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SECTION THREE
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BASIC SYSTEMS
Ear, nose and throat
Michael J. Wareing and Elinor Warner
22
Introduction
This chapter describes the assessment of potential
diseases of the ear, nose and throat. The formal title
of the specialty is otorhinolaryngology, also known as
ear, nose and throat (ENT). The specialty has many
interactions with oral and maxillofacial specialties,
although extensive details of the latter are too
specialized for an undergraduate textbook.
A close functional and anatomical relationship
exists between the ear, the nose and the throat.
Disease in one area may have manifestations in
another area. Symptoms in one area may likewise
refer to another area, so an accurate assessment
requires a thorough history and examination of the
entire area to elucidate a cause. Ear, nose and throat
is a highly clinical subject because much is visible,
especially with modern examination techniques, and
so a lot of imaging and other investigations are often
unnecessary.
The ear
Anatomy
The ear (Fig. 22.1) consists of the external, middle and
inner ears. The external ear consists of the pinna and
external auditory canal (meatus). The cartilaginous
pinna is covered with perichondrium and skin,
forming the helix and antihelix. The meatus has an
outer cartilaginous and an inner bony component.
The skin overlying the external auditory meatus
contains hair cells and modified sebaceous glands,
which produce wax (cerumen). Desquamated skin
debris, mixed with cerumen, migrates outward from
the drum and deep canal and makes the external ear
a self- cleaning system.
The opaque or semitranslucent eardrum (tympanic membrane) separates the middle and external
ears (Fig. 22.2). The pars tensa, the lower part of the
drum, is formed from an outer layer of skin, a middle
layer of fibrous tissue and an inner layer of middle
ear mucosa. It is attached to the annulus, a fibrous
ring that stabilizes the drum to the surrounding bone.
The pars flaccida, the upper part of the drum, may
retract if there is prolonged negative middle ear pressure secondary to Eustachian tube dysfunction. The
malleus, incus and stapes are three small connecting
bones (ossicles) (Fig. 22.3) that transmit sound across
the middle ear from the drum to the cochlea. The
handle of the malleus lies within the fibrous layer of
the pars tensa.
Within the middle ear, the head of the malleus
articulates with the incus in the attic, the upper
portion of the middle ear space. The long process
of the incus articulates with the stapes. This
articulation (the incudostapedial joint) is liable
to disruption from trauma or chronic infection
owing to a tenuous blood supply, which may
be compromised when these situations occur.
The stapes footplate sits in the oval window, and
transmits and amplifies sound to the fluid- filled
inner ear. The inner ear has two portions. The
cochlea (Fig. 22.4), the spiral organ of hearing, is a
transducer that converts sound energy into digital
nerve impulses that are transmitted by the eighth
cranial nerve (cochlear) to the brainstem and
thence to the auditory cortex. The organ of Corti
(Fig. 22.5) within the cochlea contains hair cells
that detect frequency- specific sound energy; lowfrequency sounds are detected in the apical region
and high- frequency sounds are detected in the
basal region. The inner ear is also concerned with
balance. The semicircular canals and the vestibule
contain receptors that detect angular and linear
motion in the three cardinal x, y and z planes. The
inner ears are only one component of the balance
system; visual input and proprioception from joints
and muscles are also important.
The facial (seventh cranial) nerve (Fig. 22.6) is
important in otological practice. It runs from the
brainstem through the cerebellopontine angle to the
internal auditory meatus (IAM) with the cochlear
and vestibular (eighth) nerves. The facial nerve passes
through the temporal bone and leaves the skull
through the stylomastoid foramen near the mastoid
process. It may be damaged in cases of suppurative
middle ear disease or trauma. The chorda tympani
leaves the descending portion of the facial nerve in
the temporal bone to provide taste fibre innervation
to the anterior two- thirds of the tongue. The facial
464
Semicircular canals, utricle and saccule
middle ear
membrane)
(epitympanic
Head of
Incudomalleolar
Long process of incus
A
process
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Attic of
middle ear
recess)
Malleus
Incus
Pinna
External
auditory
meatus
Crura of
stapes
Eardrum
(tympanic
Cavity of
Facial nerve
Footplate of stapes in oval window
Vestibule
Internal acoustic meatus
Cochlear nerve
Vestibular nerve
Facial nerve
Scala vestibuli
Cochlear duct
containing organ
of Corti
Scala tympani
Pharynx
Eustachian tube
Cochlea
Figure 22.1 Anatomy of the ear.
