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) .

Killian's Dehiscence, Waldeyer's Ring And Pharyngeal Spaces

Killian's Dehiscence

Inferior constrictor muscle has two parts; thyropharyngeus
with oblique fibres and cricopharyngeus with transverse
fibres. Between these two parts exists a potential
gap called Killian's dehiscence. It is also called the "gateway
of tears" as perforation can occur at this site during
oesophagoscopy. This is also the site for herniation of
pharyngeal mucosa in cases of pharyngeal pouch.

Waldeyer's Ring:

Scattered throughout the pharynx in its subepithelial
layer is the lymphoid tissue which is aggregated at places
to form masses, collectively called Waldeyer's ring. The
masses are:
l. Nasopharyngeal tonsil or the adenoids
2. Palatine tonsils or simply the tonsils
3. Lingual tonsil
4. Tubal tonsils (in fossa of Rosenmuller)
5. Lateral pharyngeal bands
6. Nodules (in posterior pharyngeal wall).

Pharyngeal Spaces

There are two potential spaces in relation to the pharynx
where abscesses can form.
1. Retropharyngeal space, situated behind the pharynx
and extending from the base of skull to the bifurcation
of trachea (see page 246).
2. Parapharyngeal space, situated on the side of pharynx.
It contains carotid vessels, jugular vein, last
four cranial nerves and cervical sympathetic chain

Parapharyngeal Space Abscess: Causes, Features, Treatment, Complications

Anatomy: Parapharyngeal space is pyramidal in shape with its base
at the base of skull and its apex at the hyoid bone.
Relations:
Medial: Buccopharyngeal fascia covering the constrictor
muscles .
Posterior: Prevertebral fascia covering prevertebral
muscles and transverse processes of cervical
vertebrae.
Lateral: Medial pterygoid muscle, mandible and deep
surface of parotid gland.
Styloid process and the muscles attached to it divide
the parapharyngeal space into anterior and posterior
compartments. Anterior compartment is related to tonsillar
fossa medially and medial pterygoid muscle laterally.
Posterior compartment is related to posterior part of lateral
pharyngeal wall medially and parotid gland laterally.
Through the posterior compartment pass the carotid
artery, jugular vein, IXth, Xth, XIth, XIIth cranial nerves
and sympathetic trunk.
It also contains upper deep cervical nodes.
Parapharyngeal space communicates with other
spaces, viz. retropharyngeal, submandibular, parotid,
carotid and visceral.

Aetiology:
Infection of parapharyngeal space can occur from:
1. Pharynx. Acute and chronic infections of tonsil and
adenoid, bursting of peritonsillar abscess.
2. Teeth. Dental infection usually comes from the lower
last molar tooth.
3. Ear. Bezold's abscess, petrositis.
4. Other spaces. Infections of parotid , retropharyngeal
and submaxillary spaces.
5. External trauma. Penetrating injuries of neck, injection
of loc al anaesthetic for tonsillectomy or
mandibular nerve block.
Clinical Features
Clinical features depend on the compartment involved.
Anterior compartment infections produce a triad of
symptoms: (i) prolapse of tonsil and tonsillar fossa, (ii)
trismus (due to spasm of medial pterygoid muscle) and
(iii) external swelling behind the angle of jaw. There is
marked odynophagia associated with it.
Posterior compartment involvement produces (i) bulge
of pharynx behind the posterior pillar, (ii) paralysis of
CN IX, X, Xl, and XII and sympathetic chain, and (iii)
swelling of parotid region. There is minimal trismus or
tonsillar prolapse.
Fever, odynophagia, sore throat, torticollis (due to
spasm of prevertebral muscles) and signs of toxaemia are
common to both compartments.
Complications
1. Acute oedema of larynx with respiratory obstruction.
2. Thrombophlebitis of jugular vein with septicaemia.
3. Spread of infection to retropharyngeal space.

4. Spread of infection to mediastinum along the
carotid space.
5. Mycotic aneurysm of carotid artery from weakening
of its wall by purulent material. It may involve common
carotid or internal carotid artery.
6. Carotid blowout with massive haemorrhage .
Treatment
Systemic antibiotics. Intravenous antibiot ics may become
necessary to combat infection.

Drainage of abscess. This is usually done under
general anaesthesia. If the trismus is marked, preoperative
tracheostomy becomes mandatory. Abscess
is drained by a horizontal incision, made 2-3 cm below
the angle of mandible. Blunt dissection along the inner
surface of media l pterygoid muscle towards styloid
process is carried out and abscess evacuated . A drain
is inserted . Transoral drainage should never be done
due to danger of injury to great vessels which pass
through this space.

