Anatomy

External ear
The pinna ( Fig. 26.1 ) is made of fibroelastic cartilage. The external auditory meatus has
an outer cartilage portion; the inner part is formed by the tympanic bone ( Fig. 26.2 ). It is
lined by squamous epithelium and contains ceruminous glands that produce wax. There is
very little subcutaneous tissue and soft tissue swelling is very painful.

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Fig. 26.1
Anatomy of the pinna.
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Fig. 26.2
Anatomy of the ear.

Middle ear
The vibrating tympanic membrane is conical and attached to the margin of the bony ear canal
laterally and to the handle of the malleus, the first of the three ossicles, medially ( Fig.
26.2 ). The head of the malleus is attached to the body of the incus in the space superior to
the middle ear known as the attic. The long process of the incus attaches to the head of the
stapes via its lenticular process. The stapes is joined to the oval window margin by the
annular ligament. The middle ear is lined by simple cuboidal epithelium containing some
mucus-secreting cells. The middle ear space is connected to the nasopharynx by the
Eustachian tube, which maintains the middle ear at atmospheric pressure.

The inner ear

The inner ear membrane encloses a labyrinth filled by a fluid called endolymph. This is
surrounded by a bony labyrinth, the otic capsule, which is filled with perilymph. The cochlea,
the hearing component of the inner ear, is a tube linking the oval and round windows, coiled
up like a shell. The vestibular (balance) portion of the inner ear consists of three semicircular
canals, together with their vestibule, which contains the saccule and utricle, medial to the
stapes footplate. The cochlear and vestibular nerves combine in the internal auditory meatus
and pass medially to the brainstem. The facial nerve enters the temporal bone through the
internal auditory meatus and passes laterally to the geniculate ganglion, where it turns
posteriorly (the first genu). It passes through the middle ear above the oval window and turns
inferiorly (the second genu) to exit at the stylomastoid foramen.

Physiology
The pinna funnels sound into the ear canal. The tympanic membrane lever mechanism, the
ossicular lever mechanism and the large size of the drum relative to the stapes footplate act as
an impedance-matching transformer. Vibrations in air are thus transferred to the cochlear
fluids without excessive loss of energy. The cochlea converts these endolymph vibrations into
electrical impulses in the auditory nerve, by stimulation of hair cells in the organ of Corti.
The maximum response to high frequencies occurs in the basal turn of the cochlea. Low
frequencies maximally stimulate the apex. Auditory neurons connect via the brainstem to the
auditory cortex, where again different groups of cells are stimulated by nerve impulses coded

for different frequencies. The hair cells in the ampullae of the semicircular canals are
stimulated by angular acceleration. The saccule and utricle are stimulated by linear
acceleration. Information from the labyrinths, eyes and limbs is combined within the
brainstem. Connections from the vestibular nuclei pass to the cortex and the cerebellum
( Fig. 26.3 ).

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Fig. 26.3
The vestibular system.

Assessment
Clinical features
Disorders of the external or middle ear can impair sound transmission to the inner ear and
cause conductive deafness. Sensorineural deafness results from lesions of the cochlea or its
nerve. Deafness is often associated with a noise in the ear (tinnitus). Ear pain (otalgia) may be
due to ear disease but may also be referred from other sites ( Table 26.1 ). Ear-related
disorders of balance usually cause a sensation of movement (vertigo), most often rotation.
Unsteadiness however, typically has a non-otological cause. Patients with ear disease
occasionally fall to the ground but never lose consciousness.

