CHAPTER 25
EXAMINATION OF HEARING
AND BALANCE
● ●
Brian C. Kung and Thomas O. Willcox, Jr.
Hearing loss and balance disorders are two of the most common
reasons that patients visit their physicians. Varying degrees of
hearing loss can affect patients at any age. One of every 1000
newborns is affected by some degree of hearing loss, and the
prevalence of hearing loss rises with advancing age.1 By age 60,
one of every three individuals is affected by hearing loss, and
by age 85, one of every two is affected.1
Balance disorder, or “dizziness,” is the ninth most common
complaint for which patients visit primary care physicians and
the third most common complaint for 65- to 75-year-old
patients.2-4 Hearing and balance disorders have a myriad of
manifestations and etiologies, some of which are difficult to
piece together. Treatment is often multidisciplinary, involving
the neurologist, otolaryngologist, audiologist, neurosurgeon,
and physical therapist, among others. It is important to recog-
nize the signs and symptoms associated with specific types of
hearing loss and balance disorders for the patient to receive
proper referrals and proper treatment. The purpose of this
chapter is to provide a better understanding of the otolaryn-
gologist’s approach to the hearing and balance examination.
HEARING EXAMINATION
There are three main forms of hearing loss: conductive, sen-
sorineural, and mixed. Each can be caused by a wide variety of
conditions, ranging from benign conditions, such as cerumen
impaction, to potentially life-threatening diseases, such as
squamous cell carcinoma of the temporal bone. Usually, con-
ductive hearing loss is caused by a disorder in the external or
middle ear, whereas a sensorineural hearing loss is caused by a
disorder of the inner ear or neural structures leading from the
inner ear to the central nervous system. Hearing loss can lead
to speech and developmental delays in children and significant
communication problems and decreased quality of life in both
children and adults. Many of these conditions are treatable and
early recognition is important. A structured hearing evaluation
consists of a history, physical examination, and audiological
testing; often radiological testing is necessary to lead to the
proper diagnosis.
History
A thorough history is one of the most important aspects of a
hearing evaluation. Often, this gives the physician clues as to
318
● ●
what to look for during the subsequent physical examination
and audiological and/or radiographic tests in order to arrive at
the correct diagnosis. The severity of the patient’s hearing loss
can be assessed just by conversing with the patient in a normal
or soft voice and observing whether the patient responds appro-
priately. If the patient speaks in a very loud voice, it may indi-
cate a sensorineural cause of hearing loss, and if the patient
speaks very softly, it may point to a conductive cause, as the
patient’s voice may sound louder to the patient (just as a normal
hearing person’s would if his or her ears were plugged). Some-
times, discrepancies between the patient’s behavior in conver-
sation and during diagnostic tests can point to malingering as
a possible diagnosis.
When taking a history of present illness, specific points
should be emphasized. These include the patient’s perception
of the degree of hearing loss, whether the hearing loss is uni-
lateral or bilateral, and the onset of the hearing loss (sudden
within 3 days, rapidly progressive within 1 week, slowly pro-
gressive over weeks to years, fluctuating, or stable). The patient
may have associated symptoms, such as aural fullness, tinnitus,
vertigo, disequilibrium, otalgia, otorrhea, headache, visual
problems, and other neurological complaints (facial numbness
or weakness, ataxia, oscillopsia, etc.), that may help point to
specific causes of hearing loss. The past medical history is also
very helpful: cardiovascular, renal, rheumatological, hemato-
logical, endocrine, and neurological conditions can predispose
a patient to certain types of hearing loss.5 Past surgical history
should also be obtained, with special emphasis on head trauma
and previous otological or neurological surgery. A history of
noise exposure is also important, as excessive noise exposure,
either suddenly or over a period of time, can lead to hearing
loss. A full account of the patient’s recent medications, includ-
ing potentially ototoxic medications, should be taken. It is very
important to know whether there is a family history of hearing
loss, as there is a genetic predisposition for many types of
hearing loss, and many genes associated with deafness and pre-
disposition to hearing loss have been identified.1,5
Physical Examination
A complete head and neck examination can give many clues to
the cause of a patient’s hearing loss. The auricle and the postau-
ricular area should be examined for deformities, surgical inci-
sions, the presence of a hearing aid, and patency of the external
 chapter 25 examination of hearing and balance
auditory canal. Something as simple as cerumen impaction can
be the cause of hearing loss in some patients, but other condi-
tions, such as foreign bodies, exostoses, canal stenosis/atresia,
and carcinoma of the external canal, can be more troublesome.
Pneumatic otoscopy can then be used to examine the tympanic
membrane and middle ear. Here, the presence of a tympanos-
tomy tube, tympanosclerosis (scarring of the tympanic mem-
brane), tympanic membrane perforation, retraction pocket,
fluid in the middle ear, middle ear masses, or otorrhea can be
assessed. It is important to obtain a good seal with the specu-
lum in order to assess the mobility of the tympanic membrane.
External and middle ear abnormalities usually point to a con-
ductive component of hearing loss.
Tuning fork testing is an essential part of the physical exam-
ination and can help determine if the cause of hearing loss is
conductive, sensorineural, or mixed. The three types of tuning
forks that can be used are 256 Hz (middle C), 512 Hz (octave
above middle C), and 1024 Hz (two octaves above middle C).
The Rinne test is useful in determining if there is a conductive
hearing loss and is performed by striking the tuning fork and
placing it on the mastoid bone (testing bone conduction). Once
the patient stops hearing the sound, the tines of the tuning fork
are then placed in front of the external canal (testing air con-
duction) with the tines oriented in the head-frontal plane, and
the patient indicates whether he or she can hear the sound. If
the patient can hear the sound, air conduction is greater than
bone conduction, and the result is normal, or “positive.” If the
patient cannot hear the sound, bone conduction is greater than
air conduction, and the result is abnormal, or “negative.” The
degree of conductive hearing loss can be estimated based on
the results of the Rinne test. A test that is negative at 256 Hz
and positive at 512 and 1024 Hz indicates a mild 20- to 30-
decibel (dB) conductive loss. A test that is negative at 256 and
512 Hz and positive at 1024 Hz indicates a moderate 30- to
45-dB conductive loss. A negative test at all three frequencies
indicates a severe 45- to 60-dB conductive loss.6,7 The Weber
test is a test used to lateralize the hearing loss. The tuning
fork is struck and placed on the patient’s vertex, nasal bones,
or maxillary teeth in the midline. The single most clinically
useful fork used here is the 512-Hz variety, as the 256-Hz fork
can be overly sensitive, leading to many false-positive results,
and the 1024-Hz fork may not be sensitive enough.7-9 Lateral-
ization of sound to one ear during the Weber test indicates
either a conductive hearing loss in that ear or a greater sen-
sorineural loss in the opposite ear.7 Simple tuning fork tests
using only a few frequencies are far from comprehensive. If
both ears are symmetrically affected by a sensorineural hearing
loss, both the Rinne and Weber tests will be normal, provided
the patient is able to hear the tuning fork at all.