Nasal Septum: Anatomy

Nasal septum consists of three parts:
1. Columellar septum. It is formed of columella
containing the medial crura of alar cartilages united
together by fibrous tissue and covered on either side by
skin.
2. Membranous septum. It consists of double layer
of skin with no bony or cartilaginous support. It lies
between the columella and the caudal border of septal
cartilage. Both columellar and membranous parts are
freely movable from side to side.
3. Septum proper. It consists of osteocartilaginous
framework, covered with nasal mucous membrane.
Its principal constituents are:
(i) the perpendicular plate of ethmoid
(i i) the vomer, and
(iii) a large septal (quadrilateral) cartilage wedged
between the above two bones anteriorlv. Other
bones which make minor contribution- at the
periphery are: crest of nasal bones, nasal spine of
frontal bone, rostrum of sphenoid, crest of palatine
bones and the crest maxilla, and the anterior nasal
spine of maxilla.
Septal cartilage not only forms a partition between the
right and left nasal cavities but also provides support to the
tip and dorsum of cartilaginous part of nose. Its destruction,
e.g. in septal abscess, injuries, tuberculosis or excessive
removal during septal surgery, leads to depression of lower
part of nose and drooping of the nasal tip .
Septal cartilage lies in a groove in the anterior edge of
vomer and rests anteriorly on anterior nasal spine. During
trauma, it may get dislocated from anterior nasal spine or

vomerine groove causing caudal septal deviation or septa
spur respectively. This compromises the nasal airway.
Septal cartilage is also intimately related to the upper lateral
cartilages of nose and is in fact fused with them in the
upper third. For this reason septal deviation may be associated
with deviation of cartilaginous part of external nose.

Blood Supply:

Internal Carotid System
(a) Anterior ethmoidal artery} Branches of ophthalmic
(b) Posterior ethmoidal artery artery
External Carotid System
(a) Sphenopalatine artery (branch of maxillary artery)
gives nasopalatine and posterior medial nasal
branches.
(b) Septal branch of greater palatine artery (Br. of maxillary
artery).
(c) Septal branch of superior labial artery (Br. of facial
artery) .

Nerve supply:

Nasal septum is supplied by branches of sphenopalatine ganglion and the anterior ethmoidal nerve.

Little's area or Kiesselbach's plexus: This is the vascular
area in the antero-inferior part of nasal septum ju •
above the vestibule. Anterior ethmoidal, sphenopalatine
greater palatine and septal branch of superior labial arteries
and their corresponding veins form an anastomostis
here. This is the commonest site for epistaxis. This is also
the site for origin of the "bleeding polypus" (haemangioma)
of nasal septum.

Organ of Corti

Organ of corti is the sense organ of hearing and is situated
on the basilar membrane. Important components of
the organ of corti are:
1. Tunnel of Corti, which is formed by the inner and
outer rods. It contains a fluid called cortilymph. The exact
function of the rods and cortilymph is not known.
2. Hair cells. They are important receptor cells of
hearing and transduce sound energy into electrical energy.
Inner hair cells form a single row while outer hair cells are
arranged in three or four rows. Inner hair cells are richly
supplied by afferent cochlear fibres and are probably more
important in the tranmission of auditory impulses. Outer
hair cells mainly receive efferent innervation from the
olivary complex and are concerned with modulating the
function of inner hair cells.
3. Supporting cell. Deiters' cells are situated between
the outer hair cells and provide support to the latter.
Cells of Hensen lie outside the De iters' cells.
4. Tectorial membrane. It consists of gelatinous
matrix with delicate fibres. It overlies the organ of Corti.
The shearing force between the hair cells and tectorial
membrane produces the stimulus to hair cells.
Nerve Supply of Hair Cells: 95% of afferent fibres of spiral ganglion
supply the inner hair cells while only 5% supply the outer
hair cells. Efferent fibres to the hair cells come from the
olivocochlear bundle. Their cell bodies are situated in
superior olivary complex. Each cochlea sends innervation
to both sides of the brain.

