2558 CHAPTER 400  Hearing and Equilibrium

400 
HEARING AND EQUILIBRIUM
ROBERT W. BALOH AND JOANNA C. JEN

  DISORDERS OF THE AUDITORY SYSTEM

  DEFINITION
The normal ear can detect sound frequencies ranging between 20 and 20,000 Hz;
the upper range drops off fairly rapidly with advancing age. The ear is most
sensitive between 500 and 4000 Hz, which roughly corresponds to the fre-
quency range most important for understanding speech. The hearing level in
this range has several practical implications in terms of the degree of handicap
and the potential for useful correction with amplification. A 30- to 40-dB
hearing level in the speech range would impair normal conversation, whereas
an 80-dB hearing level would make everyday auditory communication almost
impossible (the social definition of deafness).

  EPIDEMIOLOGY
About 5% of the world population suffers from disabling hearing loss (defined
by the World Health Organization as greater than 40 dB in the better hearing
ear in adults and greater than 30 dB in the better hearing ear in children). The
prevalence of disabling hearing loss is twice as high in poorer countries com-
pared with richer countries. The prevalence increases with every age decade,
and it is higher in men than in women across all age decades. Hearing loss is
independently associated with accelerated cognitive decline, incident cognitive
impairment, and a higher risk of accidental injury1 in community-dwelling
older adults.

  PATHOBIOLOGY
Localization of Lesions within the Auditory Pathways
Conductive hearing loss results from lesions involving the external or middle
ear. It is typically characterized by an approximately equal loss of hearing at
all frequencies and by well-preserved speech discrimination once the threshold
for hearing is exceeded. Patients with conductive hearing loss can hear speech
in a noisy background better than in a quiet background because they can
understand loud speech as well as anyone.
Sensorineural hearing loss results from lesions of the cochlea or auditory
division of the eighth cranial nerve, or both. With sensorineural hearing loss,

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 CHAPTER 400  Hearing and Equilibrium
 
2558.e3

ABSTRACT KEYWORDS
The neural pathways subserving hearing and those most important for equi- hearing loss
librium and spatial orientation are anatomically proximate in much of their sudden deafness
course from their end organs in the inner ear to their termination in the superior tinnitus
portion of the temporal lobe. Because of the close anatomic linkage, disorders vertigo
that affect hearing often affect equilibrium, and vice versa. Nevertheless, sub- benign paroxysmal positional vertigo
stantial pathophysiologic differences make clinical examination of the two Meniere disease
systems different. The auditory system is relatively isolated physiologically, acoustic neuroma
so that function and dysfunction can be tested independently of other neural
systems. In contrast, the vestibular system has many close physiologic links
with other neural systems (particularly the visual-oculomotor, somatosensory,
and autonomic systems) and can be difficult to test in isolation of these other
systems. Abnormalities of the auditory system lead to only a few well-defined
and unique symptoms (i.e., hearing loss or tinnitus). Abnormalities of the
vestibular system can mimic disorders of other neural structures when they
cause dizziness, visual distortion (oscillopsia), imbalance, nausea, vomiting,
and even syncope.