The physical examination should also include an assessment
of any craniofacial deformities or stigmata that may be associ-
ated with hereditary causes of hearing loss or associated sys-
temic diseases. Also, a full cranial nerve examination should be
performed, as asymmetries in any of the cranial nerves may
indicate that hearing loss is just one component of more severe
or extensive disease, such as a skull base neoplasm. A decreased
corneal blink reflex and hypesthesia of the external auditory
canal (Hitselberger’s sign) can be suspicious for an acoustic
neuroma. Finally, attention to the nose, nasopharynx, oral
cavity, oropharynx, larynx, and hypopharynx can reveal other
causes of hearing loss (e.g., the presence of nasopharyngeal
carcinoma as the cause of serous otitis media).
319
Audiological Testing
Audiological testing has been available for decades, but devel-
opments over the years have advanced the field of audiology to
include tests and procedures that can determine the site of
lesion with far greater accuracy than before. Otolaryngologists
and audiologists often need to rely on one another to diagnose
accurately the cause of a patient’s hearing loss using a combi-
nation of the history, physical examination, and results of
various audiological tests. The audiological test battery
includes audiometry (pure tone and speech), acoustic immit-
tance testing (tympanometry and acoustic reflex testing),
electrophysiological testing (auditory brainstem response and
electrocochleography), and otoacoustic emission testing.
Pure-Tone Audiometry
Pure-tone audiometry is the most commonly used test to
measure auditory sensitivity. Pure-tone signals are delivered to
the ear via air conduction and bone conduction at a variety of
frequencies, and the patient responds to the sound by signal-
ing the examiner with a button or by raising a hand. The
response can be modified for pediatric patients or patients who
lack the capacity to respond in the conventional manner.
Although the entire range of human hearing is from 20 to
20,000 Hz, the typical range of frequencies tested runs from 250
to 8000 Hz, which is the range necessary to understand
speech.10
The intensity of a sound presented is represented by a ratio
of its sound pressure to a reference sound pressure, defined as
the amount of pressure that can just be sensed by a normal
human ear at its most sensitive frequency (0.0002 dyne/cm2).11
As the pressure level of a presented sound is often many times
the reference sound pressure, the simplest way to present this
ratio is to use the decibel, a logarithmic unit:
dB = 20 log10(P2/P1)
where P2 is the presented sound pressure and P1 is the
reference sound pressure.
A sound referenced to the reference sound pressure is known
as the absolute sound level, presented as decibels sound pres-
sure level (dB SPL). The normal human ear is variably sensi-
tive to different frequencies throughout its range, so clinically,
the easiest reference level to use is the sound pressure level for
each tested frequency that can be heard by a normal ear. The
sound level is presented as decibels hearing loss, or dB HL.11
For example, if a normal hearing patient responds to a sound
P2 that is equal to P1 (what another normal person would
hear), then that patient has 20 log10 1 = 20(0) = 0 dB HL. If a
patient with hearing loss responds to a sound P2 that is 100
times what a normal person would hear, then that patient has
20 log10 (100/1) = 20(2) = 40 dB HL. If a patient with hyperacu-
sis (supersensitive hearing) responds to a sound P2 that is
1/10 what a normal person would hear, then that patient has
20 log10 (1/10) = 20(−1) = −20 dB HL. These examples help to
illustrate that dB is indeed a comparison between sound levels
and that 0 dB or negative dB does not mean that there is no
sound⎯it just means that the sound is the same as or lower
than the reference sound level, respectively.
Auditory threshold is defined as the lowest signal intensity
at which the signal can be identified 50% of the time.12 Air
320 Section V Neuro-Otology
conduction thresholds are determined by presenting sound to
the ears via headphones or insert earphones, and bone con-
duction thresholds are determined by vibrating the mastoid
directly. Air conduction thresholds measure the sensitivity of
the entire auditory system from the external ear to the audi-
tory cortex. When analyzed alone, they do not provide much
information regarding the etiology of hearing loss. However,
when they are analyzed together with bone conduction thresh-
olds, which measure the degree of sensorineural hearing loss,
they can provide valuable information regarding both the type
and severity of the hearing loss.12 When air conduction thresh-
olds are elevated relative to bone conduction thresholds, an
“air-bone gap” exists, indicating a conductive hearing loss. Air
conduction and bone conduction thresholds showing the same
amount of hearing loss indicate a sensorineural hearing loss. A
mixed hearing loss is present when both air and bone conduc-
tion thresholds are elevated, but air conduction thresholds are
more elevated than bone conduction thresholds.
The normal region on the audiogram is from 0 to 20 dB HL
for adults and from 0 to 15 dB HL for children. Mild hearing
loss is 20 to 40 dB HL, moderate loss is 40 to 55 dB HL,
moderately severe loss is 55 to 70 dB HL, severe loss is 70 to
90 dB HL, and profound loss is above 90 dB HL. Hearing
sensitivity within the speech frequencies is known as the
pure-tone average (PTA) and can be calculated by adding the
thresholds obtained at 500, 1000, and 2000 Hz and dividing the
result by 3.11
For audiometric results to be valid, the patient must respond
to stimulation of the ear being tested. When noninsert ear-
phones are used, sounds greater than 40 dB HL presented to
one ear can cross over to the opposite ear, most likely with the
vibration of the earphone against the skull acting as a bone con-
ductor. The amount of sound needed for crossover to occur is
known as the interaural attenuation, which for air conduction
is about 50 dB HL for lower frequencies and 60 dB HL for higher
frequencies. The interaural attenuation is considerably higher
when insert earphones are used. For bone conduction, inter-
aural attenuation is less than 10 dB HL.11 To correct for the
presence of interaural attenuation when a true hearing loss is
present, masking techniques are used. A narrow band “white”
noise is presented to the nontest ear when the true stimulus is
being given to the test ear, and with adequate masking, any
sound crossing over to the nontest ear is masked by the noise.