External Acoustic (Auditory) Canal

It extends from the bottom of the concha to the tympanic
membrane and measures about 24 mm along its
posterior wall. It is not a straight tube; its outer part is
directed upwards, backwards and medially while its inner
part is directed downwards, forwards and medially.
Therefore, to see the tympanic membrane, the pinna has
to be pulled upwards, backwards and laterally so as to
bring the two parts in alignment.
The canal is divided into two parts: (a) cartilaginous
and (b) bony.
(a) Cartilaginous Part
It forms outer one-third (8 mm) of the canal. Cartilage is
a continuation of the cartilage which forms the framework
of the pinna. It has two deficiencies-the "fissures of
Santorini" in this part of the cartilage and through them
the parotid or supelficial mastoid infections can appear
in the canal, or vice versa. The skin, covering the cartilaginous
canal is thick and contains ceruminous and
pilosebaceous glands which secrete wax. Hair is only
confined to the outer canal and therefore furuncles
(staphylococcal infection of hair follicles) are seen only
in the outer one third of the canal.
(b) Bony Part
It forms inner two-thirds (16 mm). Skin lining the bony
canal is thin and continuous over the tympanic membrane.
It is devoid of hair and ceruminous glands. About
6 mm lateral to tympanic membrane, the bony meatus
presents a narrowing called the isthmus. Foreign bodies
lodged medial to the isthmus, get impacted, and are difficult
to remove. Antero-inferior part of the deep meatus,
beyond the isthmus, presents a recess called the anterior
recess which acts as a cesspool for discharge and debris
in cases of external and middle ear infections. Anteroinferior
part of the bony canal may present a deficiency
(foramen of Huschl<e) in children up to the age of four or
sometimes in adults, permitting infections to and from
the parotid.

Middle Ear Anatomy

The middle ear together with the eustachian tube, aditus,
antrum and mastoid air cells is called the middle ear
cleft  . It is lined by mucous membrane and filled
with air.
The middle ear extends much beyond the limits of
tympanic membrane which forms its lateral boundary
and is sometimes divided into (i) mesotympanum (lying
opposite the pars tensa) , (ii) epitympanum or the attic
(lying above the pars tensa but medial to Shrapnell's
membrane and the bony lateral attic wall), (iii) hypotympanum
(lying below the level of pars tensa) (Fig, 1.5).
The portion of middle ear around the tympanic orifice of
the eustachian tube is sometimes called the protympanum.
Middle ear can be likened to a six-sided box with a
roof, a floor, medial, lateral, anterior and posterior walls.
The roof is formed by a thin plate of bone called
tegmen tympani. It also extends posteriorly to form the
roof of the aditus and antrum. It separates tympanic cavity
from the middle cranial fossa.
The floor is also a thin plate of bone which separa tes
tympanic cavity from the jugular bulb. Sometimes, it is
congenitally deficient and the jugu lar bulb may then
project into the middle ear; separated from the cavity
only by the mucosa.

The anterior wall has a thin plate of bone which separates
the cavity from internal carotid artery. It also has
two openings; the lower one for the eustachian tube and
the upper one for the canal of tensor tympani muscle,
The posterior wall lies close to the mas toid air cells.
It presents a bony projection called the pyramid through
the summit of which appears the tendon of the stapedius muscle to get attachment to the neck of stapes. Aditus, an opening through which attic communicates with the
antrum, lies above the pyramid . Facial nerve runs in the
posterior wall just behind the pyramid. Facial recess or
the posterior sinus is a depression in the posterior wall lateral
to the pyramid. It is bounded medially by the vertical
part of VlIth nerve, laterally by the chorda tympani and
above, by the fossa incudis (Fig. l.7) . Surgically, facial
recess is important, as direct access can be made through
this into the middle ear without disturbing posterior
canal wall (intact canal wall technique, see page 72).
The medial wall (Fig. 1.8) is formed by the labyrinth.
It presents a bulge called promontory which is due to the
basal coil of cochlea; oval window into which is fixed the
footplate of stapes; round window or the fenestra cochleae
which is covered by the secondary tympanic membrane.
Above the oval window is the canal for facial nerve. Its
bony cove ring may sometimes be congenitally dehiscent

and the nerve may lie exposed making it very vulnerable
to injuries or infection. Above the canal for facial nerve
is the prominence of lateral semicircular canal. Just anterior
to the oval window, the medial wall presents a hooklike
projection called the processus cochleariformis. The
tendon of tensor tympani takes a turn here to get attachment
to the neck of malleus. The cochleariform process
also marks the level of the genu of the facial nerve which
is an important landmark for surge ry of the facial nerve.
Med ial to the pyramid is a deep recess called sinus tympani
which is bounded by the subiculum be low and the
ponticulus above .
The lateral wall is formed largely by the tympanic
membrane and to a lesser extent by the bony outer attic
wall called the scutum. The tympanic membrane is semi transparent
and forms a 'window' into the middle ear. It is