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 CHAPTER 400  Hearing and Equilibrium
Hearing Impacted cerumen
Loss Otitis media
Abnormal Cholesteatoma
History Ear Drum perforation
examination Trauma
Normal
Drugs
Noise exposure Pure tone Sensorineural
Hereditary factors audiogram hearing loss
Intrauterine factors
Trauma Conductive
hearing loss
Otosclerosis
Ossicular chain
Impedance dysfunction
audiometry Serous otitis
Eustachian tube
dysfunction
FIGURE 400-1.  Evaluation of hearing loss. BAER = brain stem auditory evoked response; C-P = cerebellopontine.
the hearing levels for different frequencies are usually unequal, typically result-
ing in better hearing for low- than for high-frequency tones. Patients with
sensorineural hearing loss often have difficulty in hearing speech that is mixed
with background noise and may be annoyed by loud speech. Three important
manifestations of sensorineural lesions are diplacusis, recruitment, and tone
decay. Diplacusis and recruitment are common with cochlear lesions; tone
decay usually accompanies eighth nerve involvement.
Central hearing disorders result from lesions of the central auditory pathways.
As a rule, patients with central lesions do not have impaired hearing for pure
tones, and they can understand speech as long as it is clearly spoken in a quiet
environment. If the listener’s task is made more difficult with the introduction
of background noise or competing messages, performance deteriorates more
markedly in patients with central lesions than in normal subjects.
  DIAGNOSIS
Evaluation
Bedside Test
A quick test for hearing loss in the speech range is to observe the response to
spoken commands at different intensities (whisper, conversation, shouting).
Tuning fork tests permit a rough assessment of the hearing level for pure tones
of known frequency. The clinician can use his or her own hearing level as a
reference standard. In the Rinne test, nerve conduction is compared with
bone conduction by holding a tuning fork (preferably 512 Hz) against the
mastoid process until the sound can no longer be heard. It is then placed 1
inch from the ear and, in normal subjects, can be heard about twice as long
by air as by bone. If bone conduction is better than air conduction, the hearing
loss is conductive, but care must be taken to ensure that the bone conduction
is not heard in the normal ear. In the Weber test, the tuning fork is placed on
the patient’s forehead or upper teeth. Normally, this sound is referred to the
center of the head. If it is referred to the side of unilateral hearing loss, the
hearing loss is conductive; if it is referred away from the side of unilateral
hearing loss, the loss is sensorineural.
Audiometry
Pure tone testing is the cornerstone of most auditory examinations. Pure tones
at selected frequencies are presented through either earphones (air conduc-
tion) or a vibrator pressed against the mastoid portion of the temporal bone
(bone conduction), and the minimal level that the subject can hear (threshold)
is determined for each frequency. Two speech tests are routinely used. The
speech reception threshold is the intensity at which the patient can correctly
repeat 50% of the words presented. The speech reception threshold is a test
of hearing sensitivity for speech and should reflect the hearing level for pure
tones in the speech range. The speech discrimination test is a measure of the
patient’s ability to understand speech when it is presented at a level that is
easily heard. In patients with eighth nerve lesions, speech discrimination scores
can be severely reduced, even when pure tone thresholds are normal or nearly
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2559
Acoustic neuroma
Other C-P angle
Neuroimaging tumor
Multiple sclerosis
Brain stem infarct
Abnormal
BAER
Normal Perilymph
Abnormal
fistula
Fistula
test Labyrinthitis
Labyrinthine
infarct
Normal
Meniere disease
Presbycusis
Noise induced
normal; by comparison, in patients with cochlear lesions, discrimination tends
to be proportional to the magnitude of hearing loss.
Brain stem auditory evoked responses can be recorded from scalp electrodes
at 0 to 10 msec (early), 10 to 50 msec (middle), and 50 to 500 msec (late)
following a click (a high-frequency stimulus). The early potentials reflect elec-
trical activity at the cochlea, eighth cranial nerve, and brain stem; the later
potentials reflect cortical activity. Computer averaging of the responses to
1000 to 2000 clicks separates the evoked potential from background noise.
Early evoked responses may be used to estimate the magnitude of hearing
loss and to differentiate among cochlea, eighth nerve, and brain stem lesions.
Differential Diagnosis
Conductive Hearing Loss
The history, examination, and audiometry usually provide the key differential
features for identifying common causes of hearing loss (Fig. 400-1). Asym-
metric hearing loss in adults in usually idiopathic.2
Otosclerosis commonly produces progressive conductive hearing loss by
immobilizing the stapes with new bone growth in front of and below the oval
window. The hearing loss is typically conductive, although in some persons
the cochlea may be invaded by foci of otosclerotic bone, producing an addi-
tional sensorineural hearing loss. Otosclerosis usually stabilizes when the
hearing level reaches 50 to 60 dB and rarely progresses to deafness.
The most common cause of reversible conductive hearing loss is impacted
cerumen in the external canal. This benign condition is usually first noticed
after bathing or swimming when a droplet of water closes the remaining tiny
passageway. The most common serious cause of conductive hearing loss is
inflammation of the middle ear, otitis media, either infective (suppurative;
see Fig. 398-9) or noninfective (serous). Chronic otitis media with perfo-
ration of the tympanic membrane can result in an invasion of the middle
ear and other pneumatized areas of the temporal bone by keratinizing squa-
mous epithelium (cholesteatoma). Cholesteatomas can produce erosion of
the ossicles and bony labyrinth, thereby resulting in a mixed conductive and
sensorineural hearing loss. Barotrauma to the middle ear arises with otalgia and
hearing loss and can be associated with serous effusion or hematotympanum
(see Fig. 398-10). Other causes of conductive hearing loss include trauma,
congenital malformations of the external and middle ear, and glomus body
tumors.
Sensorineural Hearing Loss
Hereditary Deafness
Genetically determined deafness, usually from hair cell aplasia or deteriora-
tion, may be present at birth or may develop in adulthood. The diagnosis of
hereditary deafness rests on the finding of a positive family history. Mutations
in connexin 26, a key component of gap junctions in the inner ear, account
for most cases of recessively inherited deafness. Intrauterine factors resulting in
congenital hearing loss include infection (especially rubella); toxic, metabolic,
2560 CHAPTER 400  Hearing and Equilibrium
and endocrine disorders; and anoxia associated with Rh incompatibility and
difficult deliveries.
Cochlear Damage
Acute unilateral deafness usually has a cochlear basis. Bacterial or viral infec-
tions of the labyrinth, head trauma with fracture or hemorrhage into the cochlea,
or vascular occlusion of a terminal branch of the anterior inferior cerebellar
artery can extensively damage the cochlea and the vestibular labyrinth. An
isolated sudden unilateral sensorineural hearing loss is presumed to reflect a
viral infection of the cochlea and auditory nerve terminals. High-dose steroids
followed by a rapid taper are recommended (see Treatment).
Sudden unilateral hearing loss often associated with vertigo and tinnitus
can result from a perilymphatic fistula. Such fistulas may be congenital or may
follow stapes surgery or head trauma.
Drugs
Drugs cause acute and subacute bilateral hearing impairment. Salicylates, furo-
semide, and ethacrynic acid have the potential to produce transient deafness