To work, the masking noise presented to the nontest must be
greater than the threshold of hearing for the nontest ear.11 This
can be a problem when bilateral hearing loss (especially con-
ductive) exists, as masking presented to the nontest ear can
cross back over to the test ear. This is known as a “masking
dilemma.”10 In air conduction testing, masking should be used
when there is a difference between the air conduction presen-
tation level to the test ear and the bone conduction threshold
of the nontest ear of greater than 40 dB for lower frequencies
and greater than 60 dB for higher frequencies. In bone con-
duction testing, masking should be used whenever there is any
difference in the air and bone conduction thresholds.10
Speech Audiometry
Commonly measured speech tests include the speech detection
threshold (SDT), the speech reception threshold (SRT), and
speech discrimination or word recognition. The SDT is the
softest level at which the patient can barely detect the presence
of a speech signal 50% of the time.12 The SRT is the softest level
at which the patient can repeat 50% of balanced disyllabic
words, or spondees (e.g. “hot dog,” “baseball”), correctly.10,12
The SDT should correspond to the PTA, whereas the SRT is
usually about 8 to 9 dB higher than the PTA.12 Both SDT and
SRT can be measured with bone conduction testing and can be
masked if necessary. Discrepancies between the PTA and the
SDT or SRT can indicate malingering.
The speech discrimination score is a test of the patient’s
ability to identify monosyllabic words, or phonemes, at a
suprathreshold level, usually about 40 dB above the SRT.10 The
speech discrimination score is important in that it helps assess
the patient’s ability to understand speech, to communicate
effectively, and to benefit from amplification. It also provides
some information regarding the patient’s central auditory
function.12
In general, patients with conductive hearing loss tend to
have excellent speech discrimination scores when presented
with sounds loud enough for them to hear. Patients with
cochlear sensorineural loss tend to have lower speech discrim-
ination scores, and patients with retrocochlear sensorineural
loss (from lesions of the eighth cranial nerve to the auditory
cortex) have even lower speech discrimination scores. They
may even have lower speech discrimination in the presence of
normal pure-tone thresholds.12
Tympanometry
Acoustic immittance refers to either acoustic admittance (the
ease with which energy flows through a system) or acoustic
impedance (the blockage of energy flow through a system).12 In
tympanometry, acoustic immittance measures are used to
determine the status of the tympanic membrane and middle
ear. A probe is placed in the ear canal and an airtight seal is
obtained. A tone is introduced into the ear canal and the pres-
sure in the canal is varied. When the pressure in the ear canal
is equal to the middle ear pressure, the tympanic membrane
will be at its most compliant (highest admittance) and will
absorb the sound. This results in a tympanometric peak.10
If eustachian tube function is normal, the middle ear pres-
sure is equal to the atmospheric pressure and the peak occurs
at 0 mm H2O⎯this corresponds to a type A tympanogram. If
there is negative middle ear pressure, the peak occurs at a neg-
ative pressure, corresponding to a type C tympanogram. If there
is no peak (flat or type B tympanogram), there is no compli-
ance of the tympanic membrane (no admittance), indicating a
middle ear effusion, tympanic membrane perforation, or patent
tympanostomy tube. These can be distinguished using ear canal
volume measurements, with higher volumes corresponding
to a hole in the tympanic membrane. Other types of tym-
panograms include As (shallow peak and low compliance at
0 mm H2O), indicating ossicular chain fixation or middle ear
effusion, and Ad (very high peak and high compliance at 0 mm
H2O), indicating ossicular chain discontinuity or a monomeric
tympanic membrane.10
Acoustic Reflex
In acoustic reflex testing, acoustic immittance measures are
used to assess the neural pathway surrounding the stapedial
 chapter 25 examination of hearing and balance
reflex, which occurs in response to a loud sound (70 to 90 dB
above threshold).10 The afferent limb of the stapedial reflex is
the ipsilateral eighth nerve, which leads to the brainstem.
Complex pathways in the brainstem involving the ipsilateral
ventral cochlear nucleus, trapezoid body, and bilateral medial
superior olives lead from the eighth nerve on the ipsilateral
(stimulated) side to the motor nucleus of the facial nerve on
both sides of the brainstem.7,10-12 The efferent limb is the ipsi-
lateral and contralateral facial nerves, which innervate the
stapedius muscles. When the stapedius muscle contracts, the
ossicular chain stiffens, causing a small change in compliance
in the middle ear system that is detected by the probe.11
Patients with mild to moderate cochlear sensorineural
hearing loss have reflexes bilaterally at about the same inten-
sity level as those with normal hearing, but patients with severe
or profound hearing loss have absent reflexes when the affected
ear is stimulated.10
A conductive hearing loss results in absent reflexes when the
affected ear is stimulated, as sound will not be loud enough to
stimulate the reflex. Even when the normal ear is stimulated,
the ear with the conductive loss does not have a reflex, as the
middle ear condition prevents the stapedius from contracting.10
A lesion of the eighth nerve should result in absent reflexes
bilaterally when the affected ear is stimulated, but reflexes
should be present bilaterally when the nonaffected ear is stim-
ulated. This can be confused with the reflex result associated
with profound unilateral hearing loss (>70 dB) of cochlear
origin. Lesions of the brainstem affecting the central crossed
pathways may result in present ipsilateral reflexes when each
ear is stimulated but absent contralateral reflexes. A facial nerve
lesion results in an absent reflex on the affected side, no matter
which side is stimulated, provided the lesion is proximal to the
branching of the nerve to the stapedius muscle.10
Auditory Brainstem Response
The auditory brainstem response (ABR) is an electrophysiolog-
ical recording of responses of the distal auditory pathway
(eighth nerve and brainstem) to sounds.11 The ABR involves
placement of electrodes on the patient’s head and presentation
of sound to the ear. When sound is presented to a normal ear,
either in click form or frequency-specific tones, five to seven
peaks occurring within 10 milliseconds make up the ABR.12
Usually only the first five peaks are considered. Wave I repre-
sents the action potentials from the eighth nerve near the
cochlea. Wave II comes from the eighth nerve near the cochlear
nucleus in the brainstem. Waves I and II are the only waves
generated by ipsilateral structures. All subsequent waves rep-
resent bilateral crossed pathways. Wave III comes from the
caudal pons with contributions from the cochlear nucleus,
trapezoid body, and superior olive. Wave IV probably comes
from the lateral lemniscus. Wave V, the most prominent wave,
comes from the lateral lemniscus as it approaches the inferior
colliculus.11
For audiological purposes, the latencies and amplitudes of
waves I, III, and V are analyzed, and comparisons between sides
are made. In normal hearing, the latencies of waves I, III, and
V are within normal ranges and the latencies between ears are
within 0.2 to 0.4 milliseconds of each other. In conductive
hearing loss, the absolute latency of wave I is prolonged, but
the latencies between waves and the amplitudes are not
321
affected. In cochlear sensorineural loss, the wave I latency is
slightly delayed and is small in amplitude, but the latencies
between waves are not affected. In retrocochlear (neural)
hearing loss, wave I tends to be normal, but latencies between
waves I-III and I-IV are abnormally prolonged.10,11
In practice, the ABR is a good tool to definitively test hearing
in uncooperative patients (newborns) and in suspected malin-
gerers, and it can be used to evaluate the eighth nerve and
brainstem structures in patients with suspected retrocochlear
hearing loss. It is also used in neurotological surgical proce-
dures, such as vestibular nerve section and acoustic neuroma
removal.11
Electrocochleography
Electrocochleography is a test of the electrical activity gener-
ated by the cochlea and eighth nerve. It is most often used to
aid in the diagnosis of Ménière disease, but it can also be used
for intraoperative monitoring of the cochlear and eighth nerve.