possible to see some struc tures of the middle ear through
the normal tympanic membrane, e.g. the long process of
incus, incudostapedial joint and the round window.
Mastoid Antrum
It is a large, air-containing space in the upper part of mastoid
and communicates with the attic through the aditus.
I ts roof is formed by the tegmen antri which is a continuation
of the tegmen tympani and separa tes it from the middle
cranial fossa. The lateral wall of antrum is formed by
a plate of bone which is on an average 1.5 cm thick in the
adult. It is marked externally on the surface of masto id by
suprameatal (MacEwen's) C1-iangle (Fig. 1.9).
Aditus ad Antrum
Aditus is an opening through wh ich the attic communicates
with the antrum. The bony prominence of the horizonta
l canal lies on its medial side while the fossa
incudis, to which is attached the short process of incus,
lies laterally. Facial nerve courses just below the aditus.

The Mastoid and its Air Cell System:
The mastoid consists of bone cortex with a "honeycomb"
of ai r cells underneath. Depending on development of air
cell, three types of mastoid have been described.
(i) Well-pneumatised or cellular. Mas toid cells are well
developed and intervening septa are thin.
(ii) Diploetic. Mastoid consists of marrow spaces and
a few air cells.
(iii) Sclerotic or acellular. There are no cells or marrow
spaces.
With any type of mastoid pneumatisation, antrum is always
present. In sclerotic mastoids, antrum is usually small and
the sigmoid sin us is anteposed.
Depending on the location, mastoid air cells are
d ivided into:
(i) zygomatic cells (in the root of zygoma).
(ii) tegmen cells (extending into the tegmen tympani).
(iii) perisinus cells (overlying the sinus plate).
(iv ) retrofacial cells (round the facial nerve).
(v) perilabyrinthine cells (located above, below and
behind the labyrinth, some of them pass through
the arch of superior semicircular canal. These cells
may communicate with the petrous apex).
(vi) peritubal (around the eustachian tube. Along with
hyporympanic cells they also communicate with
the petrous apex).
(vii) tip cells which are quite large and lie medial and
lateral to the digastric ridge in the tip of mastoid.
(viii) marginal cells (lying behind the sinus plate and
may extend into the occipi tal bone).
Ox) squamosal cells (lying in the squamous part of temporal
bones).

Abscesses may form in relation to these air cells and
may sometimes be located far from the mastoid region.
Development of Mastoid
Mastoid develops from the squamous and petrous bones.
The petrosquamosal suture may persist as a bony platethe
Komer's septum, separating superficial squamosa l
cells from the deep petrosal cells. Korner's septum is surgically
important as it may cause difficulty in locating the
antrum and the deeper cells, and thus lead to incomplete
removal of disease at mastOidectomy (Fig. 1.11). Masto id
antrum cannot be reached unless the Korner's septum
has been removed.
Ossicles of the Middle Ear (Fig. 1.12)
There are three ossicles in the middle ear- the malleus,
incus and stapes.
The maLLeus has head, neck, handle (manubrium), a
lateral and an anterior process. Head and neck of malleus

lie in the attic. Manubrium is embedded in the fibrous
layer of the tympanic membrane. The lateral process
forms a knob-like projection on the outer surface of the
tympanic membrane and gives attachment to the anterior
and posterior malleal (malleolar) folds.
The incus has a body and a short process, both of
which lie in the attic, and a long process which hangs
vertically and attaches to the head of stapes.
The stapes has a head, neck, anterior and posterior
crura and a footpl ate. The footplate is held in the oval
window by annular ligament.
The ossicles conduct sound energy from the tympanic
membrane to the oval window and then to the inner ear
fluid .
Intratympanic Muscles
There are two muscles-tensor t)'mpani and the stapedius;
the former attaches to the neck of malleus and tenses the
tympanic membrane while the latter attaches to the neck