Figure 22.2 A normal left tympanic membrane.
nerve supplies the facial muscles through upper and
lower divisions that arise as it passes through the
parotid gland.
Symptoms of ear disease
The five main symptoms of ear disease are:
Otalgia: earache or pain
Otorrhoea: discharge
Hearing loss
Tinnitus: a perception of sound in the absence of
an appropriate auditory stimulus
Vertigo: an illusion of movement
malleus
Neck of
malleus
Lateral
process
nterior
Manubrium
of malleus
Anterior crus
Footplate of stapes
articulation
Short process
of incus
Body of
incus
Incudostapedial
articulation
Posterior
crus
Figure 22.3 The ossicles.
Otalgia
Pain from disease of the external ear, tympanic
membrane and middle ear reaches the brain by
branches of the fifth, ninth and tenth cranial nerves,
together with nerves from C2 and C3 roots. Because
branches of these nerves also supply the larynx and
pharynx, as well as the temporomandibular joint
and teeth, diseases of these structures may give rise
to referred pain in the ear. Therefore, if otoscopic
examination is normal, examination of these other
sites should be considered. In half of patients with
otalgia, the pain is referred.
The main causes of otalgia are listed in Box 22.1.
Of the otological causes, acute infection of the
cartilage caused by the pinna (perichondritis) can be
Scala media
Cochlear
nerve
Inner
Tectorial
Outer
Cells of
Inner
nerve
Greater superficial
Cervical
Stylomastoid foramen
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(Cochlear duct)
Scala
vestibuli
Lateral semicircular
petrosal nerve
Superior semicircular canal
canal
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Brainstem
Porus of internal
auditory canal
465
Organ of
Corti
Scala tympani
Figure 22.4 Section through the cochlea.
Inner
rod
hair cell
Cochlear
sulcus cells
Hensen
Cells of
Claudius
membrane
Basement
membrane
hair cells
Cells of
Deiters
Outer
rod
Tunnel
of Corti
Figure 22.5 The organ of Corti.
very painful. Malignant otitis externa (also known
as necrotizing otitis externa) is not neoplastic. It
is due to infection (usually Pseudomonas) and can
spread to the skull base, especially in diabetic or
immunocompromised patients, and its incidence is
increasing exponentially in the UK.
Otorrhoea
Pus draining from the ear varies in character
depending on its origin (Table 22.1). A profuse
mucoid discharge with pulsation suggests a tympanic
membrane perforation. The length of history is
important. Persistent discharge suggests chronic otitis
media with perforation (Table 22.2). Cholesteatoma
usually begins with tympanic membrane retraction
and blockage of migrating desquamated skin from
the drum and external meatus. The retraction
deepens and infection leads to destruction of middle
ear structures, sometimes causing damage to the
facial nerve or inner ear. The infection may spread
outside the temporal bone, even causing meningitis
or intracranial abscess. Bleeding from a chronically
Posterior semicircular canal
To stapedius muscle
Chorda tympani nerve
Zygomatic
Temporal
Buccal
Mandibular
Figure 22.6 The course of the peripheral facial nerve.
Box 22.1
Causes of otalgia
Otological
Acute otitis media, mastoiditis
Acute otitis externa
Barotrauma
Furunculosis
Perichondritis
Herpes zoster (Ramsay Hunt syndrome—shingles of the
facial nerve)
Myringitis bullosa—viral myringitis
Necrotizing external otitis (malignant otitis externa)
Neoplasia
Non- otological
Tonsillitis or quinsy
Dental disease
Temporomandibular joint pathology
Cervical spine disease
Carcinoma in the upper air and food passages
discharging ear is usually caused by infection, but
may rarely indicate malignant change. Cranial trauma
followed by bleeding and leakage of cerebrospinal
fluid (CSF) indicates fracture of the base of the skull.