An electrode is placed in the ear canal, on the tympanic mem-
brane, or on the promontory of the cochlea in the middle ear.
The three main signals detected by electrocochleography are
the cochlear microphonic, the summating potential, and the
action potential. The cochlear microphonic and summating
potential reflect cochlear electrical activity, and the action
potential reflects eighth nerve activity and is the same as wave
I of the ABR. The calculation of interest is the summating
potential/action potential ratio. An abnormally high ratio is
suggestive of endolymphatic hydrops characteristic of
Meniere’s disease.10,11
Otoacoustic Emissions
Otoacoustic emissions (OAEs) represent auditory signals pro-
duced by the cochlear outer hair cells that can be picked up by
a very sensitive microphone in the ear canal.12 Although they
are a measure of cochlear function, abnormalities anywhere
between the microphone and cochlea (e.g. middle ear) block
any signals going from the cochlea to the microphone⎯they
will not be detectable in the presence of conductive hearing
loss.10 The three main types of OAEs are spontaneous, transient
evoked, and distortion product.
Spontaneous OAEs occur in the absence of a stimulus, but
they only occur in less than one half to 60% of normal hearing
individuals.10,11 Transient evoked OAEs (OAEs) are elicited by a
brief click or tone burst. Distortion product OAEs (OAEs) are
generated when two pure-tone stimuli of different frequencies
are presented to the ear simultaneously. In response to these
tones, the outer hair cells generate signals called distortion
products that are related to the frequencies of the presented
tones. Transient evoked OAEs are used to determine mainly if
there is good cochlear function, whereas distortion product
OAEs can be used to generate a curve resembling an audiogram
based on frequency-specific responses of the cochlea.10-12
OAEs are useful in that they are specific to cochlear func-
tion. They are not present in conductive hearing loss or
cochlear hearing loss greater than 25 to 30 dB HL. However,
they can be present in retrocochlear (neural) hearing loss,
which can help differentiate cochlear from retrocochlear
lesions.10 OAEs are noninvasive and easy to perform⎯they can
be used to screen hearing in infants, to confirm audiometric
322 Section V Neuro-Otology
testing in young children, to monitor the effects of ototoxic
medications, to detect cochlear abnormalities in patients
with tinnitus and normal audiograms, and to help detect
malingerers.10,11
Radiographic Testing
Radiographic testing is indicated in certain patients with either
conductive or sensorineural hearing loss. A CT scan of the tem-
poral bones can be useful to detect the presence of congenital
inner ear malformations, middle ear masses, erosive skull base
neoplasms, and temporal bone fractures. It is also important
in assessing the patient’s surgical anatomy and in planning
for procedures such as cholesteatoma removal or cochlear
implantation.
Magnetic resonance imaging (MRI) of the internal auditory
canals is extremely useful in the diagnosis of unilateral or
asymmetric sensorineural hearing loss. It is more sensitive and
specific than ABR for the detection of acoustic neuromas and
is the gold standard in the diagnosis of acoustic neuromas as
a cause of retrocochlear (neural) hearing loss.5,13 MRI with
gadolinium enhancement is able to detect small tumors less
than 1 cm in diameter, which results in better facial and hearing
function after tumor removal.13 MRI should also be heavily con-
sidered in the face of sudden sensorineural hearing loss, even
if it resolves with steroids, because as many as 19% of patients
with acoustic neuromas can present with sudden hearing loss.14
Some reports state that as many as 47.5% of cases of sudden
hearing loss may be caused by an acoustic neuroma.14,15
BALANCE EXAMINATION
The diagnosis and treatment of patients with “dizziness” can be
very challenging and frustrating for the patient, the neurolo-
gist, the otolaryngologist, and the audiologist. A huge variety
of disorders can cause the patient to have a sensation of dizzi-
ness, and a huge variety of terms can be used to describe it
(lightheadedness, spinning, “swimming sensation,” “things not
being right in the head”).16 Often, the diagnosis is made by
piecing together many different pieces of information. It is
important to realize that not every case of dizziness can be com-
pletely cured or diagnosed exactly. An organized, systematic
approach is necessary in order to make a reasonably accurate
diagnosis and to avoid confusion. Key components in the eval-
uation of dizziness include the history, physical examination,
electronystagmography, rotary chair testing, and computerized
dynamic posturography testing.
History
Obtaining a careful history is probably the most important step
in the diagnosis of dizziness, but it often requires patience.
Symptoms are often vague and difficult for the patient to
describe. It may seem faster to begin by asking a lot of leading
questions, but the physician will actually save time by allowing
the patient to describe what he or she is feeling in the patient’s
own words. Especially important is the patient’s description of
the first episode of dizziness, although this may be difficult to
elicit in patients who are so consumed by their dizziness that
they cannot focus on the initial event and in patients who have
already seen multiple specialists and/or lawyers.16
When the patient describes his or her symptoms, it is impor-
tant to distinguish whether the patient is experiencing a sen-
sation of movement, such as a spinning sensation or a falling
sensation. Vertigo, a false sensation of movement, should be
distinguished from dizziness, which is any kind of altered sense
of orientation.17 Lightheadedness refers to a sensation charac-
teristic of presyncope, which may include temporary blurred
vision and pale facial color. It should be distinguished from
vertigo and is usually caused by nonvestibular problems such
as the cardiac or vasovagal reflex, both of which can result in
cerebral hypoxia.17 A sense of imbalance refers to the inability
to maintain the center of gravity, which causes the patient to
feel unsteady and as if he or she is going to fall.17 This can be
caused by both vestibular and nonvestibular disorders.