when they are taken in high doses. More toxic to the cochlea are aminoglycoside
antibiotics (gentamicin, tobramycin, amikacin, kanamycin, streptomycin, and
neomycin). These agents can destroy cochlear hair cells in direct relation to
their serum concentrations. Some antineoplastic chemotherapeutic agents,
particularly cisplatin, cause severe ototoxicity.
Meniere Disease
Subacute relapsing cochlear deafness occurs with Meniere disease, a condition
associated with fluctuating hearing loss and tinnitus, recurrent episodes of
abrupt and often severe vertigo, and a sensation of fullness or pressure in the
ear. Recurrent endolymphatic hypertension (hydrops) is believed to cause
the episodes. On pathologic examination, the endolymphatic sac is dilated,
and the hair cells become atrophic. The resulting deafness is subtle and revers-
ible in the early stages but subsequently becomes permanent and is character-
ized by diplacusis and loudness recruitment. The disorder is usually unilateral,
but in about 20 to 40% of patients, bilateral involvement eventually occurs.
Presbycusis
The gradual, progressive, bilateral hearing loss commonly associated with
advancing age is called presbycusis. Presbycusis is not a distinct disease entity
but rather represents multiple effects of aging on the auditory system. It may
include conductive and central dysfunction, although the most consistent
effect of aging is on the sensory cells and neurons of the cochlea. The typical
audiogram of presbycusis is a symmetrical high-frequency hearing loss gradu-
ally sloping downward with increasing frequency. The most consistent patho-
logic finding associated with presbycusis is degeneration of sensory cells and
nerve fibers at the base of the cochlea.
Noise
The recurrent trauma of noise-induced hearing loss affects approximately the
same region at the base of the cochlea and is also common, particularly among
those with exposure to loud explosive or industrial noises. Loud, blaring,
modern music has become a recent offender. The loss almost always begins
at 4000 Hz and does not affect speech discrimination until late in the disease
process. With only brief exposure to loud noise (hours to days), there may
be only a temporary threshold shift, but with continued exposure, permanent
injury begins. The duration and intensity of exposure determine the degree
of permanent injury, but estimates suggest that nearly 25% of American adults
have some degree of noise-induced hearing damage or loss.3
Acoustic Neuroma
Progressive unilateral hearing loss, which arises insidiously, initially in the
high frequencies, and worsens by almost imperceptible degrees, is characteristic
of benign neoplasms of the cerebellopontine angle, most commonly acoustic
neuromas. In about 10% of cases, the hearing loss can be acute, apparently
due to either hemorrhage into the tumor or compression of the labyrinthine
vasculature. Magnetic resonance imaging (MRI) with contrast enhancement
reliably identifies small acoustic neuromas.
Central Hearing Loss
Central hearing loss is unilateral only if it results from damage to the pontine
cochlear nuclei on one side of the brain stem from conditions such as ischemic
infarction of the lateral brain stem (e.g., occlusion of the anterior inferior cer-
ebellar artery [Chapter 379]), a plaque of multiple sclerosis (Chapter 383), or,
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rarely, invasion or compression of the lateral pons by a neoplasm or hematoma
(Chapters 180 and 371). Bilateral degeneration of the cochlear nuclei accom-
panies some of the rare recessive inherited disorders of childhood. As noted,
clinically important unilateral hearing loss never results from neurologic disease
arising rostral to the cochlear nucleus. Although bilateral hearing loss could, in
theory, result from bilateral destruction of central hearing pathways, in practice
this is rare because involvement of neighboring structures in the brain stem
or hemisphere would usually produce overwhelming neurologic disability.
TREATMENT 
If an underlying disorder has not yet destroyed the auditory system and can
be ameliorated medically or surgically, hearing may be improved or preserved.4
Most patients with otosclerosis respond to stapedectomy. Closure of a perilymph
fistula may improve hearing. Antibiotic and decongestive treatment of otitis
media (Chapter 398) should prevent permanent hearing loss.
A brief course of high-dose steroids is commonly used for patients with
idiopathic sudden unilateral sensorineural deafness, but the evidence to support
this approach is limited. Intratympanic corticosteroid treatment (four doses of
40 mg/mL of methylprednisolone during 2 weeks) is not inferior to oral treatment
(60 mg/day of oral prednisone followed by a 5-day taper) for idiopathic sudden
sensorineural hearing loss, A1  and combination oral and intratympanic therapy
may be better than either alone. A2  A low-salt diet and diuretics are effective in
selected cases of Meniere disease. Folic acid supplementation appears to reduce
the rate of hearing loss in the elderly. Hearing aids amplify sound, usually with
the goal of making speech intelligible. Patients with conductive hearing loss
require simple amplification, but those with sensorineural hearing loss often
need frequency-selective amplification to make hearing aids useful. Cochlear
implants can markedly help patients of all ages with profound hearing loss if
they have some intact auditory nerve fibers.5 Intense postoperative speech
recognition training is required.
  PREVENTION
Noise-induced hearing loss can be prevented with the use of ear plugs and
other noise-reducing interventions. A3  Recent evidence also suggests that ebselen
(a glutathione peroxidase 1 mimic at 400 mg twice daily 2 days before and 2
days after a noise challenge) can prevent noise-induced damage. A4 
  Tinnitus
  DIAGNOSIS
As many as 10% of U.S. adults may complain of tinnitus. The evaluation of
common causes of tinnitus (Fig. 400-2) begins with a careful history to identify
common offending drugs.6
Objective Tinnitus
With objective tinnitus, the patient hears a sound arising external to the audi-
tory system, a sound that can usually be heard by the examiner with a stetho-
scope. Objective tinnitus usually has benign causes, such as noise from
temporomandibular joints, opening of eustachian tubes, or repetitive muscle
contractions. Sometimes, in a quiet room, the patient can hear the pulsatile
flow in the carotid artery or a continuous hum of normal venous outflow
through the jugular vein. The latter can be obliterated by compression of the
jugular vein or extreme lateral rotation of the neck. Pathologic objective tin-
nitus occurs when patients hear turbulent flow in vascular anomalies or tumors
(e.g., glomus jugulare tumor). Objective tinnitus may also be an early sign of
increased intracranial pressure. Such tinnitus, which probably arises from
turbulent flow through compressed venous structures at the base of the brain,
is usually overshadowed by other neurologic abnormalities.
Subjective Tinnitus
Subjective tinnitus can arise from sites anywhere in the auditory system. The
sounds most frequently reported are metallic ringing; buzzing; blowing; roaring;
or, less often, bizarre clanging, popping, or nonrhythmic beating. Tinnitus
heard as a faint, moderately high pitched, metallic ring can be observed by
almost anyone who concentrates attention on auditory events in a quiet room.
Sustained louder tinnitus accompanied by audiometric evidence of deafness
occurs in association with both conductive and sensorineural hearing loss.
Tinnitus observed with otosclerosis tends to have a roaring or hissing quality,
and that associated with Meniere disease often produces sounds that vary
widely in intensity with time and quality, sometimes including roaring or
clanging. Tinnitus with auditory nerve lesions tends to be higher pitched and
 CHAPTER 400  Hearing and Equilibrium
 
