The document discusses the anatomy, course, branches and clinical aspects of the facial nerve (cranial nerve VII). Some key points: - The facial nerve has both motor and sensory components. It innervates the muscles of facial expression and provides parasympathetic innervation to certain glands. - The course of the nerve can be divided into intracranial, intratemporal and extracranial parts as it exits the brainstem and travels through the temporal bone. - Common causes of facial nerve palsy include Bell's palsy (idiopathic), herpes zoster infection, fractures of the temporal bone, parotid surgery and tumors in the parot

1. Anila

3. Anatomy and Functions
• Facial Nerve is a mixed nerve having motor
and a sensory root
• The sensory root (nerve of Wrisberg) also
carries secretomotor fibres to the lacrimal
gland and salivary glands, and brings fibres of
taste and general sensation
• There are 2 efferent and 2 afferent pathways

6. Components of facial nerve
Components of facial nerve Function
Supplies the muscles of facial
expression, auricular muscles
(vestigial) stylohyoid, posterior belly
of digastric and stapedius
Parasympathetic innervation of the
lacrimal, submandibular and
sublingual glands and the smaller
secretory glands of nasal mucosa
and the palate
Taste sensation from the anterior 2/3
of tongue via chorda tympani . Hard
and soft palates via greater petrosal
nerve.
General sensation from the concha,
posterosuperior part of external
canal and the tympanic membrane.

7. • Motor nucleus situated in the pons.
• Receives fibres from the precentral gyrus.
• Upper part of the nucleus which
innervates forehead muscles receives
fibres from both the cerebral
hemispheres.
• Lower part of nucleus which supplies
lower face gets only crossed fibres from
one hemisphere.
• The function of forehead is preserved in
supranuclear lesions because of bilateral
innervation.
• Facial nucleus also receives fibres from the
thalamus by alternate routes and provides
involuntary control to facial muscles
• Emotional movements such as smiling and
crying are thus preserved in supranuclear
palsies because of these fibres fron
thalamus

9. • Motor fibres originate from the nucleus of VIIth nerve, hook
around the nucleus of VIth nerve and are joined by the sensory
root (nerve of Wrisberg).
• Facial nerve leaves the brainstem at pontomedullary junction,
travels through posterior cranial fossa and enters the internal
acoustic meatus
• At the fundus of the meatus (lateral most part of the meatus),
the nerve enters the bony facial canal, traverses the temporal
bone and comes out of the stylomastoid foramen .
• It crosses the styloid process and divides into terminal
branches.

10. • Thus the course of the nerve can be divided in to :
1) Intracranial part – From pons to internal acoustic meatus (15-
17 mm)
2) Intratemporal part – From internal acoustic meatus to
stylomastoid foramen. It is further divided into:
a. Meatal segment – with in internal acoustic meatus
b. Labyrinthine segment – From fundus of meatus to the
geniculate ganglion where nerve takes a turn posteriorly
forming a “genu”. Nerve in the labyrinthine segment has the
narrowest diameter (0.61 – 0.68 mm) and the bony canal in
this segment is also the narrowest . Thus edema or
inflammation can easily compress the nerve and cause
paralysis . This is also the shortest segment of the nerve – 4.0
mm
c. Tympanic /horizontal segment – From geniculate ganglion to
just above the pyramidal eminence. It lies above the oval
window and below the lateral semicircular canal
d. Mastoid or vertical segment – From pyramid to stylomastoid
foramen. Between the tympanic and mastoid segment is the
second genu of the nerve

11. 3) Extracranial part – From stylomastoid foramen to the termination of
its peripheral branches

12. Branches of Facial Nerve
1. Greater superficial petrosal nerve – Arises from the geniculate
ganglion & carries secretomotor fibres to lacrimal gland and the
glands of nasal mucosa
2. Nerve to stapedius – Arises at the level of second genu and
supplies stapedius muscle.
3. Chorda tympani – Arises from the middle of vertical segment,
passes between the incus and neck of malleus, and leaves the
tympanic cavity through petrotympanic fissure. Carries fibres to
submandibular & sublingual glands and brings taste from
anterior two-thirds of tongue.
4. Communicating branch – It joins the auricular branch of vagus
and supplies the concha, retroauricular grove, posterior meatus
and the outer surface of tympanic membrane
5. Posterior auricular nerve – Supplies muscles of pinna , occipital
belly of occipitofrontalis and communicates with auricular
branch of vagus.

