Facial Nerve

ANATOMY AND FUNCTIONS OF
FACIAL NERVE
Facial nerve is a mixed nerve, having a motor root and a
se nsory root. Motor root, supplies all the mimetic muscles
of face which develop from the 2nd branchial arch.
Sensory root (nerve of Wrisberg) , carr ies secretomotor
fibres to the lacrimal, submandibular and sublingual sa li va
ry glands and to those in the nose and palate. It also
carries taste from the anterior two-thirds of tongue via
chorda tympani and soft and hard palate via greater superficial
petrosal nerve distributed through palatine branches
of sphenopalatine ganglion and general sensation from
the concha and retroauricular skin.
Nucleus of Facial Nerve
Motor nucleus of the nerve is situated in the pons. It
receives fibres from the precentral gyrus. Upper part of
[be nucleus which innervates forehead muscles receives
fibres from both the cerebral hemispheres, while the
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. The emotional movemenrs
such as smiling and crying are thus preserved in supranuclear
palsies because of these fibres from the thalamus
Course of Facial Nerve
Motor fibres take origin from the nucleus of VlIth nerve,
hook round the nucleus of VIth nerve and are joined by
the sensory root (nerve of Wrisberg). Facial nerve leaves
the brainstem at ponto medullary junction, travels through
posterior cra nial fossa and enters the internal acoustic
mea tus. A t the fundus of the meatus (lateralmost part of
meatus), the nerve enters the bony facial canal, traverses
the temporal bone and comes out of the stylomastoid
foramen. Here it crosses the styloid process and divides
into terminal branches. The course of the nerve (Fig. 14.2)
can thus be divided into:
1. Intracranial part. From pons to internal acoustic
meatus (15- 17 mm).
2. Intratemporal part. From internal acous tic meatus
to stylomastoid foramen. It is further divided into:
(a) Meatal segment. Within internal acoustic meatus
(8-10mm).(b) Labyrinthine segment. From fundus of meatu~ to the
geniculate ganglion where nerve takes a turn posteriorly
forming a "genu". The nerve in the labyrinthine
segment has the nalTowest diameter (0.61-0.68 mm)
and the bony canal in this segment is also the narrowest.
Thus oedema or inflammation can easily
compress the nerve and cause paralysis. This is also
the shortest segment of the nerve-only 4.0 mm.
(c) Tympanic or horizontal segment. From geniculate
ga nglion to just above the pyramidal eminence. It
lies above the oval window and below the lateral
semicircular canal (11.0 mm).
(d) Mastoid or vertical segment. From the pyramid to stylomastoid
foramen. Between the tympanic and mastoid
segments is the second genu of the nerve (13.0 mm).
3. Extracranial part. From sty lomastoid foramen to
the termination of its peripheral branches.
Branches of Facial Nerve
1. Greater superficial petrosal nerve. It arises from
geniculate ganglion and carries secretomotor fibres to
lacrimal gland and the glands of nasal mucosa.
2. Nerve to stapedius. It arises at the level of second
genu and supplies the staped ius muscle.
3. Chorda tympani. It arises from the middle of ve rtical
segment, passes between the incus and neck of
malleus, and leaves the tympanic cavity through petrotympanic
fissure. It carries secretomotor fibres to submandibular
and sublingual glands and brings taste from anterior
two-thirds of tongue.
4. Communicating branch. It joins auricular branch
of vagus and supplies the concha, retroau ricular groove,
posterior meatus and the ou ter surface of tympanic
membrane
5. Posterior auricular nerve. It supplies muscles of
pinna, occipital belly of occipitofrontalis and communicates
with auricular branch of vagus.
6. Muscular branches to sty lohyoid and posterior
belly of digastric.
7. Peripheral branches. The nerve trunk, after
crossing the stylo id process, forms two divisions, 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 pes anseTinus (goose-foot). They supply all the
muscles of facial expression.
Blood Supply of Facial Nerve
It is derived from four blood vessels: (i) Anterior-inferior
cerebellar artery supplying 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 (Lv) 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 inteTnal plexus
(Fig. 14.3).
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. ShoTt pTOcess of incus. Facial nerve lies medial co the
short process of incus at the level of aditus.4. Pyramid. Nerve runs behind the pyramid and the
posterior tympanic sulcus.
5. TympanomCLStoid 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.
For parotid surgery (Fig. 14.4)
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 digCLStric. 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.