Hearing loss
Deafness may be gradual or sudden, bilateral or
unilateral. There may be an obvious precipitating
cause, such as trauma or noise exposure. There are
two characteristics of hearing loss: to use the analogy of a radio, a decrease in volume or a change
in the tuning corresponding to impaired speech
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Table 22.1 Characteristics of otorrhoea in relation to site and aetiology
Diagnosis Purulent Mucopurulent Mucoid Serous Watery
Acute otitis externa (OE) ✓✓ ✓ ✓
Chronic OE ✓✓ ✓ ✓✓
Acute otitis media (AOM) ✓ ✓✓ ✓
Chronic OM ✓ ✓✓ ✓✓
Cerebrospinal fluid leak ✓ ✓✓
Table 22.2 Classification of chronic otitis media (COM)
COM
classification
(synonym) Otoscopic abnormalities
Healed COM
(healed
perforation
with or without
tympanosclerosis)
Inactive mucosal
COM (dry
perforation)
Active mucosal
COM (discharging
perforation)
Inactive
squamous
epithelial COM
(retraction)
Active squamous
epithelial COM
(cholesteatoma)
Thinning and/or local or generalized
opacification of the pars tensa without
perforation or retraction
Permanent perforation of the pars
tensa, but the middle ear mucosa is
not inflamed
Permanent defect of the pars tensa
with an inflamed middle ear mucosa
that produces mucopus which may
discharge
Retraction of the pars flaccida or pars
tensa (usually posterosuperior) which
has the potential to become active with
retained debris
Retraction of the pars flaccida or
tensa that has retained squamous
epithelial debris and is associated with
inflammation and the production of
pus, often from the adjacent mucosa
Box 22.2
Conductive
Occluding wax in the external meatus
Middle ear effusion: otitis media with effusion
Acute otitis media
Chronic otitis media: perforation, ossicular erosion,
cholesteatoma
Otosclerosis
Trauma to the drum or ossicular chain
Otitis externa
Congenital atresia of the external meatus or congenital
ossicular fixation
Carcinoma of the middle ear
Sensorineural
Age- associated hearing loss: presbycusis
Noise- induced hearing loss
Genetic: syndromal or non- syndromal
Ménière’s disease
Infective: meningitis, measles, mumps, syphilis
Sudden sensorineural hearing loss: idiopathic
Perinatal: hypoxia, jaundice
Prenatal: rubella
Trauma: head injury, surgery
Ototoxicity: aminoglycosides, diuretics, cytotoxics
Neoplastic: vestibular schwannoma, other
cerebellopontine angle lesions
Causes of deafness
discrimination so that words are not clear even
with a hearing aid. Hearing loss may be conductive, sensorineural or mixed, with both conductive
and sensorineural components (Box 22.2). Conductive deafness is caused by disease in the external ear canal, tympanic membrane or middle ear.
Characteristically, the patient retains normal speech
discrimination. Sensory deafness implies pathology
in the cochlea, and neural deafness implies pathology in the cochlear nerve or the central connections
of hearing. In practice this distinction is difficult to
make and rarely useful, and the term sensorineural deafness is used instead. Sensorineural deafness
causes impairment of speech discrimination with
recruitment; the latter is an abnormal perception
of the increase of intensity of sound with increasing signal volume that results from damage to the
hair cells in the cochlea. This leads to a decreased
functional dynamic range, so that a small increase
in sound intensity is uncomfortable (which is why a
deaf grandparent might not be able to hear you one
minute, but as you raise your voice, then ask you
not to shout). The patient may also notice an apparent difference in the pitch or frequency of a tone
between the two ears (diplacusis).
Most hearing loss is gradually progressive and
related to ageing. There are also occupational causes
of deafness, owing to loud sound exposure through
work or social noise exposure and a predisposition to
an early onset of hearing loss is often inherited. Many
drugs are ototoxic, and there are associations between
hereditary hearing loss and neurological and renal
disorders. Occasionally, sensorineural hearing loss
occurs suddenly. A cause is only rarely identifiable.
Tinnitus
Tinnitus is a ringing, rushing or hissing sound in the
absence of an appropriate auditory stimulus. It can
be caused by almost any pathology in the auditory
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pathways. It is strongly associated with hearing loss,
although it occasionally occurs with normal hearing.
It is common, affecting up to 18% of the population
of industrialized countries. In a small proportion
(0.5%), daily life is affected. Correction of coexisting
depressive illness may be of value. Management of
tinnitus includes the use of hearing aids, masking
devices and stress management techniques. It usually
improves with time, but in most cases there is no
specific treatment.
Vertigo
Vertigo is an illusion of movement such that the
patient either feels the world moving or has a
sensation of moving in the world. Patients frequently
have difficulty describing the symptom. Higher
centre dysfunction, as in anxiety states or drug
effects, may also cause dizziness. There are therefore
many causes for symptomatic ‘dizziness’ (Box 22.3).