13. 6. Muscular branches – To stylohyoid and posterior belly of digastric
7. Peripheral branches – Nerve trunk after crossing the styloid process,
forms two division , an upper temporofacial and a lower
cervicofacial, which further divide into smaller branches. These are
the temporal, zygomatic buccal, mandibular and cervical and
together form pesansernius (goose-foot). They supply all the
muscles of facial expression.

14. Blood supply of facial nerve
It is derived from four blood vessels: (i) Anterior-inferior cerebellar artery
supplies the nerve in CP angle; (ii) labyrinthine artery, branch of anterior
inferior cerebellar artery, supplies the nerve in internal auditory canal; (iii)
superficial petrosal artery, a branch of middle meningeal artery, which
supplies geniculate ganglion and the adjacent region; and (iv) stylomastoid
artery, branch of posterior auricular artery, which supplies the mastoid
segment. All the arteries form an external plexus which lies in the
epineurium and feeds a deeper intraneural internal plexus
Anterior inferior
cerebellar artery
Labyrinthine artery
Superficial petrosal
Stylomastoid artery

15. Surgical landmarks of Facial nerve
For middle ear and mastoid surgery
• 1. Processus cochleariformis. It demarcates the
geniculate ganglion which lies just anterior to it.
Tympanic segment of the nerve starts at this level.
• 2. Oval window and horizontal canal. The facial nerve
runs above the oval window (stapes) and below the
horizontal canal.
• 3. Short process of incus. Facial nerve lies medial to
the short process of incus at the level of aditus.
• 4. Pyramid. Nerve runs behind the pyramid and the
posterior tympanic sulcus.
• 5. Tympanomastoid suture. In vertical or mastoid
segment, nerve runs behind this suture.
• 6. Digastric ridge. The nerve leaves the mastoid at the
anterior end of digastric ridge.

16. • For parotid surgery
• 1. Cartilaginous pointer. The nerve lies 1 cm deep and sightly
anterior and inferior to the pointer. Cartilaginous pointer is a sharp
triangular piece of cartilage of the pinna and "points" to the nerve.
• 2. Tympanomastoid suture. Nerve lies 6-8 mm deep to this suture.
• 3. Styloid process. The nerve crosses lateral to styloid process.
• 4. Posterior belly of digastric. If posterior belly of digastric muscle
is traced backwards along its upper border to its attachment to the
digastric groove, nerve is found to lie between it and the styloid
process.

17. STRUCTURE OF NERVE

18. From inside out, nerve consists of
• Axon,
• Myelin sheath,
• Neurilemma,
• Endoneurium
A group of nerve fibres is enclosed in a sheath
called perineurium to form a fascicle and the
fascicles are bound together by epineurium

19. Severity of Nerve Injury
• Degree of nerve injury will determine the
regeneration of nerve & its function.
• Earlier nerve injuries were divided into
(Seddon’s Classification):
Neuraparaxia, a conduction block, where flow
of axoplasm through the axons was partially
obstructed
Axonotmesis – injury to axons
Neurotmesis – injury to nerves

20. Seddon’s Classification

21. Sunderland classification

22. Sunderland classification is now widely accepted.
Sunderland classified nerve injuries into five
degrees of severity based on anatomical
structure of the nerve
1ᵒ= Partial block to flow of axoplasm; no morphological changes
seen. Recovery of function is complete (Neuraparaxia).
2ᵒ= Loss of axons, but endoneurial tubes remain intact. During
recovery, axons will grow into their respective tubes, and the
result is good (axonotmesis).
3ᵒ= Injury to endoneurium. During recovery, axons of one tube
can grow into another. Synkinesis can occur (neurotmesis).
4ᵒ= Injury to perineurium in addition to above. Scarring will
impair regeneration of fibres (partial resection).
5ᵒ= Injury to epineurium in addition to above (complete nerve
transection).

23. The first three degrees are seen in viral and inflammatory
disorders while fourth and fifth are seen in surgical or accidental
trauma to the nerve or in neoplasms. The prognosis is poor for
degrees 3 onwards.