Structure of Nerve
From inside out, a nerve fibre consists of axon, myelin
sheath, neurilemma and 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
(Fig. 14.5).
Severity of Nerve Injury
Degree of nerve injury will determine the regeneration
of nerve and its function. Earlier nerve injuries were
divided into:
(a) Neurapraxia, a conduction block, where flow ofaxoplasm
through the axons was partially obstructed.
(b) Axonotmesis-injury to axons.
(c) Neurocmesis-injury to nerve.
Sunderland classified nerve injuries into five degrees
of severity based on anatomical structure of the nerve,
and this classification is now widely accepted.
1 ° = Partial block to flow of axoplasm; no morphological
changes are seen. Recovery of function is
complete (neurapraxia) .
2° = Loss ofaxons, but endoneurial tubes remain
intact. During recovery, axons will grow into
their respective tubes, and the result is good
(axonotmesis).
3° = Injury to endoneurium. During recovery, axons
of one tube can grow into another. Synkinesis
can occur (neurotmesis).
4° = Injury to perineurium in addition to above.
Scarring will impair regeneration of fibres (partial
transection) .
5° = Injury to epineurium in addition to above (complete
nerve transection).
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.
Electrodiagnostic Tests
These tests are useful to differentiate between neurapraxia
. and degeneration of the nerve. They also help to predict
prognosis and 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 n ormal and paralysed side in
conduction block. In other injuries, where degeneration sets
in, nerve excitability is gradually lost. \Vhen 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.
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 visua lly
graded as equal, decreased or absent, with maximal stimulation
indicating degeneration and incomplete recovery.
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
imilar 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
(han 14 days has a still poorer prognosis. ENoG is most
useful between 4 and 21 days of the onset of complete
paralysis.
4. Electromyography (EMG). This tests the motor
activity of facial muscles by direct insertion of needle
electrodes usually in orbicular oculi and orbicularis oris
1uscles and the recordings are made during rest and
\-oluntary contraction of muscle.
In a normal resting muscle, biphasic or triphasic
(:,otentials are seen every 30-50 milliseconds.
In a denervated muscle spontaneous involuntary action
potentials called fibrillanon 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
inical evidence of facial fun ction and thus provide the
earliest evidence of recovery.
Voluntary contraction causes motor discharge. DiminIShed
or no response to voluntary contraction is seen
.after nerve inj ury.
Electromyography is useful in planning reanimation
- rocedures. Presence of normal or polyphasic potentials
lfter 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.
Thus ENoG and EMG are complimentary and help to
rngnosticate in cases of facial paralysis and in deciding
FACIAL NERVE AND ITS DISORDERS
the procedure for reanimation, i.e. nerve substitution
versus muscle transposition or sling operation.
CAUSES OF FACIAL PARALYSIS
The cause may be central or peripheral. The peripheral lesion
may involve the nerve in its intracranial, intratemporal or
extratemporal parts. Peripheral lesions are more common
and about two-thirds of them are of the idiopathic variety
(Table 14.1).
Table 14.1 Causes of facial paralysis
1. Central
Brain abscess
Pontine gliomas
Poliomye litis
Multiple sclerosis
2. Intracranial port (cerebellopontine angle)
Acoustic neuroma
Meningioma
Congenital cholesteatoma
Metastatic carcinoma
Meningitis
3. Intratemporal port
(0) Idiopathic
Bell's palsy
Melkersson's syndrome
(b) I nfecti ons
Acute suppurative otitis media
Chr'onic suppurative otitis media
Herpes zoster oticus
Malig nant otitis externa
(c) Trauma
Surgical: Mastoidectomy
Stapedectomy
Accidental: Fractures of temporal bone
(d) Neoplasms
Malignancies of external and middle ear
Glomus jugulare tumour
Facia I nerve neuroma
Metastasis to temporal bone (from cancer of
breast, bronchus, prostate)
4. Extrocranial port
Malignancy of parotid
SUI'gery of parotid
Accidental injury in parotid region
Neonatal facial injury (obstetrical forceps)
5. Systemic diseases
Diabetes mellitus
Hypothyroid ism
Uraemia
Polyarteritis nodosa
Wegener's granulomatosis
Sarcoidosis (Heerfor'dt's syndrome)
Leprosy
Leukaemia
Demyelinating disease

Bell's Palsy
Sixty to seventy-five percent of facial paralysis is due to
Bell's palsy. It is defined as idiopathic, peripheral facial paral),
sis or paresis of acute onset. Both sexes are affected with
equal frequency. Any age group may be affected though
incidence rises with increasing age. A positive family history
is present in 6-8% of patients. Risk of Bell's palsy is
more in diabetics (angiopathy) and pregnant women
(retention of fluid).