Table 26.1
Causes of referred otalgia

Pharynx and larynx

Tonsillitis

Tonsillectomy

Tumours
Mouth

Dental disease

Tumour
Temporomandibular joints (TMJ)

TMJ dysfunction

Arthritis
Neck

Cervical spondylosis

Tumour

Paranasal sinuses

Maxillary sinusitis

Examination
The ear canal and tympanic membrane are inspected with an otoscope, a rigid telescope or a
microscope. Microscopy can assist in wax or discharge removal. Tuning fork tests
differentiate between conductive and sensorineural hearing loss (Rinne's test). In health or
sensorineural deafness, a tuning fork is heard better via the ear canal (air conduction) than via
the mastoid process (bone conduction). When there is a conductive hearing loss, the tuning
fork is heard better by bone conduction. When hearing is symmetrical, a tuning fork placed in
the centre of the forehead is heard equally well in both ears (Weber's test). If a conductive
hearing loss is present in one ear, the tuning fork is heard better in the deaf ear if the loss is
conductive which can be easily shown by occluding one ear and applying the fork to your
own head. Conversely, in a unilateral sensorineural deafness, the sound is louder in the good
ear.

Audiometry
Hearing by air conduction can be assessed by pure tone audiometry, in which sounds of
known pitch and loudness are presented to each ear in turn via headphones. Bone conduction
(cochlear function) can be separately tested by applying sounds to the mastoid process. A
masking tone is needed if the two cochleae are to be tested separately. The difference between
the air and bone conduction gives the level of conductive hearing loss ( Figures
26.4and 26.5 ). The patient's ability to hear speech can be tested by presenting lists of
words via headphones. The percentage correctly identified at different loudness levels allows
derivation of a speech reception threshold (50% of words correct) and a discrimination score.
Middle ear function (compliance) can be assessed by tympanometry. The amount of sound
from a probe reflected back from the drum is measured while the pressure in the ear canal is

made to vary. The compliance is maximal when the pressure in the ear canal equals the
pressure in the middle ear, because when pressure is the same on both sides of the drum it is
maximally mobile. Tympanometry is most often used to confirm the presence of fluid in the
middle ear.

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Fig. 26.4
Audiogram showing conductive deafness.
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Fig. 26.5
Audiogram showing sensorineural deafness.

Temporal bone imaging

In patients with unilateral sensorineural hearing loss, MRI is used to detect an acoustic
neuroma ( Fig. 26.6 ). MRI also demonstrates the presence of normal fluid in the cochlea
before attempting cochlear implantation. CT scans can be used to demonstrate temporal bone
anatomy, congenital abnormalities and fractures or unusual pathology.

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Fig. 26.6
Magnetic resonance imaging (MRI) of the cerebellopontine angle.
A Normal MRI scan of cerebellopontine angle. Thin arrow = IAM
(internal auditory meatus). B MRI showing an acoustic neuroma. Thick
arrow = lesion compressing cerebellum.

Diseases of the pinna

Bat ears
A developmental abnormality results in absence of the antihelical fold (seeFig. 26.1 ). This
produces prominent ears that cause embarrassment. The abnormality can be corrected
surgically.

Trauma
Trauma to the ear may result in a haematoma, which strips the perichondrium off the
underlying cartilage. Secondary infection may lead to loss of cartilage, resulting in a
cauliflower ear. Haematomas should therefore be drained under strict aseptic conditions.

Tumours
Basal cell and squamous carcinomas may occur on the pinna and require excision ( Fig.
26.7 ).

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Fig. 26.7
Squamous carcinoma of the pinna.

Diseases of the external auditory meatus

Wax
Wax (cerumen) is normally found in the ear canal. The ear canal has a migratory epithelium
that carries wax to the opening of the external auditory meatus. Wax seldom causes deafness,
unless it becomes packed against the eardrum.

Otitis externa
This is an inflammatory condition of the ear canal skin. Secondary infection with bacteria or,
less frequently, fungi may occur. It is managed by cleaning the ear, followed by local
treatment with eardrops, sprays or ointment containing a steroid, with or without antiseptic,
or a weak acid solution (which controls the typical causative anaerobic organisms). Adults
tend to develop skin sensitivities to the components of topical antibiotic preparations which
are thus best avoided. Antibiotics also predispose to fungal superinfection. Both phenomena
simply exacerbate the severity of this painful condition. Keeping water out of the ear with
Vaseline-coated plugs helps prevent any recurrence. Uncommonly, chronic otitis externa
causes stenosis of the ear canal.