2561

Synchronous Patent eustachian

with respiration tube

Aneurysm
Audible Synchronous Vascular malformation
sounds with pulse Vascular tumor
Venous hum

Tinnitus Venous hum

Continuous
Acoustic emissions

History Ear
examination Impacted cerumen
Conductive Chronic otitis
hearing loss Acoustic neuroma
Otosclerosis
Common No audible Other C-P angle
offending drugs: sounds tumors
Quinidine Abnormal Vascular
Salicylates (neural) compression
Neurologic Sensorineural
Indomethacin Normal Audiogram BAER
examination hearing loss
Carbamazepine Normal Noise damage
Propranolol (cochlear) Ototoxic drugs
Levodopa Brain stem
Labyrinthitis
Aminophylline signs
Meniere disease
Caffeine Idiopathic
Normal Perilymph fistula
Multiple sclerosis tinnitus
Presbycusis
Tumor
Ischemic infarction

FIGURE 400-2.  Evaluation of tinnitus. BAER = brain stem auditory evoked response; C-P = cerebellopontine.

ringing in quality. Audiometric and brain stem evoked response testing can
help distinguish between lesions involving the conducting apparatus, the
cochlea, and the auditory nerve. Tinnitus without observable deafness appears
sporadically and for variable lengths of time in many persons without other
evidence of an ongoing pathologic process.
TREATMENT  or away from the cupula, bending the cilia and, depending on the direction
Most patients with tinnitus can be helped by a careful evaluation to exclude
serious underlying conditions and by subsequent reassurance when appropri-
ate.7 Often, exacerbating factors such as chronic anxiety and depression can
be treated. In patients with hearing loss and tinnitus, a hearing aid may improve
tinnitus because the amplification of ambient sound may effectively mask the
tinnitus. This mechanism probably explains the frequent observation that removal
of cerumen from the external auditory canal to improve ambient hearing also
improves tinnitus. Also, when cerumen is attached to the tympanic membrane,
tinnitus may result from local mechanical effects on the conductive system.
For patients who find their tinnitus most obtrusive when trying to sleep, recorded
masking sounds (e.g., white noise, rainfall, mountain stream) can be helpful. A
careful drug history should be taken (see Fig. 400-2), and a drug-free trial period
should be considered when possible.
No medications are approved for the treatment of tinnitus in the United
States or Europe. Benzodiazepines (e.g., diazepam, 2 to 5 mg every 8 hours) or
tricyclic amines (e.g., amitriptyline, 25 to 75 mg at bedtime) may provide tem-
porary symptomatic relief of tinnitus, but cognitive-behavioral therapy, which
can be administered face-to-face or via the Internet, is a more effective long-
term approach that can significantly decrease tinnitus and improve health-
related quality of life. A5  A6  Furthermore, some patients have varying degrees of
,
acceleration and two otolith structures, the utricle and saccule, that detect
linear acceleration (including gravitational). Like the cochlea, these organs
possess hair cells that act as force transducers, converting the forces associated
with head acceleration into afferent nerve impulses. The hair cells of the three
semicircular canals, each of which is oriented at right angles to the others, are
located in the crista, where their cilia are embedded in a gelatinous mass called
the cupula. Movement of the head causes the endolymph to flow either toward
of endolymphatic movements, either exciting or inhibiting the afferent nerves
at the base of the hair cells. The hair cells of the utricle and saccule are located
in an area called the macule. The macule of the utricle lies approximately in
the plane of the horizontal canal, and the macule of the saccule is approximately
in the plane of the anterior canal. The hair cell cilia are embedded in a mem-
brane that contains calcium carbonate crystals or otoliths; the density of otoliths
is considerably greater than that of the endolymph. Linear accelerations of
the head combine with the linear acceleration of gravity to distort the otolith
membrane, thereby bending the cilia of the hair cells and modulating the
activity of the afferent nerve terminals at the base of the hair cells.
The afferent vestibular nerves have their cell bodies in the Scarpa ganglion. The
nerve fibers travel in the vestibular portion of the eighth cranial nerve contigu-
ous to the acoustic portion. Fibers from different receptor organs terminate in
different vestibular nuclei at the pontomedullary junction. There are also direct
connections with many portions of the cerebellum, the greatest representation
being in the flocculonodular lobe, the so-called vestibular cerebellum.
  DIAGNOSIS
Evaluation

spontaneous improvement.8 In patients with concomitant profound bilateral

sensorineural hearing loss, cochlear implants can improve hearing and often History
decrease tinnitus. Most vestibular problems presented to the physician are episodic, and often
there are neither symptoms nor signs when the physician examines the patient.
The history therefore can become paramount for identifying vestibular dys-
function. The history should attempt to distinguish vertigo (the illusion of
  EQUILIBRIUM–VESTIBULAR SYSTEM movement in space) from other types of dizziness (see later).
About 12% of patients with vertigo have a central cause, and about 88%
  PATHOBIOLOGY have a problem with the peripheral vestibular apparatus. In general, peripheral
Anatomy and Physiology of the Vestibular System vertigo is more severe, is more likely to be associated with hearing loss and
The paired vestibular end organs lie within the temporal bones next to the tinnitus, and often leads to nausea and vomiting. Nystagmus associated with
cochlea. Each organ consists of three semicircular canals that detect angular peripheral vertigo is usually inhibited by visual fixation. Central vertigo is