f tapes and helps to dampen very loud sounds thus pre\'
enting noise trauma to the inner ear. Stap dius is a 2nd
arch muscle and is supplied by a branch of CN VII while
tensor tympani develops from the 1st arch and is supplied
by a branch of mandibular nerve (V3)·
Tympanic Plexus
It lies on the promontory and is formed by (i) tympanic
branch of glossopharyngeal and (ii) sympathetic fibres from
the plexus round the internal carotid artery. Tympanic
plexus supplies innervation co the medial surface of the
tympanic membrane, tympanic cavity, mastoid air cells
and the bony eustachian tube. It also carries secretomotor
fibres for the parotid gland. Section of tympanic
branch of glossopharyngeal nerve can be carried out in
the middle ear in cases of Frey's syndrome.
Course of secretomotor fibres to the parotid:
Inferior salivary nucleus --- CN IX --- Tympanic
branch --- Tympan ic plexus --- Lesser petrosal nerve ---
Otic ganglion --- Auriculotemporal nerve --- Parotid
gland.
Chorda Tympani Nerve
It is a branch of the facial nerve which enters the middle
ear through posterior canaliculus, and runs on the medial
surface of the tympanic membrane between the handle
of malleus and long process of incus, above the attachment
of tendon of tensor tympani. It carries taste from
anterior two-thirds of tongue and supplies secretomotor
fibres to the submaxillary and sublingual salivary glands.
Lining of the Middle Ear Cleft
Mucous membrane of the nasopharynx is continuous
with that of the middle ear, aditus, antrum and the mastoid
air cells. It wraps the middle ear structures-the ossicles,
muscles, ligaments, and nerves-like peritoneum wraps
various viscera in the abdomen-raising several folds and
dividing the middle ear into various compartmenrs. Middle
ear contains nothing but the air; all the structures lie
outside the mucous membrane.
Histologically, the eustachian tube is lined by ciliated
epithelium which is pseudostratified columnar in the
cart ilaginous part, columnar in the bony part with several
mucous glands in the submucosa. Tympanic cavity is
lined by ciliated columnar epithelium in its anterior and
inferior part which changes to cuboidal type in the posterior
part. Epitympanum and mastoid air cells are lined
by flat, nonciliated epithelium.
Blood Supply of Middle Ear
Middle ear is supplied by six arteries, out of which two
are the main, i.e.
(i) Anterior tympanic branch of maxillary artery which
supplies tympanic membrane.
(ii) Stylomastoid branch of posterior auricular artery
which supp lies middle ear and mastoid air cells.

Four minor vessels are:
(i) Petrosal branch of middle meningeal artery (runs
along greater petrosal nerve).
(ii) Superior tympanic branch of middle meningeal
artery traversing along the canal for tensor tympani
muscle.
(iii) Branch of artery of pterygoid canal (runs along
eustachian tube).
(iv) Tympanic branch of internal carotid.
Veins drain into pterygoid venous plexus and superior
petrosal sinus.
Lymphatic Drainage
Lymphatics from the middle ear drain into retropharyngeal
and parotid nodes while those of the eustachian tube
drain into retropharyngeal group.

Tympanic Membrane Anatomy

It forms the partition between the external acoustic canal
and the middle ear. It is obliquely set and as a result, its posterosuperior
part is more lateral than its antero-inferior
part. It is 9-10mm tall, 8-9 mm wide and 0.1 mm thick.
Tympanic membrane can be divided into two parts:
(a) Pars Tensa
It forms most of tympanic membrane. Its periphery is
thickened to form a fibrocartilaginous ring called the
annulus tympanicus which fits in the tympanic sulcus. The
central part of pars tensa is tented inwards at the level of
the tip of malleus and is called the umbo. A bright cone
of light can be seen radiating from the tip of malleus to
the periphery in the anteroinferior quadrant (Fig. 1.2).
(b) Pars Flaccida (Shrapnel's Membrane)
This is situated above the lateral process of malleus between
the notch ofRivinus and the anterior and posterior
malleal folds (earlier called the malleolar folds). It is not
so taut and may appear slightly pinkish. Various landmarks
seen on the lateral surface of tympanic membrane
are shown in Fig. 1.2.
Layers of Tympanic Membrane
Tympanic membrane consists of three layers:
(i) Outer epithelial layer, which is continuous with
the skin lining the meatus.

(ii) Inner mucosal layer, which is continuous with the
mucosa of the middle ear.

(iii) Middle fibrous laye r, which encloses the handle of
malleus and has three types of fibres-the radial,
circular and the parabolic.
Fibrous layer in the para flacc ida is thin and not organised
into various fibres as in pars tensa.

Nerve Supply:

(i) Anterior half of lateral surface: auriculotemporal
(V 3)'
(il) Posterior half of lateral surface: auricular branch of
vagus (CN X):
(iii) Medial surface: Tympanic branch of CN IX
(Jacobson's nerve).