A feeling of the room spinning associated with
nausea or vomiting suggests an acute labyrinthine
cause, especially if there are changes in hearing or
tinnitus. Fortunately, most acute vestibular events are
self- limiting, because even if one vestibular system
is abnormal, the central connections can ‘reset’ the
system over a period of a few days. The elderly are
less able to compensate. In all age groups, vertigo
may cause residual vague imbalance, particularly in
association with movement or after alcohol ingestion.
It is important to test for positional changes; the
most common cause of vestibular vertigo is benign
paroxysmal positional vertigo (BPPV), secondary to
loose debris floating in the posterior semicircular
canal.
Clinical examination of the ear and hearing
Pinna and postauricular area
First, inspect the pinna and the surrounding
skin. Congenital abnormalities may be associated
with accessory skin tags, abnormal cartilaginous
fragments in the skin surrounding the ear or small
pits and sinuses. Look also for any lymphadenopathy
(associated with otitis externa or scalp cellulitis) and
for surgical scars. A hot, tender postaural swelling,
pushing the pinna forward, suggests mastoid
infection or mastoid abscess (Fig. 22.7). Incomplete
development of the ear (microtia) occurs with
narrowing (atresia) of the external meatus, but the
auricle can also be displaced from its normal position
(melotia) or pathologically enlarged (macrotia).
These abnormalities may be associated with cysts or
infection in a preauricular sinus.
External ear canal
Inspect the external auditory canal using a handheld otoscope (Fig. 22.8). To bring the cartilaginous
meatus into line with the bony canal, retract the
pinna backwards and upwards. Always use the largest speculum that will comfortably fit the ear canal.
Box 22.3
Of sudden onset
Acute viral labyrinthitis
Vestibular neuritis
Migraine
With focal features
Brainstem ischaemia (transient ischaemic attack)
Multiple sclerosis
Migraine
Temporal lobe epilepsy
With deafness and tinnitus
Ménière’s disease
Vestibular schwannoma
Migraine
With positional change
Benign paroxysmal positional vertigo (BPPV)
Cervical vertigo
After trauma
BPPV
Perilymph fistula
With motion
Motion sickness
Drug- induced
Vestibulotoxic drugs (e.g. aminoglycosides, salicylate,
quinine, furosemide, platinum- based chemotherapy)
With aural discharge
Middle ear disease
With systemic disorders
Postural hypotension
Syncope
Cardiac dysrhythmia
Carotid sinus hypersensitivity
Anxiety and panic attacks
Hyperventilation syndrome
Hold the otoscope like a pen between thumb and
index finger, with the ulnar border of your hand
resting gently against the side of the patient’s head.
In this way, any movement of the patient’s head
during the examination causes synchronous movement of the speculum, limiting any risk of accidental injury to the ear canal. With a young child, sit
him on his parent’s lap with the head and shoulder
held (Fig. 22.9).
Wax may be removed with a Jobson Horne probe
or wax hook or by syringing with water. Never
syringe if there is a history of previous perforation
or discharge. It is important to use water at 37°C
lest vertigo be induced by caloric stimulation of
the labyrinth. Keratin debris, pus or mucopus in
the meatus can be removed and can be sent for
microbiology. Foreign bodies in the ear canal are
sometimes found in children; they may be difficult
to remove without a general anaesthetic.
Causes of vertigo
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A
Figure 22.8 Examining the ear in an adult.
B
Figure 22.7 Acute mastoiditis (A) before and (B) after incision.
The tympanic membrane
The hand- held otoscope is satisfactory for most
examinations, but the outpatient microscope offers
the best view. Be familiar with the variability in
appearance of the normal drum. The most common
abnormality is tympanosclerosis (Fig. 22.10), which
consists of white chalky patches in the drum caused
by hyaline degeneration of the fibrous layer due to
previous infection.
Prolonged negative middle ear pressure may
cause the drum to become thinned and atelectatic (Fig. 22.11), either diffusely or with a retrac-
tion pocket. Eustachian tube dysfunction and/or
acute otitis media may cause a middle ear effusion
(Fig. 22.12). Fluid behind the drum is often obvious,
but when the drum is opaque, increased vascularity
and retraction are useful clues.
Perforations of the pars tensa are either central or
marginal (Fig. 22.13). Marginal perforations extend
to the annulus and may be associated with cholesteatoma (Fig. 22.14), whereas with central perforations
a rim of membrane is retained between the defect
and the annulus. Both are described by their position in relation to the handle of the malleus (anterior,
posterior or inferior) and by their size (Fig. 22.15).