Aetiology
(a) Viral infection. Most of the evidence supportS
the vira l aetiology due to herpes simplex, herpes zoster or
the Epstein-Barr virus. Other cranial nerves may also be
involved in Bell's palsy which is thus considered a part of
the total picture of polyneuropathy.
(b) Vascular ischaemia. It may be primary or secondary.
Primary ischaemia is induced by cold or emotional stress.
Secondnr)' ischaemia is the result of primary ischaemia
which causes increased capillary permeability leading to
exudation of fluid, oedema and compression of microcirculation
of the nerve.
(c) Hereditary. The fallopian canal is narrow because
of hereditary predisposition and this makes the nerve susceptible
to early compression with the slightest oedema.
Ten percent of the cases of Bell's palsy have a positive
family history.
(d) Autoimmune disorder. T-lymphocyte changes
have been observed.
Clinical Features (Fig. 14.6)
Onset is sudden. Patient is unable to close his eye. On
attempting to close the eye, eyeball turns up and out (Bell's
phenomenon). Saliva drihbles from the angle of mouth.
Face becomes asymmetrical. Tears flow down from the eye
(epiphora). Pain in the ear may precede or accompany
the nerve paralysis. Some complain of noise intolerance
(stapedial paralysis) or loss of taste (involvement of
chorda tympani). Paralysis may be complete or incomplete.
Bell's palsy is recurrent in 3-10% of patients.
Diagnosis
Diagnosis is always by exclusion. All other known causes
of peripheral facial paralysis should be excluded. This
requires careful history, complete otological and head
and neck examination, x-ray studies, blood tests such as
total count, peripheral smear, sedimentation rate, blood
sugar and serology.
Nerve excitability tests are done daily or on alternate
days and compared with the normal side to monitor
nerve degeneration.
Localising the site of lesion (topodiagnosis) helps in
establishing the aetiology and also the si te of surgical
decompression of nerve, if that becomes necessary.
Treatment
General
1. Reassurance.
2. Relief of ear pain by analgesics.
3. Care of the eye as outlined on page 97. Eye must be
protected aga inst exposure keratitis.
4. Physiotherapy or massage of the facial muscles gives
psychological support to the patient. It has not been
shown to influence recovery. Active facial movements
are encouraged when there is return of some
movement to the facial muscles.
Medical management
Steroids. Their utility has not been proved beyond doubt
in carefully controlled studies. Prednisolone is the drug
of choice. If patient reports within 1 week, the adu lt dose
of prednisolone is 1 mg/kg/day divided into morning and
evening doses for 5 days. Patient is seen on the 5th day.
If paralysis is incomplete or is recovering, dose is tapered
during the next 5 days. If paralysis remains complete, the
same dose is continued for another 10 days and thereafter
tapered in next 5 days. ( total of 20 days). Contraindications
to use of steroids include pregnancy, diabetes,
hypertension, peptic ulcer, pulmonary tuberculosis and
glaucoma. Steroids have been found useful to prevent
incidence of synkinesis, crocodile tears and to shorten the
recovelY time of facial paralysis. Steroids can be combined
with acyclovir for Herpes zoster oticus or Bell's palsy.
Other drugs. Vasodilators, vitamins, mast cell inhibitors,
antihistaminics have not been found usefu l.
Surgical treatment. Nerve decompression relieve
pressure on the nerve fibres and thus improves the microcirculation
of the nerve. Vertica l and tympanic segments
of nerve are decompressed. Some workers have suggested
total decompression including labyrinthine ' e~mcnr by
postaural and middle fossa approach .
Prognosis
Eighty- fi ve to ninety percent of the pa tients recover
fully. 10-15% recover incompletely and may be left with
ome stigmata of regeneration . Recurrent facial palsy may
not recover full y. Prognosis is good in incomplete Bell's
r alsy (95% complete recovery) and in those where clinical
recovery starts within 3 weeks of onse t (75% comple te
recovery) .