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2562 CHAPTER 400  Hearing and Equilibrium
Focal
neurologic Neuroimaging
Vertigo signs
History Examinations
Hearing loss
Drugs Audiometry
Trauma Normal
Hereditary factors
Migraine
Positional
nystagmus in
plane of canal
Positive
head-thrust
test
FIGURE 400-3.  Evaluation of vertigo. BAER = brain stem auditory evoked response; C-P = cerebellopontine; ENG = electronystagmography.
generally less severe than peripheral vertigo and is often associated with other
signs of central nervous system disease.9 The nystagmus of central vertigo is
not inhibited by visual fixation and frequently is prominent when vertigo is
mild or absent.
Common Causes of Vertigo
Physiologic Vertigo
Physiologic vertigo includes common disorders that occur in healthy people,
such as motion sickness, space sickness, and height vertigo (Fig. 400-3). In these
conditions, vertigo (defined as an illusion of movement) is minimal while
autonomic symptoms predominate. With height vertigo, patients may experi-
ence acute anxiety and panic reaction. Individuals with motion sickness and
space sickness typically develop perspiration, nausea, vomiting, increased
salivation, yawning, and generalized malaise. Gastric motility is reduced and
digestion impaired. Even the sight or smell of food is distressing. Hyperven-
tilation is a common sign, and the resulting hypocapnia leads to changes in
blood volume, with pooling in the lower parts of the body predisposing to
postural hypotension and syncope. An unusual variant of motion-induced
dizziness occurs when the subject returns to stationary conditions after pro-
longed exposure to motion (mal de débarquement syndrome). Typically, affected
patients report that they feel the persistent rocking sensation of a boat long
after returning to solid ground. Rarely, the syndrome can last for months to
years after exposure to motion and can even be incapacitating. The cause is
unknown.
Physiologic vertigo can often be suppressed by supplying sensory cues that
help to match the signals originating from different sensory systems. Thus
motion sickness, which is caused by a mismatch of visual and vestibular signals,
is exacerbated by sitting in a closed space or reading (giving the visual system
the miscue that the environment is stationary). It may be improved by looking
out at the horizon. Height vertigo, caused by a mismatch between sensation
of normal body sway and lack of its visual detection, can often be relieved
either by sitting or by visually fixating a nearby stationary object.
Benign Paroxysmal Positional Vertigo (Canalithiasis)
Benign paroxysmal positional vertigo is by far the most common cause of
vertigo.10 Patients with this condition develop brief episodes of vertigo (less
than 1 minute) with position change, typically when turning over in bed,
getting in and out of bed, bending over and straightening up, or extending
the neck to look up (so-called top-shelf vertigo). Benign paroxysmal positional
vertigo results when otolith debris inadvertently enters one of the semicircular
canals. It can occur after head trauma or inner ear infection but most com-
monly occurs spontaneously in older people and particularly in older women
with osteoporosis. The diagnosis rests on finding characteristic positional
nystagmus in the plane of the affected canal (see later). It is important to
recognize this syndrome because, in most patients, it can be cured by simple
bedside maneuvers (Fig. 400-4). If the history or findings are atypical, the
condition must be distinguished from other causes of positional vertigo that
may occur with tumors or infarcts of the posterior fossa.
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Multiple sclerosis Peripheral
vestibulopathy
Infarction
Tumor Physiologic vertigo
Degenerative disease Ototoxicity
Normal ENG
Labyrinthitis
Sensori- Meniere disease
neural BAER Normal ENG Fistula
loss Labyrinthine
concussion
Benign Abnormal
positional
vertigo
Neuroimaging
Vestibular
neuritis Acoustic neuroma
Ototoxicity Other C-P angle tumor
Acute Peripheral Vestibulopathy (Vestibular Neuritis)
One of the most common clinical neurologic syndromes at any age is the
acute onset of vertigo, nausea, and vomiting lasting for several days and not
associated with auditory or neurologic symptoms. A viral origin is suspected,
but attempts to isolate an agent have been unsuccessful, except for occasional
findings of a herpes zoster infection. Pathologic studies showing atrophy of
one or more vestibular nerve trunks, with or without atrophy of their associ-
ated sense organs, are evidence of a vestibular nerve site and, probably, viral
cause for most patients with this syndrome. Patients gradually improve during
1 to 2 weeks, but residual dizziness and imbalance can persist for months.
Meniere Disease
Meniere disease (see earlier) accounts for about 10% of all patients with
vertigo.11 The diagnosis is based on documenting episodic severe attacks
accompanied by fluctuating hearing levels on audiometric testing beginning
in the low frequencies.
Migraine
Vertigo is a common symptom with migraine (Chapter 370). It can occur
with headaches or in separate isolated episodes, and it can predate the onset
of headache. So-called benign paroxysmal vertigo of childhood is often the
first symptom of migraine. The mechanism of vertigo with migraine is not
clear, but both peripheral and central types of nystagmus can occur with attacks.
A few develop typical features of Meniere disease.
Post-traumatic Vertigo
Vertigo, hearing loss, and tinnitus often follow a blow to the head (Chapter
371) that does not result in temporal bone fracture, termed labyrinthine con-
cussion. Blows to the occipital or mastoid region are particularly likely to produce
labyrinthine damage. Transverse fractures of the temporal bone typically pass
through the vestibule of the inner ear, tearing the membranous labyrinth and
lacerating the vestibular and cochlear nerves. Complete loss of vestibular and
cochlear function is the usual sequela, and the facial nerve is interrupted in
approximately 50% of cases. Examination of the ear often reveals hemotym-
panum (see Fig. 398-10), but bleeding from the ear seldom occurs because
the tympanic membrane usually remains intact. As noted earlier, benign par-
oxysmal positional vertigo is also a common sequela of head trauma. Fistulas
of the oval and round windows can result from impact noise, deep-water
diving, severe physical exertion, or blunt head injury without skull fracture.
Clinically, the rupture leads to the sudden onset of vertigo or hearing loss, or
both. Surgical exploration of the middle ear is warranted when there is a clear
relationship between the onset of vertigo or hearing loss, or both, and the
onset of severe exertion, barometric change, head injury, or impact noise.
Postconcussion Syndrome
The so-called postconcussion syndrome refers to a vague dizziness (not vertigo)
associated with anxiety, difficulty in concentrating, headache, and photophobia
induced by a head injury resulting in concussion (Chapter 371). On occasion,
 CHAPTER 400  Hearing and Equilibrium
 
2563

1 2

A 4

2 3

B
FIGURE 400-4.  Modified Epley (A) and Semont (B) maneuvers for benign positional vertigo affecting the right posterior semicircular canal. The procedure is reversed to treat the
left posterior semicircular canal. The entire sequence should be repeated until no nystagmus is elicited. (From Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for
benign paroxysmal positional vertigo [an evidence-based review]: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2008;70:2067-2074.)

similar but less pronounced symptoms are associated with mild head injury at the bedside with a head-thrust test (bilateral corrective saccades; see later).
judged to be trivial at the time. The cause is unknown, but animal studies Caloric and rotational testing can confirm the vestibular loss. The best treat-
indicate that small multifocal brain lesions (petechiae) commonly occur after ment is prevention. If the drug is discontinued early during the course of
concussive brain injury. symptoms, the disorder may stabilize or improve.