When the patient describes vertigo, further information
must be gathered in order to differentiate whether it is caused
by a peripheral or central lesion. Vertigo can be caused by
lesions anywhere from the vestibular end organs (utricle,
saccule, and semicircular canals), the vestibular nuclei, the
cerebellum, brainstem pathways, and the cortex (rarely).17 An
important characteristic to ascertain is whether the vertigo is
episodic or continuous. If episodic, how long the attacks last,
how often they occur, and whether they occur with head move-
ment or positioning are important points to know. Associated
auditory symptoms, such as hearing loss, aural fullness, and
tinnitus, are all important to ask about. Also important are
associated neurological symptoms, such as headache with or
without aura, visual changes, oscillopsia, numbness, weakness,
ataxia, seizure, and loss of consciousness. Asking if the vertigo
is more intense with a Valsalva maneuver is also helpful. A full
otological history including history of infection, otalgia, otor-
rhea, and previous otological surgery is essential. In addition,
it is imperative to obtain a full past medical history, past sur-
gical history, history of head trauma, recent medications (with
attention to ototoxic medications, blood pressure medications,
stimulants, depressants, and illegal drugs), diet, allergies, social
history, and family history of hearing loss or vestibular
problems.16
Sorting out the history is important in suggesting possible
diagnoses as well as recognizing more extensive and complex
conditions. Episodic intense vertigo lasting up to one minute
associated with head positioning or movement and not associ-
ated with other auditory symptoms is characteristic of benign
paroxysmal positional vertigo (BPPV),17 but brief 5- to 10-
second episodes associated with head movement may also be a
sign of vascular compression of the eighth nerve complex.2
Episodic vertigo lasting minutes to hours sometimes associated
with fluctuating hearing loss, tinnitus, and/or aural fullness is
suggestive of Meniere’s disease, but vertigo lasting 2 to 20
minutes may be associated with transient ischemic attacks,
especially when associated with visual changes, ataxia, and
other neurological findings.17 An isolated attack of continuous
vertigo lasting longer than 24 hours with a sudden onset is sug-
gestive of vestibular neuronitis when not associated with
hearing loss and with viral labyrinthitis when associated with
hearing loss.17 However, sudden-onset vertigo associated
with hearing loss and tinnitus can also represent a brainstem
stroke.18 Vertigo brought about by straining or other Valsalva-
like maneuvers are associated with perilymphatic fistula, Chiari
malformation, and superior semicircular canal dehiscence.17
There is also vertigo induced by sound, which is known as the
Tullio phenomenon. This can be associated with perilymph
 chapter 25 examination of hearing and balance
fistula, Meniere’s disease, congenital inner ear malformations,
Lyme disease, and superior semicircular canal dehiscence.19
Taking the history of the dizzy patient may be the most dif-
ficult part of the balance examination, but when done in an
organized fashion, sometimes with the help of a questionnaire
or preprinted template, it can be extremely useful in knowing
what to look for in subsequent tests and examinations.
Physical Examination
The physical examination of a patient with a balance disorder
should contain a complete head and neck examination, includ-
ing a detailed neurotological examination specifically using
oculomotor function testing, positional testing, and postural
control testing.
Head and Neck Examination
The head and neck examination is similar to that described pre-
viously. Additional information can be found by performing a
fistula test, which can be done by either tragal pressure or
pneumatic otoscopy. The patient is instructed to look straight
ahead, and continuous positive and negative pressure is applied.
Normally, the eyes will not drift, but a positive fistula test (Hen-
nebert’s sign) is manifest by the eyes drifting away from the
tested ear with positive pressure and toward the tested ear with
negative pressure. A positive fistula test is associated with a per-
ilymph fistula, Meniere’s disease, or superior semicircular canal
dehiscence.17,19
The cranial nerve examination should be as thorough as pos-
sible, as every cranial nerve may be potentially affected in
disease processes that cause vertigo. Oculomotor examination
documenting the function of cranial nerves III, IV, and VI
should be performed. Internuclear ophthalmoplegia produced
by lesions in the medial longitudinal fasciculus of the lower
midbrain and pons is important to recognize, as vertigo may be
one of the manifesting signs of multiple sclerosis.16 Subtle
abnormalities in cranial nerves V, VII, and VIII may indicate a
retrocochlear lesion. These can be tested by closely examining
facial symmetry at rest and during movement, performing
the corneal blink reflex test, and performing tuning fork
testing. Usually, though, patients with retrocochlear lesions
will present with hearing loss rather than tinnitus or vertigo.16
Finally, cranial nerves IX, X, XI, and XII should be thoroughly
examined.
Oculomotor Function Testing
The basis for nystagmus and oculomotor testing revolves
around the vestibulo-ocular reflex (VOR). The VOR is a pathway
that associates the activity of paired semicircular canals to a set
of extraocular muscles.20 There are two main types of VOR: the
angular reflex associated with the semicircular canals and the
linear reflex associated with the utricle and saccule. The pur-
poses of the reflex are to maintain binocular vision and to
stabilize images on the fovea during head movement.2 The
pathway involves the vestibule, the vestibular nuclei, and the
oculomotor nuclei with modulation between cerebellar centers.
The easiest reflex pathway to test is the paired horizontal semi-
circular canals with cranial medial and lateral recti muscles.
For example, in a normal individual, there is an equal tonic
323
firing rate of both vestibular nerves in the absence of head
movement, but when the head turns to the left, the endolymph
in the left horizontal canal moves to the right. This displaces
the cupula and consequently the cilia toward the kinocilium,
leading to an increased firing rate in the left superior vestibu-
lar nerve. The opposite effect occurs on the right side. Path-
ways in the brainstem then cause activation of the left medial
rectus and the right lateral rectus, while the left lateral rectus
and right medial rectus are inhibited. The eyes then move con-
jugately to the right in the exact opposing fashion to head rota-
tion until they reach a limit. At this point, a saccade to the left
brings the eyes back to the midline.