The fistula test is indicated if the patient is dizzy
with middle ear pathology. Press on the tragus to
occlude the meatus and then apply more pressure.
If the labyrinth is open, this pressure change will be
applied to the inner ear. The patient will be dizzy
and nystagmus may be induced. Typical computerized tomography (CT) scan findings of a positive fistula test are shown in Figure 22.27.
The facial nerve
Test the facial movements. Unilateral weakness
is much easier to identify than bilateral weakness.
A peripheral facial palsy can be graded using the
House- Brackmann scale (Table 22.3). Function of
the greater superficial petrosal nerve can be tested
with Schirmer’s test: absorbent paper strips are
applied to the inferior margin of the eye to detect
tear formation (see Chapter 21). Chorda tympani
function can be tested by the sense of taste and by
electrogustometry, although this is rarely used in
practice.
Clinical assessment of hearing
Conversational hearing will indicate any possible
deafness. The television may be too loud or varying
amounts of background noise make conversation
Establish which is theunexpectedly difficult.
patient’s better- hearing ear. Test using words or
numbers. Stand to the side of the ear to be tested
and mask the non- test ear by gently rubbing the
tragus. The test starts with a whispered voice at 60
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Figure 22.9 Examining the ear in a child.
469
Figure 22.10 A right tympanic membrane showing marked
posterior tympanosclerosis and a small anterior perforation.
Figure 22.11 A left tympanic membrane showing atelectasis and
posterior retraction on to the long process of the incus.
Figure 22.12 A left tympanic membrane with a middle ear
effusion.
Figure 22.13 A left tympanic membrane with an anterior central
perforation.
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Figure 22.14 A left tympanic membrane with cholesteatoma in
the posterosuperior quadrant.
Table 22.3 The House- Brackmann facial nerve grading scale
Grade Function
I Normal
II Normal at rest
Slight weakness on close inspection
Complete eye closure with minimal effort
Slight asymmetry of mouth with movement
Good to moderate forehead movement
Normal at rest
Obvious asymmetry on movement
Synkinesis ± hemifacial spasm
Complete eye closure with effort
Slight to moderate forehead movement
Slight weakness of mouth with maximal
effort
III Normal at rest
Asymmetry on movement is disfiguring
Incomplete eye closure
No perceptible forehead movement
Asymmetrical mouth motion with maximal
effort
IV Asymmetric at rest
Barely noticeable movement
No forehead movement
Incomplete eye closure
Slight mouth movement with effort
No facial function perceptible
Figure 22.15 A left tympanic membrane with a subtotal
perforation. The chorda tympani and long process of the incus can
clearly be seen, as can the round window niche.
cm (approximate intensity 15 dB) and proceeds
with a whispered voice at 15 cm (35 dB). If there
is no response, try a conversational voice at 60 cm
(50 dB); this is then repeated, if necessary, at 15
cm (55–60 dB) from the test ear. With experience,
a surprisingly accurate assessment can be made. It
is valuable in correlating the history and results of
more formal audiometry.
The Rinne test (Fig. 22.16) compares hearing by
air and bone conduction using a 512- or 256- Hz
tuning fork. Strike the tuning fork and hold it near
the external ear canal with the prongs vibrating
towards the meatus (air conduction) and then
against the mastoid process (bone conduction). Ask
the patient which sound was louder. In subjects with
normal hearing and those with sensorineural loss, air
conduction is better than bone conduction (Rinne
positive). In conductive deafness, bone conduction
is louder (Rinne negative), although patients with a
small conductive loss (up to 30 dB) may remain Rinne
positive; it is only when the difference between air
and bone conduction exceeds 40 dB that the Rinne
test is consistently negative. Moreover, patients with
a profound unilateral sensorineural hearing loss will
report a Rinne- negative response if the contralateral
ear has normal or reasonable hearing. This is because,
although the vibrating tuning fork held adjacent to
the test ear will only be heard in that ear, the same
tuning fork placed on the mastoid process will also be
heard in the non- test ear. For these reasons, masking
(by rubbing) the non- test ear should always validate
a negative response. If there is doubt, a Barany box
should be used to mask the contralateral ear.