Other Peripheral Causes of Vertigo Vascular Insufficiency

Vertigo can be associated with chronic bacterial otomastoiditis, either from direct
invasion of the inner ear by the bacteria or by erosion of the labyrinth by a
cholesteatoma. Radiographic studies of the temporal bone readily identify
these disorders. Autoimmune inner ear disease typically arises with episodic
vertigo and fluctuating hearing levels similar to Meniere disease, but it is more
fulminant with early bilateral involvement. It can occur in isolation or with
other systemic features of autoimmune disease. About two thirds of patients
have antibodies directed against heat shock protein 70. The aminoglycosides
streptomycin and gentamicin are remarkably selective for vestibular ototoxic-
ity. The patient may suffer acute vertigo if the toxic effect is asymmetrical.
More often, there is a progressive symmetrical loss of vestibular function
leading to imbalance but not vertigo. Unfortunately, many patients being treated
with ototoxic drugs are initially bedridden and unaware of the vestibular
impairment until they recover from their acute illness and try to walk. They
then discover that they are unsteady on their feet and that the environment
tends to jiggle in front of their eyes (oscillopsia). The diagnosis can be made
Vertebrobasilar insufficiency is a common cause of vertigo in older people.
Whether the vertigo originates from ischemia of the labyrinth, brain stem, or
both structures is not always clear because the blood supplies to the labyrinth,
eighth cranial nerve, and vestibular nuclei originate from the same source, the
basilar vertebral circulation (Chapter 378). Vertigo with vertebrobasilar insuf-
ficiency is abrupt in onset, usually lasting several minutes, and is frequently
associated with nausea and vomiting. Associated symptoms resulting from
ischemia in the remaining territory supplied by the posterior circulation include
visual illusions and hallucinations, drop attacks and weakness, visceral sensa-
tions, visual field defects, diplopia, and headache. These symptoms occur in
episodes either in combination with the vertigo or alone. Vertigo may be an
isolated initial symptom of vertebrobasilar ischemia, but repeated episodes
of vertigo without other symptoms should suggest another diagnosis. Verte-
brobasilar insufficiency is usually caused by atherosclerosis of the subclavian,
vertebral, and basilar arteries. MRI of the brain is usually normal because the
vascular insufficiency is transient and function returns to normal between