Tumours
Squamous carcinoma of the ear canal occurs uncommonly. It is treated by a combination of
surgery and radiotherapy.

Diseases of the middle ear

Acute suppurative otitis media
This is a bacterial infection of the middle ear space, usually caused byStreptococcus
pneumoniae or Haemophilus influenzae , most commonly occurring in young children (3
years of age and under) . Children present with a combination of ear pain (otalgia), fever and
malaise. On examination, dilated blood vessels are seen on the drum surface in the early
stages. The drum then becomes red and begins to bulge. Perforation with discharge frequently
occurs, usually followed by spontaneous healing. Antibiotic therapy remains controversial:
the majority of cases resolve spontaneously in a few days ( EBM 26.1 ). Antibiotics are
useful in high risk patients (e.g. immunosuppression) as they shorten the episodes and reduce
the rate of infective complications such as mastoiditis, facial palsy or meningitis.

26.1
Clinicians need to evaluate whether the minimal short-term benefit from longer treatment of
antibiotics is worth exposing children to a longer course of antibiotics. Kozyrskyj et al.
Short-course antibiotics for acute otitis media. Cochrane Database of Systematic Reviews
2010, Issue 9. Art. No.: CD001095. DOI: 10.1002/14651858.CD001095.pub2
For further information: www.cochrane.org

Antibiotics for acute otitis media in children

Otitis media with effusion (OME), or glue ear

In this condition, fluid accumulates in the middle ear space, usually in children. A minority of
adult cases are caused by nasopharyngeal tumours and systemic disease. Childhood OME

causes hearing loss and may interfere with the acquisition of language and performance at
school. Virtually all cases resolve spontaneously, but this may take as long as 10 years. Initial
management involves documentation of the presence of effusion and the degree of hearing
loss during a period of watchful waiting. If the effusions persist, hearing may be improved by
drainage of the effusion (myringotomy) and insertion of a ventilation tube ( Fig. 26.8 ). In
children, removal of the adenoids leads to more effective resolution. Spontaneous resolution
may also occur in adults, but often effusions persist. Ventilation tubes can also be of value,
but some cases are better managed with a hearing aid.

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Fig. 26.8
Surgical treatment of otitis media with effusion.
A Myringotomy. B Grommet insertion.

Chronic suppurative otitis media

This causes aural discharge and deafness.

Tubotympanic or mucosal disease

This is characterized by the presence of a perforation of the tympanic membrane, which
typically discharges. Swimming and other activities that involve water entering the ear may
exacerbate the discharge. The hearing loss is worse when the ossicles are eroded, most
commonly the incus long process. Discharge can be controlled by cleaning the ear and
introducing eardrops. To minimize the risks of ototoxicity, drops should be used for a
maximum of 2 weeks. Surgery is indicated to prevent discharge, improve hearing or allow the
patient to swim. The operation to repair a perforation is called a myringoplasty. Defects of the
ossicular chain can be repaired by removing the incus and repositioning it to bridge the gap
between the malleus and stapes or by using a prosthesis (ossiculoplasty).

Atticoantral or squamous disease

A cholesteatoma forms as a retracted area of the drum in which keratin accumulates. The
drum tissue at the periphery of the cholesteatoma produces a number of chemical mediators
that stimulate osteoclast activity. Hence the cholesteatoma can erode surrounding bone and
cause complications such as disruption of the ossicular chain, facial palsy and intracranial
sepsis. The primary treatment goal is to eliminate the disease. Surgical treatment
(mastoidectomy) is mandatory in all but the very elderly and those who are medically unfit.

SUMMARY BOX 26.1

Acute otitis media is extremely common under the age of 3 years

The child typically awakes crying at night with a painful ear. The diagnosis is confirmed by a
red, inflamed bulging tympanic membrane on otoscopy

Pain relief is important. Antibiotics should be given to prevent the development of

complications

Otitis media with effusion (glue ear) occurs transiently in many children and is manifested by
temporary hearing impairment. Most cases settle spontaneously. Bilateral persistent hearing
impairment may demand surgery (adenoidectomy, or insertion of a grommet)

Chronic otitis media involves the middle ear and mastoid mucosa. There is permanent
perforation of the tympanic membrane, hearing loss and a mucopurulent discharge. Inactive
ears require closure of the perforated membrane (myringoplasty) and rebuilding of the
ossicular chain. Ears with cholesteatoma may require surgical removal of the posterior canal
wall to open the attic or mastoid cavity and so reduce the risk of meningitis, intracranial
abscess and facial palsy.

