound. Complete seventh nerve
lesion will therafore alter auditory acuity on the affected side.
 It contributes to forced eye opening and ptosis is not a feature of the
seventh palsy. However, there will be weakness in clenching the eyelids to
bury the eyelashes.
 Test platysma and wiggle the ears


Disorders of facial nerve function
 Facial weakness – two types
 Peripheral / lower motor neuron
 Central / upper motor neuron


Peripheral facial palsy
 Flaccid weakness of all the muscles of facial
expression on the involved side –
prosopoplegia


 Bell’s phenomenon
 Levator sign of Dutemps and Cestan – patient to look down, then close
the eyes by the slowly, because of the function of the LPS is no longer
counteracted by orbicularis oculi, the upper eyelid on the paralysed side
moves slowly upwards
 Bergera Wartenberg sign – loss of fine vibrations palpable with the
thumbs or fingertips resting lightly on the lids as the patient tries to close
the eyes as tightly as p ossible.
 Platysma sign of Babinski – asymmetrtic contraction of the platysma, less
on the affected side, when the mough is opened.
 House-Breckman scale, Burres-Fisch Index, facial nerve function index


 Lack of tearing – indicates very proximal involvement, above the origin of
GSPN.
 Corneal reflex – direct limb absent, consensual reflex present


Bell’s Palsy
 Idiopathic, peripheral facial paralysis or paresis of acute onset
 Both the sexes equally affected
 Any age may be affectedbut incidence rises with increasing age
 Positive family h/o in 6-8 %
 Risk factors – diabetes, pregnancy
 Clinical features :
 Sudden onset, unable to close eyes
 Bell’s phenomenon
 Dribbling of saliva, epiphora, assymetrical face


 Pain in ear precede or accompany the paralysis
 Noise intolerance and loss of taste
 Etiology :
 Viral infection – HSV, herpes zoster, EBV
 Vascular ischemia – primary ischemia induced by cold / emotional stress
 Hereditary – fallopian tube is narrow making it susceptible to early
compression
 Autoimmune disorder – T lymphoccyte changes observed


 Diagnosis :
 History, ENT examination
 Nerve excitability test
 Treatment :
 Reassurance, pain relief
 Eye care
 Facial physiotherapy


 Medical management :
 Steroids – prevents synkinesis, shortens the
recovery time
 Others – vasodilators, vitamins, mast cell
inhibitors, anti HT – not proven
 Surgical treatment
 Nerve decompression relieves pressure and
improves microcirculation


Brainstem causes / Nuclear causes
 Motor neurons of CN VII nucleus
 Motor neuron disease, Mobius syndrome
 Progressive bulbar palsy
 Mobius Syndrome (Congenital oculofacial paralysis)
 It is the association of congenital facial nerve palsy with paraolysis of
EOMS , esp lateral rectus due to hypoplasia or aplasia of the CN nuclei.
 It is sporadic


Pontine lesions
 Fascicular lesions may / not involve tearing and taste
 Ischemic lesions are common
 Millar – Gubler syndrome :
 Ipsilateral facial palsy with contralateral hemiparesis – due to pontine
stroke, hemorrhage or tumor.
 CN VI palsy is often but incorrectly included as a part of MGS.
 Foville syndrome :
 Ipsilateral facial palsy with horizontal gaze palsy with contralateral
hemiparesis.
 Eight and half syndrome :
 Is one and half syndrome with facial weakness due to pontine lesion.


 Other lesions :
 Abscess, syringobulbia, demyelinating disease, trauma.


CPA lesions
 Acoustic neuroma, meningioma, epidermoid - commonly involve CN VII,
NI, CN VIII, CN V, the cerebellar peduncles and cerebellum.
 No hyperacusis due to associated hearing loss.
 Findings – hearing loss, facial sensory changes, ipsilateral ataxia,
nystagmus, facial weakness.


Ramsay Hunt syndrome
 Herpes zoster oticus, Hunt sydrome, geniculate herpes
 Reactivation of varicella zoster visur involving the
geniculate ganglion.
 Facial weakness is accompanied with taste impairment,
hyperacusis, dimunition of salivary and lacrimal secretion.
 Pain in and behind the ear +
 Vesicles on the TM, EAC, lateral surface of pinna and
mastoid process.
 Two types :
 Otalgic form – pain in the ear
 Prosolgic form – pain deep in the face


 Preherpetic neuralgia – pain and dysesthesias preceeding the
development of rash.
 Attacs beyond the facial nerve occur frequently.
 Tinnitus, hearing loss, nausea, vomitting, tagmus from the vertigo,
nystagmus – from the involvement of CN VIII are common.
 c/f Bells’ palsy, Ramsay Hunt syndrome patients have more severe
paralysis and less likely to recover completely.
 Diabetes – four to five fold increased risk of developing acute PFP.


Trauma
 Petrous bone fractures – may injure facial nerve.
 Longitudinal fractures along the long axis of petrous bone – the facial
nerve injury is due to edema, does not occur immidiately and tends to
resolve spontaneously.
 Transverse fractures – comes on immediately, may be permanent., nerve
is often lacerated, contused or severed.
 Rupture of the ear drum, bleeding from the ear – indicate longitudinal
fracture.
 CSF otorrhoea – common with transverse fractues.


Other causes
 Melkersson syndrome (Melkersson-Rosenthal syndrome) is characterized
by recurrent attacks of facial palsy, nonpitting facial and lip edema, and a
congenitally furrowed and fissured tongue (lingua plicata, scrotal tongue);
 It is sometimes familial and usually begins in childhood.
 Its cause is unknown.
 Myasthenia gravis
 Marked facial weakness, bilateral, difficulty in both closing and opening
the eyes
 Myasthenic smile – may look like a snarl.
 Ectropion – worse in the afternoon, responds to antiCE


 Facial hemiatrophy – Parry-Romberg syndrome, Wartenberg syndrome
 Conginetal failure or progressive atrophy
 Bilateral facial weakness :
 Bells’ palsy, sarcoidosis, Lyme disease, diabetes, trauma, HIV, GBS,
carcinomatous / lymphomatous meningitis, pontine tumor, Leprosy.
 Middle ear surgery – chorda tympani may be damaged.


Central facial paralysis
 Lesions are most often in the cortex or internal capsule.
 Occasionally, a lesion as far caudal as the medulla can cause a CFP
because of involvement of the aberrant pyramidal tract.
 The upper face is not necessarily completely spared, but it is always
involved to a lesser degree than the lower face.
 There may be subtle weakness of the orbicularis oculi, the palpebral
fissure may be slightly wider on the involved side, and there may be a
decrease in palpable lid vibrations.
 However, involvement of the corrugator and frontalis is unusual, and the
patient should be able to elevate the eyebrow and wrinkle the forehead
with no more than minimal asymmetry.
 Inability to independently wink the involved eye may be the only
demonstrable deficit.


Hemifacial spasm
 Repeated uncontrollable twitching of the facial muscles
 2 types – 1) cause unknown
 2) secondary – acoustic neuroma, congenital cholesteatoma, glomus
tumor
 Irritation of the nerve
 Microvascular decompression had met with surgical success.
 Botulinum toxin – used in affected muscle


blephaspasm
Twitcing and spasms are limitged to the orbicularis oculi – both sides
Eyes are closed
Cause is undertain
Lesion – basal ganglia
Treated by selective section of nerves

Facial nerve

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