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2564 CHAPTER 400  Hearing and Equilibrium
episodes. Magnetic resonance angiography can identify occlusive vascular
disease most commonly involving the vertebral-basilar junction.
Vertigo is a common symptom with infarction of the lateral brain stem or
cerebellum (Chapter 379), or both. The diagnosis is usually clear, based on
the characteristic acute history and pattern of associated symptoms and neu-
rologic findings. On occasion, cerebellar infarction or hemorrhage arises with
severe vertigo, vomiting, and ataxia without associated brain stem symptoms
and signs that might suggest the erroneous diagnosis of an acute peripheral
vestibular disorder. The key differential is the finding of clear cerebellar signs
(extremity and gait ataxia); direction-changing, gaze-evoked nystagmus; and
a normal head-thrust test. Such patients must be watched carefully for several
days because they may develop progressive brain stem dysfunction due to
compression by a swollen cerebellum.
Cerebellopontine Angle Tumors
Most tumors growing in the cerebellopontine angle (e.g., acoustic neuroma,
meningioma, epidermal cyst) grow slowly, allowing the vestibular system to
accommodate so that they produce only a vague sensation of disequilibrium
rather than acute vertigo (Chapter 180). On occasion, however, episodic vertigo
or positional vertigo heralds the presence of a cerebellopontine angle tumor.
In virtually all patients, retrocochlear hearing loss is present, best identified
by audiometric testing. MRI with contrast enhancement is the most sensitive
diagnostic study for identifying a cerebellopontine angle tumor.
Other Central Causes of Vertigo
Acute vertigo may be the first symptom of multiple sclerosis (Chapter 383),
although only a small percentage of young patients with acute vertigo eventu-
ally develop multiple sclerosis. Vertigo in multiple sclerosis is usually transient
and often associated with other neurologic signs of brain stem disease, in
particular, internuclear ophthalmoplegia or cerebellar dysfunction. Vertigo
may also be a symptom of parainfectious encephalomyelitis or, rarely, parainfec-
tious cranial polyneuritis. In this instance the accompanying neurologic signs
establish the diagnosis. The Ramsay Hunt syndrome (geniculate ganglion herpes)
is characterized by vertigo and hearing loss associated with facial paralysis
and, sometimes, pain in the ear. The typical lesions of herpes zoster (Chapter
351), which may follow the appearance of neurologic signs, are found in the
external auditory canal and over the palate in some patients. Rarely is herpes
zoster responsible for vertigo in the absence of the full-blown syndrome.
Granulomatous meningitis (Chapter 384) or leptomeningeal metastasis and cere-
bral or systemic vasculitis (Chapter 254) may involve the eighth nerve, produc-
ing vertigo as an early symptom. In these disorders, cerebrospinal fluid analysis
usually suggests the diagnosis (Chapter 368). Patients suffering from temporal
lobe epilepsy (Chapter 375) occasionally experience vertigo as the aura. Vertigo
in the absence of other neurologic signs or symptoms is never caused by
epilepsy or other diseases of the cerebral hemispheres.
Bedside Tests
Hyperventilation
If the history is not clear, bedside provocative tests to mimic the symptom
may assist in making a pathophysiologic diagnosis. Hyperventilation, which
lowers the arterial partial pressure of carbon dioxide (Paco2) and decreases
cerebral blood flow, causes a lightheaded sensation associated with syncope.
Patients with compressive lesions of the vestibular nerve, such as with an
acoustic neuroma or cholesteatoma, or with demyelination of the vestibular
nerve root entry zone may develop vertigo and nystagmus after hyperventila-
tion. Presumably, metabolic changes associated with hyperventilation trigger
the partially damaged nerve to fire inappropriately.
Vestibulospinal Function
Bedside tests of vestibulospinal function are often insensitive because most
patients can use vision and proprioceptive signals to compensate for any ves-
tibular loss. Patients with acute unilateral peripheral vestibular lesions may
past-point or fall toward the side of the lesion, but within a few days, balance
returns to normal. Patients with bilateral peripheral vestibular loss have more
difficulty compensating and usually show some imbalance on the Romberg
and tandem walking tests (Chapter 368), particularly with eyes closed.
Doll’s-Eye and Head-Thrust Tests
The vestibulo-ocular reflex can be tested at the bedside with the doll’s-eye
and head-thrust tests. In an alert human, rotating the head back and forth in
the horizontal plane induces compensatory horizontal eye movements that
are dependent on both the visual and vestibular systems. The doll’s-eye test
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is a test of vestibular function in a comatose patient (Chapter 376) because
such patients cannot generate pursuit or corrective fast components. In this
setting, conjugate compensatory eye movements indicate normally functioning
vestibulo-ocular pathways. Because the vestibulo-ocular reflex has a much
higher frequency range than the smooth pursuit system, a qualitative bedside
test of vestibular function can be made with the head-thrust test. It is performed
by grasping the patient’s head and applying brief, small-amplitude, high-
acceleration head thrusts first to one side and then the other. The patient
fixates on the examiner’s nose and the examiner watches for corrective sac-
cades, which are a sign of an inappropriate compensatory slow phase.
Caloric Test
The caloric test induces endolymphatic flow in the horizontal semicircular
canal and horizontal nystagmus by creating a temperature gradient from
one side of the canal to the other. With a cold caloric stimulus, the column
of endolymph nearest the middle ear falls because of its increased density.
This causes the cupula to deviate away from the utricle (ampullofugal flow)
and produces horizontal nystagmus with the fast phase directed away from
the stimulated ear. A warm stimulus produces the opposite effect, causing
ampullopetal endolymph flow and nystagmus directed toward the stimulated
ear (a mnemonic is COWS, meaning cold opposite, warm same). Because of
its ready availability, ice water (approximately 0° C) can be used for bedside
caloric testing. To bring the horizontal canal into the vertical plane, the patient
lies in the supine position with head tilted 30 degrees forward. Infusion of 1 to
3 mL of ice water induces a burst of nystagmus usually lasting about a minute.
Greater than a 20% asymmetry in nystagmus duration suggests a lesion on the
side of the decreased response. The ice water caloric test is a useful way to test
the integrity of the oculomotor pathways in a comatose patient. In this case
ice water induces only a slow tonic deviation toward the side of stimulation.
Positional Tests
Examination for pathologic vestibular nystagmus should include a search for
spontaneous and positional nystagmus (see Table 396-4). Because vestibular
nystagmus secondary to peripheral vestibular lesions is inhibited with fixation,
the yield is increased by impairing fixation with +30 lenses (Frenzel glasses)
or infrared video recordings. Two types of positional testing are typically
performed: moving the patient from the sitting to head-hanging-right and
head-hanging-left positions (Dix-Hallpike test) and turning the head to the
right and left while the patient lies supine.12 Induced positional nystagmus
may be paroxysmal or persistent, and it may be in the same direction in all
positions or change directions in different positions. The most common cause
of positional nystagmus is otolith debris in the semicircular canals, either free
floating (paroxysmal) or attached to the cupula (persistent). This type of
nystagmus always occurs in the plane of the affected canal—vertical torsional
for the vertical canals and horizontal torsional for the horizontal canal. By
contrast, central positional nystagmus is often pure vertical or horizontal and
cannot be explained by stimulating a single semicircular canal.
Nystagmography
Nystagmography tests oculomotor control by inducing and recording eye
movements. A standard test battery includes (1) tests of visual ocular control
(saccades, smooth pursuit, and optokinetic nystagmus), (2) a careful search
for pathologic nystagmus with fixation and with eyes open in darkness, and
(3) the measurement of induced vestibular nystagmus (caloric and rotational).
Nystagmography can be helpful in identifying a vestibular lesion and localizing
it within the peripheral and central pathways.
Evaluating the “Dizzy” Patient
The history is key because it determines the type of dizziness (Table 400-1),
associated symptoms (neurologic, audiologic, cardiac, psychiatric), precipitat-
ing factors (position change, trauma, stress, drug ingestion), and predisposing
illness (systemic viral infection, cardiac disease, cerebrovascular disease).13 The
history provides direction for both the examination and the diagnostic evalu-
ation. When focal neurologic signs are found, neuroimaging usually leads to a
specific diagnosis. When vertigo is present without focal neurologic symptoms
or signs, head-thrust and positional testing are key to localizing the lesion to
the labyrinth or eighth nerve.14 Audiometry and nystagmography are useful if
the cause of vertigo is not clear after the history and examination. Patients with
psychogenic dizziness (also called chronic subjective dizziness or persistent
perceptual-postural dizziness) should be identified early so that needless tests
are not obtained. A detailed cardiac evaluation (including loop monitoring)
often identifies the cause of episodic near-fainting (Chapters 45 and 56).
TABLE 400-1 DESCRIPTION, MECHANISM, AND FOCUS OF DIAGNOSTIC WORK-UP FOR COMMON TYPES OF DIZZINESS
TYPE OF DIZZINESS DESCRIPTION MECHANISM FOCUS OF DIAGNOSTIC EVALUATION
Vertigo Spinning (environment moves), tilt, drunkenness Imbalance in tonic vestibular activity Auditory and vestibular systems
Near-faint Lightheaded, swimming Decreased blood flow to entire brain Cardiovascular system
Psychogenic Dissociated from body, spinning inside Impaired central integration of sensory Psychiatric assessment
(environment still) signals
Disequilibrium Off balance, unsteady on feet Loss of vestibulospinal, proprioceptive, Neurologic assessment
cerebellar, or motor function