24. Electrodiagnostic Tests
 Useful to differentiate between neurapraxia and
degeneration of the nerve.
 Helps to indicate time for surgical decompression of
the nerve.
1. Minimal Nerve excitability test- The nerve is
stimulated at steadily increasing intensity till facial twitch
is just noticeable. This is compared with the normal side.
There is no difference between the normal and paralysed
side in conduction block. In other injuries, where
degeneration sets in, nerve excitability is gradually lost.
When the difference between two sides exceed 3.5
milliamperes, the test is positive for degeneration.
Degeneration of fibres cannot be detected earlier than
48-72 hours of its commencement

25. 2. Maximal stimulation test (MST) - This test is
similar to the minimal nerve excitability test but
instead of measuring the threshold of
stimulation, the current level which gives
maximum facial movement is determined and
compared with the normal side. Response is
visually graded as equal, decreased or absent.
Reduced or absent response with maximal
stimulation indicates degeneration and is
followed by incomplete recovery.

26. • 3. Electroneuronography (ENoG)
It is a sort of evoked electromyography. The facial
nerve is stimulated at the stylomastoid foramen
and the compound muscle action potentials are
picked up by the surface electrodes. Supramaximal
stimulation is used to obtain maximal action
potentials. The response of action potentials of the
paralysed side are compared with that of the
normal side on similar stimulation and thus
percentage of degenerating fibres is calculated.
Studies reveal that degeneration of 90% occurring
in the first 14 days indicates poor recovery of
function. Faster rate of degeneration occurring in
less than 14 days has a still poorer prognosis. ENoG
is most useful between 4 and 21 days of the onset
of complete paralysis

28. 4. Electromyography (EMG)
• This tests the motor activity of facial muscles by direct
insertion of needle electrodes usually in orbicular oculi
and orbicularis oris muscles and the recordings are
made during rest and voluntary contraction of muscle.
• In a normal resting muscle, biphasic or triphasic
potentials are seen every 30-50 milliseconds.
• In a denervated muscle spontaneous involuntary action
potentials called fibrillation potentials are seen. They
appear 14-21 days after denervation. With
regeneration of the nerve after injury, polyphasic
reinnervation potentials replace fibrillation potentials.
They appear 6-12 weeks prior to clinical evidence of
facial function and thus provide the earliest evidence
of recovery.

29. • Electromyography is useful in planning
reanimation procedures. Presence of normal or
polyphasic potentials after 1 year of injury
indicates that reinnervation is taking place and
there is no need for reanimation procedure. If
fibrillation potentials are seen, it indicates intact
motor end plates but no evidence of
reinnervation and need for nerve substitution.
Electrical silence indicates atrophy of motor end
plates and need for muscle transfer procedures
rather than nerve substitution.
• Voluntary contraction causes motor discharge.
Diminished or no response to voluntary
contraction is seen after nerve injury

31. • The cause may be central or
peripheral
• The peripheral lesion are
more common and may
involve the nerve in its
intracranial, intratemporal
or extratemporal parts.
• Other causes are linked to
Systemic diseases like DM,
hypothyroidism etc.

32. • Brain abscess
• Pontine gliomas
• Poliomyelitis
• Acoustic neuroma
• Meningoma
• Congenital
cholesteatoma
• Idiopathic
• Infections
• Trauma
• Neoplasms
• Malignancy of parotid
• Surgery of parotid
• Neonatal facial injury
• Diabetes mellitus
• Hypothyroidism
• Uremia
• Polyarteritis nodosa

33. Idiopathic,
peripheral facial paralysis or
paresis of acute onset
• Both sexes are equally affected.
• Any age may be affected but
incidence rises with increasing
age.
• +ve family hx in 6-8%
• Risk: diabetes and pregnancy
•sudden onset
• unable to close eyes
• Bell’s phenomenon (eyeball turns
up and out on attempting to close
the eye)
• dribbling of saliva
• asymmetrical face
• epiphora
• pain in ear precede or accompany
nerve paralysis
• noise intolerance and loss of taste

34.  Viral infection
HSV, Herpes zoster, EBV
 Vascular ischemia
-Primary ischemia (induced by cold or emotional stress)
-Secondary ischemia ( primary ischemia increased capillary
permeability exudation of fluid, edema, compression of
microcircultation).
 Hereditary
Fallopian tube is narrow making it susceptible to early
compression
 Autoimmune disorder
T-lymphocyte changes have been observed.