When a patient has a unilateral left vestibular lesion, tonic
input from the left vestibular nerve ceases, resulting in unop-
posed input from the right vestibular nerve. This leads to
conjugate eye movements to the left (slow phase), followed by
corrective saccades to the right (fast phase). The direction of
nystagmus is defined by its fast phase. This is a right-beating
spontaneous nystagmus. Right-beating torsional nystagmus
would also occur from unopposed stimulation of the right
superior and inferior canals. Upbeating or downbeating nys-
tagmus is not characteristic of peripheral vestibular lesions and
usually is caused by central lesions. Spontaneous peripheral
nystagmus can be suppressed by visual fixation. The use of
Frenzel lenses that do not allow visual fixation are useful to
increase the examiner’s sensitivity to the patient’s nystagmus.2
Nystagmus can also be enhanced by having the patient look
toward the intact side. Vestibular suppressants, alcohol, and
antiepileptic medications decrease the amplitude of the nys-
tagmus and can make evaluation difficult.16
Gaze nystagmus can be identified by having the patient look
at the examiner’s index finger held at off-center positions. Gaze-
evoked nystagmus is often a side effect of drugs such as anti-
convulsants, benzodiazepines, or alcohol, but when it is present
in the absence of these drugs, it almost always indicates a
central disorder involving the brainstem, cerebellum, or
midbrain depending on its direction, and also tends to be
direction changing.17,20
Head-shaking nystagmus is assessed by having the patient
shake his or her head very rapidly back and forth in the hori-
zontal plane while wearing Frenzel lenses. Shaking is abruptly
stopped, and nystagmus is assessed. Normal individuals usually
have just a beat or two of nystagmus, but individuals with a
unilateral vestibular lesion show nystagmus with the fast phase
toward the intact side.2 Patients with central lesions such as
cerebellar dysfunction may also have post head-shaking nys-
tagmus, often in the vertical direction.2
Nonlinearity testing, or head thrust testing, is performed by
applying quick head thrusts about 15 degrees in the plane of
each semicircular canal from the neutral position while the
patient attempts to fix his gaze on the examiner’s nose. A
normal patient is able to keep his or her gaze on the examiner’s
nose, but a patient with a lesion affecting a semicircular canal
demonstrates a corrective saccade after the head thrust toward
the lesioned side.17
Positional Testing
The first positional test that should be performed is the Dix-
Hallpike maneuver to detect the presence of benign paroxysmal
positional vertigo of the posterior semicircular canal. In this
324 Section V Neuro-Otology
test, the patient is sitting upright on an examination table and
the head is turned 45 degrees to the side in question. The head
is brought quickly down to a position where the head hangs off
the edge of the table and the patient is instructed to look
straight ahead with the eyes open (the patient may also wear
Frenzel lenses if desired).2,17 This position is held for 30
seconds, and in the presence of BPPV, classically the patient has
horizontorotary nystagmus with the fast phase beating toward
the down ear (geotropic), which is delayed in onset and fatiga-
ble. Almost all persons with BPPV have a sensation of spin-
ning.16 Nystagmus of central origin may also manifest itself
during the Dix-Hallpike maneuver, but it usually lasts indefi-
nitely while the patient is in the supine position.16
Postural Control Testing
Postural control testing is based on the vestibulospinal reflex.
These pathways work in conjunction with visual and proprio-
ceptive pathways to help the patient maintain balance. For
example, if your body leans to the left, the left leg extensors are
activated to counteract a change in the patient’s new center of
gravity. With a perceived forward motion, the body sways
forward to maintain the center of gravity.
A simple way to think of this is that balance in gravity
depends on three peripheral components: vision, propriocep-
tion, and the vestibular system. These three components are
bilateral peripheral inputs to the brain, which integrates
balance, whereas the cerebellum is considered a central input.
Taking away one of the inputs places the burden of maintain-
ing balance on the other two inputs, and taking away two of the
inputs places all of the burden on the one remaining input. This
is analogous to a person standing in darkness having to rely on
vestibular inputs and proprioception to maintain balance.16
The Romberg test was originally described for tabes dorsalis
and primarily tests proprioception.16,21 In this test, the patient
stands with both feet together with the arms either folded in
front or down at the sides. Then the patient closes his or her
eyes and attempts to keep balance. Patients with a unilateral
vestibular lesion tend to fall toward the lesioned side. The
tandem Romberg test is a variant that requires patients to stand
with one foot directly in front of the other. This increases its
sensitivity.16
The Fukuda stepping test is performed with the patient’s
arms straight out in front and the eyes closed. The patient then
marches in place. A vestibular lesion is indicated if the patient
is turned more than 30 degrees from the original position
after approximately 50 steps. Usually, patients turn toward
the diseased side. Patients with a vestibular lesion with a
positive Fukuda stepping test are usually surprised by the
result, as they do not sense that they are rotating during the
test.16
Another test of vestibulospinal function is the tandem gait
test, in which the patient is asked to step heel-to-toe with
his/her eyes closed. Normal individuals can do this for at least
10 steps, but patients with vestibular disorders fail this test.17
The past pointing test is done by having the patient and exam-
iner stand facing each other with arms extended forward and
their index fingers in contact with one another. The patient
then raises his or her arms up and brings his or her fingers into
contact again with the examiner’s, first with the eyes open and
then with the eyes closed. Failure of this test can indicate an
abnormality in the vestibulospinal pathway.2,17
Electronystagmography
Electronystagmography is a combination of tests based on the
VOR that provides important information about the vestibular
and ocular systems. Results of the electronystagmographic
battery should be used in conjunction with findings from the
history, the physical examination, and other studies to arrive at
a diagnosis.22
Electro-oculography
Electro-oculography is used to record eye movements during
electronystagmographic testing. It is based on the corneoreti-
nal potential (difference in electrical charge between the cornea
and the retina), with the long axis of the eye acting as a dipole.
Movements of the eye relative to the surface electrodes placed
around the eye produce an electrical signal that corresponds to
eye position. Recordings of eye movement are accurate to about
0.5 degree, but it is still less sensitive than visual inspection,
which can perceive movements of about 0.1 degree.2 Therefore,
visual inspection with Frenzel lenses is sometimes still
necessary to document nystagmus of low amplitude. Another
limitation of electro-oculography is that torsional eye move-
ments cannot be monitored. Again, visual inspection with
Frenzel lenses is sometimes necessary to document torsional
nystagmus.2
Fortunately, new techniques have been developed to provide
greater accuracy and breadth for oculomotor testing. The most
clinically useful technique that has been developed is the
infrared video electronystagmographic system. Here, the
patient wears goggles that illuminate the eyes with infrared
light (invisible to the patient), allowing a small video camera
to pick up and project an image of the eyes onto a monitor.