In the Weber test, the base of the vibrating tuning
fork is placed firmly on the vertex or forehead in
the midline. With eyes shut, ask the patient whether
the sound is heard in the midline or whether it is
lateralized. With normal response or with hearing
symmetrically reduced, the sound is heard in the
midline. However, when one ear is normal, the noise
will be louder on the side opposite to an ear with
pure sensorineural loss and on the same side as an
ear with purely conductive hearing loss. The Weber
test is simple and quick, but there is a high test- retest
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Normal bilateral hearing or bilateral
sensorineural hearing loss
BC
+
+++
AC
Rinne: positive bilaterally (AC>BC)
Weber: central
Right-sided sensorineural hearing
loss and normal left ear
Right-sided conductive hearing
loss and normal left ear
BC
+
+++
AC
BC
+++
+
AC
Right Rinne: negative (BC>AC)
Weber: lateralizes to the ear with conductive loss
BC
+
+++
AC
Right-sided severe sensorineural
hearing loss or dead ear
BC
+
++
AC
Rinne: positive bilaterally (AC>BC)
Weber: lateralizes to the ear with greater
cochlear function
Rinne test Weber test
BC
+
+++
AC
BC
+++
+
AC
Right Rinne: negative (BC>AC): a false negative as the
BC is heard in the normal left cochlea by
skull crossover
Weber: lateralizes to the ear with greater
cochlear function
(Note: the good ear should be masked and the test
repeated. The right-side BC should be greatly reduced
or absent)
Figure 22.16 Interpretation of tuning fork tests.
variability. Because all clinical tests of hearing have
limited reliability, accurate formal audiometry in the
ENT clinic is essential.
Clinical assessment of balance
The unsteady patient requires a full neuro- otological
examination. It is also necessary to examine the
cardiovascular system (see Chapter 13). The aim
is to localize the site of any potential lesion and
possibly confirm a diagnosis, although sometimes
BC
+
Noise
+++
AC
all that is possible is to differentiate between central
(brainstem) and peripheral (labyrinthine) lesions.
Examine the cranial nerves (see Chapter 16),
particularly testing the eyes and for nystagmus.
Nystagmus (see Chapters 16 and 21). The char-
acteristic saw- toothed nystagmus of vestibular
disease has a slow (labyrinthine) and a fast (central) component and is enhanced by movement
of the eyes in the direction of the fast phase. Eye
movements can also be assessed using Frenzel’s
glasses (Fig. 22.17). These are illuminated and
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Figure 22.17 Frenzel’s glasses.
have 20- dioptre lenses that abolish visual fixation
for the patient, thereby possibly unmasking nystagmus. Horizontal nystagmus can be peripheral
or central; pure vertical upbeat or downbeat nystagmus usually indicates a central process.
Pursuit (slow) movements, which depend on
the fovea and the occipital cortex of the brain,
are seen when the patient tracks an object
moved slowly horizontally and vertically across
the visual field about 35 cm away. If these are
jerky rather than smooth this can indicate a
central lesion.
Saccadic movements are driven by the frontal
lobes and the pontine gaze centres are seen when
the patient alternates the gaze rapidly between
two objects held approximately 30° apart.
Disorders of saccadic accuracy indicate a central
lesion.
All these eye movement disorders can be identified
by videonystagmography (Fig. 22.18) in which a
test battery is run using video cameras to monitor
the eyes and measure and record eye movements
to identify signs of vestibular (peripheral) or
neurological (central) disorders.
Romberg’s test. The patient stands with the
feet together, initially with the eyes open and
then closed. Patients with disorders of the
spinal posterior columns (impaired position
sense) will sway or fall with closed eyes, but
will stand normally if eyes are open. Patients
with uncompensated unilateral labyrinthine
dysfunction are unstable, tending to fall to the side
of the lesion. Patients with central dysfunction
sway to both sides, whether the eyes are open or
shut. Patients with persistent postural perceptual
dizziness (PPPD), a cause of chronic dizziness, will
feel excessively unsteady on Romberg’s testing
despite not exhibiting particularly pronounced
sway. Computerized dynamic posturography tests
postural stability and an ability to maintain an
upright posture under different test conditions
using information from the muscles/joints, eyes
and ears. This can be used in a rehabilitative setting
Figure 22.18 Videonystagmography.
Figure 22.19 Computerized dynamic posturography.
as well as to aid diagnosis of balance dysfunction
(Fig. 22.19).
Unterberger’s stepping test has the patient
standing with arms outstretched and eyes closed
and taking steps on the spot. Unilateral vestibular
hypofunction leads to rotation to the affected
side.
Gait assessment. The patient walks heel to toe
with eyes first open and then closed. The patient
with a cerebellar lesion is unable to do either
(ataxic gait). The patient with a peripheral
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