35. history taking
complete otological and
head and neck examination
X-ray studies
blood test (total count,
peripheral smear,
sedimentation rate, blood
sugar and serology)
nerve excitability test
General
reassurance
relief of ear pain by analgesic
care of eye
physiotherapy or massage of
facial muscles

36. Steroids - prevents incidence of synkinesis,
crocodile tears and shortens the recovery time of
facial paralysis.
Other drugs -vasodilators, vitamins, mast cell
inhibitors, antihistaminics have not found to be
useful
Nerve decompression relieves pressure on nerve
fibers and thus improves the microcirculation of the
nerve

37. Idiopathic disorder
Triad- facial paralysis, swelling of lips and fissured tongue.
Paralysis may be recurrent
seen
in bell’s palsy, melkersson’s
syndrome, diabetes,
sarcoidosis and tumors.
seen in guillian barre
syndrome, sarcoidosis, sickle
cell disease, acute leukemia,
bulbar palsy, leprosy and some
other systemic disorder.

38. • There is facial paralysis along with vesicular rash in
the external auditory canal and pinna.
• There may also be anesthesia of face, giddiness and
hearing impairment due to involvement of Vth and
VIIIth nerves. Treatment is the same as for Bell's
palsy.

39. • Fractures of temporal bone may be longitudinal,
transverse or mixed. Facial palsy is seen more often
in transverse fractures (50%). Paralysis is due to
intraneural haematoma or by compression.
• It is important to know whether paralysis was of
immediate or delayed onset.
• Delayed onset paralysis is treated conservatively like
Bell's palsy while immediate onset paralysis may
require surgery (decompression, re-anastomosis of
cut ends or cable nerve graft)

41. • Facial nerve is injured
during stapedectomy,
tympanoplasty or mastoid
surgery.
• Paralysis may be immediate
or delayed and treatment is
the same as in temporal
bone trauma.
• Sometimes, nerve is
paralysed due to pressure of
packing on the exposed
nerve and this should be
relieved first.
• Facial nerve may be injured
in surgery of parotid
tumours or deliberately
excised in malignant
tumours.
• Accidental injuries in the
parotid region can also
cause facial paralysis.
• Application of obstetrical
forceps may also result in
facial paralysis in the
neonate due to pressure on
the extratemporal part of
nerve.

42. • Carcinoma of external or middle ear, glomus tumor,
rhabdomyosarcoma and metastatic tumors of temporal bone all
result in facial nerve palsy.
• Facial nerve neuroma occurs anywhere along the course of the
nerve and produces paralysis of gradual or sudden onset.
• Treated by excision and grafting.
• High resolution CT scan and gadolinium-enhanced MRI – very
useful for facial nerve tumor
• Facial paralysis with tumor of the
parotid almost always implies
malignancy.

43. • Peripheral facial paralysis is mostly of idiopathic
• Exclusion of diabetes, hypothyroidism, leukemia,
sarcoidosis, periarteritis nodosa, Wegner’s
granulomatosis, leprosy, syphilis and demyelinating
disease.

44. LOCALISATION OF FACIAL LESION
• Central facial paralysis
Caused by cerebrovascular accidents
(hemorrhage, thrombosis, embolism), tumor or
an abscess. It causes paralysis of only the lower
half of face on the contralateral side. Forehead
movements are retained due to bilateral
innervation of frontalis muscle. Involuntary
emotional movements and the tone of facial
muscles are also retained.

45. • Peripheral Facial Paralysis
All the muscles of the face on the involved side are
paralysed. Patient is unable to frown, close the eye, purse
the lips or whistle
A lesion at the level of nucleus is identified by associated
paralysis of VIth nerve.
A lesion at cerebellopontine angle is identified by the
presence of vestibular and auditory defects and
involvement of other cranial nerves such as Vth, IXth, Xth
and XIth.
A lesion in the bony canal, from internal acoustic
meatus to stylomastoid foramen, can be localised by
topodiagnostic tests.
A lesion outside the temporal bone, in the parotid area,
affects only the motor functions of nerve. It may
sometimes be incomplete as some branches of the nerve
may not be involved in tumour or trauma.

47. Topodiagnostic Tests for Lesions in
Intratemporal Part
1. Schirmer's test
It compares lacrimation of the two sides. A strip of filter paper is
hooked in the lower fornix of each eye and the amount of
wetting of strip measured. Decreased lacrimation indicates
lesion proximal to the geniculate ganglion as the secretomotor
fibres to lacrimal gland leave at the geniculate ganglion via
greater superficial petrosal nerve.

48. 2. Stapedial reflex
Stapedial reflex is lost in lesions above the nerve
to stapedius. It is tested by tympanometry.
Persistence of the stapedial reflex in Bell’s palsy
gives a better prognosis

49. 3.Taste Test
• It can be measured by a drop of salt or sugar
solution placed on one side of the protruded
tongue, or by electrogustometry. Impairment
of taste indicates lesion above the chorda
tympani.