This can also assess eye movement in horizontal, vertical,
and torsional directions and is more accurate than electro-
oculography.22
Oculomotor Testing
Oculomotor testing measures the accuracy, latency, and veloc-
ity of eye movements in response to a stimulus (usually an LED
light). The tests performed include tests for saccades, smooth
pursuit, and optokinetic nystagmus. Saccades are rapid eye
movements that bring objects from the peripheral visual fields
onto the fovea. They are controlled by the occipitoparietal
cortex, the frontal lobe, the basal ganglia, the superior collicu-
lus, the cerebellum, and the brainstem.17 During saccade
testing, the patient follows the LED, which flashes sequentially
in positions 15 to 20 degrees to the right or left of center. The
test is repeated vertically. The latency, peak eye velocity, and
accuracy are then calculated. The latency is the time lag
between presentation of the stimulus and the beginning of a
saccade. Prolonged or shortened latency, as well as differences
in latency between eyes, are usually indicative of neurodegen-
erative disease. Abnormally slow peak velocities can be caused
by sedative drugs, drowsiness, cerebellar disorders, basal
ganglia disorders, and brainstem lesions. Abnormally fast
 chapter 25 examination of hearing and balance
velocities are found with calibration errors and eye muscle
restrictions. Asymmetrical velocities are caused by internuclear
ophthalmoplegia, eye muscle restriction, and cranial nerves III
and VI palsies. Poor accuracy, described as overshoot or under-
shoot dysmetria, usually indicates cerebellar, brainstem, or
basal ganglia abnormalities.17
Smooth pursuit describes eye movements that are generated
when tracking moving objects. In smooth pursuit testing, the
patient follows an LED moving back and forth between two
points at a constant velocity. The gain and phase are then cal-
culated. Gain is the ratio of the eye velocity to the target veloc-
ity. Abnormally low gain is suggestive of a central disorder
(brainstem or cerebellum).17 Phase is the difference in time
between eye movement and target movement. Abnormalities
here also indicate central nervous system disorders.17 The mor-
phology of the smooth pursuit tracing can be analyzed. A sac-
cadic pattern of smooth pursuit is associated with a cerebellar
disorder.22 Acute peripheral vestibular lesions can also impair
smooth pursuit when the eyes are trying to move opposite the
slow phase of spontaneous nystagmus.17
Optokinetic nystagmus is tested by having the patient look
ahead while seated in a rotating drum with black and white
stripes on it. When the patient tries to look straight ahead,
there will be small involuntary excursions of the eye (stare nys-
tagmus). When the patient follows a target, smooth pursuit is
tested (look nystagmus). Both types of nystagmus are probably
responsible for eye movement during stimulation. However,
when the lights go out, the patient with an intact optokinetic
system will continue to have nystagmus for about 25
seconds⎯optokinetic after nystagmus (OKAN).22 The optoki-
netic system is distributed widely throughout the brainstem
and cerebellum, so abnormalities are difficult to localize.
However, absence or asymmetry of OKAN can occur with
peripheral vestibular lesions. Bilateral lesions tend to greatly
reduce or eliminate OKAN, whereas unilateral lesions can
result in asymmetrical OKAN with prolonged nystagmus
directed at the site of lesion.22,23
Spontaneous and Gaze Nystagmus
The electronystagmogram can record eye movements associ-
ated with spontaneous and gaze-evoked nystagmus similar to
that described earlier (see Physical Examination). An advantage
of electronystagmography over physical examination is that eye
movements can be monitored with the eyes closed. If during
any part of the test nystagmus is identified with the eyes closed,
the patient is then told to open the eyes so that changes in nys-
tagmus can be detected. Patients with peripheral causes of nys-
tagmus and a normal central pathway are able to suppress the
nystagmus with the eyes open. This is called fixation suppres-
sion. A central lesion is suggested when there is no fixation sup-
pression and the nystagmus continues with the eyes open.22
Positional and Positioning Tests
Positional tests measure the response to changes in the direc-
tion of gravitational force. With the eyes closed, the patient is
moved slowly into a series of stationary positions, and the pres-
ence of nystagmus is assessed, which can be fixed or direction
changing. Positional nystagmus from a peripheral lesion can
fatigue with repeated testing, is usually fixed in direction, and
325
usually does not change independent of head movement.
Nystagmus that changes in direction independent of head
movement is suggestive of a central lesion.22
Positioning tests include the Dix-Hallpike maneuver, among
others. The patient is positioned as described earlier (see Phys-
ical Examination), and the presence of nystagmus is noted. If
the patient has nystagmus, the test is repeated to see if the
response fatigues. If the response fatigues, it is suggestive of a
peripheral disorder, but if it does not, it suggests a central
lesion.22
Caloric Testing
Caloric testing is a very important part of electronystagmogra-
phy in that it is one of the few tests that allows one labyrinth
to be examined independently of the other.2 Horizontal nystag-
mus is induced by stimulation of the horizontal semicircular
canal using a cold and warm stimulus (air or water). The patient
lies in the supine position with the head tilted 30 degrees
upward to bring the horizontal canal into the vertical plane
(direction of gravity), making it more sensitive to the flow of
endolymph.17 The external canal is irrigated with 250 mL of
water at 30ºC and 44ºC for about 30 seconds each. Alternatively,
air at temperatures of 24ºC and 50ºC can be used.
For example, a cold stimulus in the left ear causes the
endolymph of the horizontal canal to fall (as if the head was
turning right and the endolymph was moving left) and the
cupula moves the cilia in an ampullofugal direction away from
the kinocilium, causing a decreased firing rate in the left
vestibular nerve and inhibition of the left medial rectus and the
right lateral rectus via the VOR. The eyes then drift conjugately
to the left (slow phase) and corrective saccades bring the eyes
back to the right (fast phase)⎯this results in a right-beating
nystagmus. The opposite occurs with warm stimulation. A
mnemonic used to determine the direction of the fast phase of
nystagmus in cold and warm stimulation is “COWS”: Cold
Opposite, Warm Same.
The measured value of the induced nystagmus for each stim-
ulus is the peak slow-phase velocity averaged over a 10-second
period.17 The difference between the sides is calculated, and any
difference greater than 20% to 25% between sides is considered
significant and indicates weakness of the vestibular labyrinth
or nerve on the less active side. Directional preponderance,
which compares the peak slow-phase velocities of eye move-
ments to the right with the left, can also be calculated. A dif-
ference of 25% to 30% is considered significant and indicates
an imbalance but is a nonlocalizing measure.16
Rotational Chair Testing
Rotational chair testing measures the VOR response to small
rotations of the body around an axis. It can be useful in moni-
toring changes in vestibular function over time (especially
bilateral lesions or lesions from vestibulotoxic medications),
monitoring compensation following acute injury, and identify-
ing residual vestibular function in patients with no response
during caloric testing.22 The easiest canal to test is the hori-
zontal canal. The patient is fitted with electro-oculographic
electrodes and rotated slowly around a vertical axis with the
eyes covered. The patient then undergoes sinusoidal harmonic
acceleration, during which the patient is rotated back and forth
326 Section V Neuro-Otology
at gradually increasing frequencies to a peak angular velocity
of about 50 degrees per second.16 The three values analyzed are
phase, gain, and symmetry.