Otitis media

Otosclerosis
This is a condition in which the stapes becomes fixed by new bone formation. It is more
common in females and sometimes runs in families. It can be treated by an operation called
stapedectomy, in which the stapes is replaced by a piston attached to the incus. This produces
excellent hearing improvement in the majority of patients, but a minority suffer surgicallyinduced, permanent inner ear damage. The hearing loss can be managed with a hearing aid.

Diseases of the inner ear

Deafness
Deafness is most commonly due to changes in the cochlea. Ageing produces a gradual
deterioration in hearing acuity (presbycusis). The cochlea may be damaged by chronic noise
exposure, blast injuries and temporal bone fractures. Significant noise exposure may occur in
heavy industry and agriculture, from playing in rock bands and shooting. Deafness may also
be inherited or a manifestation of systemic disease. Some drugs, such as aminoglycosides and
cytotoxic agents like cisplatinum, can damage the cochlea. Viral infections such as mumps
and rubella can also cause sensorineural deafness. Unilateral hearing loss occurs in acoustic
neuroma (Fig. 26.6B ).
Most cases of inner ear deafness are managed with a hearing aid, but in cases of profound
deafness, hearing may be restored by a cochlear implant. This consists of a series of
electrodes surgically introduced into the cochlea. A speech processor converts sound into
electrical energy, which stimulates the cochlear nerve.

Vertigo
In some cases, balance disorders may arise from abnormalities of the vestibular portion of the
inner ear.

Benign paroxysmal positional vertigo is a very common condition in middle age and is due to
debris floating in the posterior semicircular canal which stimulates the ampulla hair cells,
producing vertigo. Episodes are triggered when the affected ear is down-most as when the
patient turns over in bed. Debris can be displaced therapeutically from the posterior canal by
positioning the head so that it floats out of the canal into the vestibule (Epley's particle
repositioning manoeuvre). If this fails, division of the ampullary (singular) nerve or occlusion
of the posterior semicircular canal is beneficial.
Vestibular neuronitis causes severe vertigo lasting for as long as several weeks. The hearing
remains normal. It is due to severe temporary reduction of vestibular function in the affected
ear. Patients are managed by bed rest and vestibular sedatives, such as prochlorperazine.
Abnormal fluctuations of fluid pressure within the inner ear (endolymphatic hydrops)
produce a combination of fluctuating deafness, tinnitus and vertigo known as Mnire's
disease. This uncommon condition is initially treated medically, using either a vasodilator
agent (e.g. betahistine) or a diuretic. If medical treatment fails, the vestibular portion of the
labyrinth may be destroyed by a middle ear injection of gentamicin. Procedures of last resort
are surgical destruction of the labyrinth, or section of the vestibular nerve.

Disorders of the facial nerve

Facial palsy may result from temporal bone fractures or surgical trauma. When the nerve is
divided, it may be repaired by end-to-end anastomosis or a cable graft derived from a sensory
nerve of the right size, such as the sural nerve. Bell's palsy is an idiopathic (lower motor
neuron) facial palsy that usually improves spontaneously. There is some evidence that it is
caused by viral infection. Steroid therapy given soon after the onset is beneficial. Herpes
zoster infection of the geniculate ganglion causes facial palsy, often associated with deafness
and vertigo (RamsayHunt syndrome). Vesicles may be seen on the palate and on the
tympanic membrane. Antiviral treatment appears helpful for RamsayHunt syndrome (unlike
Bell's palsy). Intracranial disease and malignant tumours in the parotid area of the neck can
also cause facial palsy.

Chapter contents

Ear

Anatomy

Physiology