50. 4.Submandibular salivary flow test
• It also measures function of chorda tympani.
Polythene tubes are passed into both
Wharton's ducts and drops of saliva counted
during one minute period. Decreased
salivation shows injury above the chorda.

52. 1. Incomplete recovery:
 Facial asymmetry persists
 Eye cannot be closed resulting in epiphora
 Weak oral sphincter results in drooling and difficulty
in taking food
2. Exposure keratitis:
 Dryness, exposure keratitis and corneal ulcer occurs
(eye cannot be closed and tear film from cornea
evaporates)
 Worse when tear production is also affected

53. 3. Synkinesis (mass movement):
 When the patient wishes to close the eye, corner of
the mouth also twitches or vice versa.
 It is due to cross innervation of fibers.
 There is no treatment.
4. Tics and spasms:
 Result of faulty regeneration of fibers.
 Involuntary movements are seen on the affected side
of the face.
5. Contractures:
 Results from fibrosis of atrophied muscles or fixed
contraction of a group of muscles.
 Affect movements of face but facial symmetry at rest
is good.

54. 6. Crocodile tears (gustatory lacrimation):
 Unilateral lacrimation with mastication.
 Due to faulty regeneration of parasympathetic fibers
which now supply lacrimal gland instead of the
salivary glands.
 It can be treated by section of greater superficial
petrosal nerve or tympanic neurectomy.
7. Frey’s syndrome (gustatory sweating):
 There is sweating and flushing of skin over the
parotid area during mastication.
 Results from parotid surgery.
8. Psychological and social problems:
 Drooling during eating and drinking and impairement
of speech causes social problems.

55. Hyperkinetic Disorders of Facial
Nerve
They are characterized by involuntary twitching
of facial muscles on one or both sides

56. Hemifacial Spasm
• Characterized by repeated, uncontrollable twitching of
facial muscles on one side.
2 types
a) essential/ idiopathic- cause is unknown
b) Secondary – cause is acoustic neuroma , congenital
cholesteatoma or glomus tumor.
• Many cases of facial spasm are due to irritation of
nerve because of vascular loop at the cerebellopontine
angle.
• Microvascular decompression through posterior fossa
craniotomy has met with high success rate

57. • Idiopathic type has been treated by selective section
of the branches of facial nerve in the parotid or by
puncturing the facial nerve with a needle in its
tympanic segment
• Botulinum toxin has been used in the affected
muscle. It blocks the neuromuscular junction by
preventing release of acetylcholine

58. Blepharospasm
• Twitching and spasms are limited to the
orbicularis oculi muscles on both sides.
• Eyes are closed due to muscle spasms causing
functional blindness.
• Cause is uncertain but probably lies in the
basal ganglia. It is treated by selective section
of nerves supplying muscles around the eye
on both side

59. • Botulinum- A toxin injected into the
periorbital muscles gives relief for 3-6 months.
Injection can be repeated if necessary.

60. Surgery of Facial Nerve
1) Decompression – Nerve may be compressed by
edema, hematoma or a fractured bone in its
intratemporal part. The bony canal is exposed
and uncapped. The sheath of nerve is also slit to
relieve pressure due to edema or intraneural
hematoma.
2) End to end anastomosis –This done when the
gap between severed ends of the nerves is only
a few millimeters. Its is a suitable procedure for
extratemporal part of the nerve . There should
not be any tension in the approximated ends.

61. 4) Nerve graft (cable graft) When the gap between
the severed ends cannot be closed by end to end
anastomosis, a nerve graft is more suitable than
extensive re-routing or mobilisation of nerve. Nerve
graft is taken from greater auricular, lateral
cutaneous nerve of thigh or the sural nerve. In the
bony canal, the graft may not require any suturing.
5) Hypoglossal – facial anastomosis - Hypoglossal
nerve is anastomosed to the severed peripheral end
of the facial nerve. It improves the muscle tone and
permits some movements of facial muscles, but at
the expense of atrophy of tongue on that side.
However, disability of tongue due to atrophy is not
so severe and patient adjusts to the difficulty in
chewing and articulation after a few weeks.

62. 5) Plastic procedures - They are used to improve
cosmetic appearance when nerve grafting is not
feasible or has failed. The procedures include
facial slings, face lift operation or slings of
masseter and temporalis muscle. The latter also
gives some movement to face in addition to
symmetry.

63. References
Diseases of Ear, Nose & Throat by P L Dhingra
5th edition

64. Any Questions??