Phase measures the timing of eye movement relative to head
movement. In individuals with an intact VOR, the direction of
slow phase eye velocity is exactly opposite head velocity, but
patients with a vestibular or cerebellar lesion have an abnor-
mal phase, with either a phase lead or lag. Gain is the ratio of
the slow phase eye velocity to the head velocity. Abnormally low
gain may indicate bilateral peripheral vestibular weakness,
whereas abnormally high gain may be seen in cerebellar
lesions.17 Symmetry measures the difference between slow
phase velocities associated with rightward and leftward rota-
tion and can suggest involvement of the central pathways or
peripheral vestibular dysfunction.17
Computerized Dynamic Posturography
Posturography is a quantitative test of the vestibulospinal
reflex. It has the same basis as the Romberg test, where three
peripheral inputs of vision, the labyrinth, and proprioception
are integrated for a patient to maintain balance. If one of these
inputs is taken away, the patient has to rely on the remaining
inputs to maintain balance. No one input can be measured by
itself. Patients with cerebellar lesions and certain cortical
lesions are characteristically ataxic and will have poor results
on posturography.16 There are two tests in posturography: the
sensory organization test and the motor control test.
In the sensory organization test, the patient is subjected to
six conditions. In condition 1, the patient stands on a fixed plat-
form with the eyes open and looks at a fixed visual surround.
In condition 2, the platform is fixed, but the eyes are covered,
forcing the patient to rely on proprioceptive and vestibular
cues. In condition 3, the platform is fixed and the eyes are open,
but the visual surround moves in reference to body sway,
forcing the patient to ignore the visual stimulus and rely on
proprioceptive and vestibular cues. In condition 4, the eyes are
open and the visual surround is fixed, but the platform sways,
taking away proprioception, which forces the patient to rely on
visual and vestibular cues. Patients with vestibular dysfunction
still tend to do well in condition 4. In condition 5, the platform
sways and the eyes are covered, forcing the patient to rely on
vestibular cues alone⎯patients with vestibular dysfunction
tend to fall here. In condition 6, the eyes are open, but both the
platform and visual surround move, forcing the patient to rely
on vestibular cues while ignoring inaccurate proprioceptive and
visual cues.2 Patients with vestibular dysfunction tend to fall
here as well. The parameter measured is the patient’s anterior
and posterior body sway, and is measured on a 0-to-100 scale
(fall = 0, no sway = 100).22
Motor control tests evaluate the automatic postural
responses to forward and backward horizontal movements of
the platform. The main parameter tested here is latency. A pro-
longed latency in both directions suggests a central lesion,
whereas a prolonged latency in only one direction suggests
either a peripheral or central lesion.17
Although posturography results tend not to localize lesions,
they are useful for planning vestibular rehabilitation. Postur-
ography may also aid in the detection of malingerers, who tend
to have inconsistent results and may do more poorly on condi-
tions 1 and 2 than on conditions 5 and 6.2
Other Testing
Additional tests that may be useful in the balance evaluation
are audiometric tests, radiographic tests, and blood tests.
Audiometric tests are extremely important in the evaluation of
dizziness. Every patient should at least have an audiogram and
immittance testing. A unilateral hearing loss supports a periph-
eral cause of vertigo, and reduced speech discrimination scores
may prompt a search for a retrocochlear abnormality such as
an acoustic neuroma.16 Radiographic tests such as an MRI will
be able to detect acoustic neuromas, multiple sclerosis, and
brainstem strokes. CT scans may detect middle and inner ear
anomalies such as a cholesteatoma eroding into the semi-
circular canals or a superior semicircular canal dehiscence.
Finally, blood tests looking for thyroid function, glucose toler-
ance, syphilis, rheumatoid factor, and ANA may also be useful
in helping to diagnose a dizzy patient.
K E Y P O I N T S
● Hearing loss and balance disorders are two of the most
common reasons why patients visit their physicians.
● There are three main forms of hearing loss: conductive,
sensorineural, and mixed. Each can be caused by a wide
variety of conditions, ranging from benign conditions,
such as cerumen impaction, to potentially life-threatening
diseases, such as squamous cell carcinoma of the temporal
bone.
● A thorough history is one of the most important aspects of a
hearing evaluation.
● A complete head and neck examination can give many clues
to the cause of a patient’s hearing loss.
● Audiological testing has been available for decades, but
developments over the years have advanced the field of
audiology to include tests and procedures that can deter-
mine the site of lesion with far greater accuracy than before.
Otolaryngologists and audiologists often need to rely on one
another to diagnose accurately the cause of a patient’s
hearing loss using a combination of the history, physical
examination, and results of various audiological tests.
● The diagnosis and treatment of patients with “dizziness”
can be very challenging and frustrating for the patient, the
neurologist, the otolaryngologist, and the audiologist. A
huge variety of disorders can cause the patient to have a
sensation of dizziness, and a huge variety of terms can be
used to describe it (lightheadedness, spinning, “swimming
sensation,” “things not being right in the head”).
● Often, the diagnosis is made by piecing together many
different pieces of information. Not every case of dizziness
can be completely cured or diagnosed exactly. An organized,
systematic approach is necessary to make a reasonably
accurate diagnosis and avoid confusion. Key components in
the evaluation of dizziness include the history, physical
examination, electronystagmography, rotary chair testing,
and computerized dynamic posturography testing.
 chapter 25 examination of hearing and balance
Suggested Reading
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Cueva RA: Auditory brainstem response versus magnetic resonance
imaging for the evaluation of asymmetric sensorineural hearing
loss. Laryngoscope 2004; 114:1686-1692.
Kileny PR, Zwolan TA: Diagnostic and rehabilitative audiology. In
Lustig LR, Cummings CW, eds: Cummings Otolaryngology
Head and Neck Surgery. St Louis: Mosby Elsevier, 2004, pp
3483-3502.
Satar B: Vestibular testing. In Lalwani AK, ed: Current Diagnosis
and Treatment in Otolaryngology⎯Head and Neck Surgery.
New York: McGraw-Hill, 2004, pp 643-658.
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