TABLE 400-2 TREATMENT OF COMMON VERTIGO   Grade A References

SYNDROMES
SYNDROME TREATMENT A1. Qiang Q, Wu X, Yang T, et al. A comparison between systemic and intratympanic steroid therapies
as initial therapy for idiopathic sudden sensorineural hearing loss: a meta-analysis. Acta Otolaryngol.
Benign positional vertigo 2017;137:598-605.
Posterior canal variant Epley maneuver (see Fig. 400-4) A2. Han X, Yin X, Du X, et al. Combined intratympanic and systemic use of steroids as a first-line
Horizontal canal variant Barbecue roll toward normal side (side with less treatment for sudden sensorineural hearing loss: a meta-analysis of randomized, controlled trials.
nystagmus), sleep with normal ear down Otol Neurotol. 2017;38:487-495.
A3. Tikka C, Verbeek JH, Kateman E, et al. Interventions to prevent occupational noise-induced hearing
Vestibular neuritis Methylprednisolone, 100 mg × 3 days, gradual taper loss. Cochrane Database Syst Rev. 2017;7:CD006396.
during 22 days (must start within 3 days of onset) A4. Kil J, Lobarinas E, Spankovich C, et al. Safety and efficacy of ebselen for the prevention of noise-
induced hearing loss: a randomised, double-blind, placebo-controlled, phase 2 trial. Lancet. 2017;
Meniere disease 390:969-979.
Medical Low salt (1-2 g salt/day) and either A5. Zenner HP, Delb W, Kroner-Herwig B, et al. A multidisciplinary systematic review of the treatment
hydrochlorothiazide 25-50 mg/day or for chronic idiopathic tinnitus. Eur Arch Otorhinolaryngol. 2017;274:2079-2091.
hydrochlorothiazide 25 mg/day plus triamterene A6. Beukes EW, Andersson G, Allen PM, et al. Effectiveness of guided internet-based cognitive behavioral
50 mg/day therapy vs face-to-face clinical care for treatment of tinnitus: a randomized clinical trial. JAMA
Surgical Intratympanic gentamicin, vestibular nerve section Otolaryngol Head Neck Surg. 2018;144:1126-1133.
A7. Zhang X, Qian X, Lu L, et al. Effects of Semont maneuver on benign paroxysmal positional vertigo:
a meta-analysis. Acta Otolaryngol. 2017;137:63-70.
A8. Patel M, Agarwal K, Arshad Q, et al. Intratympanic methylprednisolone versus gentamicin in patients
TREATMENT  with unilateral Ménière’s disease: a randomised, double-blind, comparative effectiveness trial. Lancet.
2016;388:2753-2762.
A9. Saliba I, Gabra N, Alzahrani M, et al. Endolymphatic duct blockage: a randomized controlled trial
Treatment of vertigo can be divided into three general categories: specific,
of a novel surgical technique for Ménière’s disease treatment. Otolaryngol Head Neck Surg. 2015;
symptomatic, and rehabilitative. When possible, treatment should be directed at 152:122-129.
the underlying disorder (Table 400-2). Specific therapies include particle reposi- A10. McDonnell MN, Hillier SL. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction.
tioning maneuvers (the Epley and Semont maneuvers; see Fig. 400-4) for benign Cochrane Database Syst Rev. 2015;1:CD005397.
paroxysmal positional vertigo. A7  For vestibular neuritis, steroids (e.g., methyl-
prednisolone, 1 mg/kg/day for 5 days, then tapered during the next 15 days)
are effective, at least for the short term, but antiviral agents are not. For Meniere GENERAL REFERENCES
disease, a low-salt diet and diuretics (e.g., 25 mg hydrochlorothiazide and 50 mg
triamterene daily) are effective in some cases. Intratympanic methylprednisolone For the General References and other additional features, please visit Expert Consult
can significantly reduce vertiginous attacks in patients with refractory unilateral at https://expertconsult.inkling.com.
Meniere disease. A8  Another option is intratympanic gentamicin, which also can
significantly reduce vertigo in patients with refractory unilateral Meniere disease,
but its ototoxicity will cause a permanent vestibular defect. Endolymphatic duct
blockage is a potential option for medically refractory Meniere disease. A9 
In many cases, however, symptomatic treatment either is combined with
specific therapy or is the only treatment available. Many different classes of
drugs have been found to have antivertiginous properties, and in most instances,
the exact mechanism of action is uncertain. All these agents produce potentially
unpleasant side effects, and the decision concerning which drug or combina-
tion to use is based on their known complications and on the severity and
duration of the vertigo. An episode of prolonged, severe vertigo is one of the
most distressing symptoms that a patient can experience. Affected patients
prefer to lie still with eyes closed in a quiet, dark room. Antivertiginous drugs,
such as dimenhydrinate (25 mg) or diazepam (5 mg), may be helpful. Prometha-
zine suppositories (25 mg) are useful in patients with vomiting.
In more chronic vertiginous disorders, when the patient is trying to carry
on normal activity, less sedating antivertiginous medications, such as meclizine
(25 mg) or transdermal scopolamine (0.5 mg every 3 days), may provide relief.
Chronic use of these drugs should be avoided.
Vestibular rehabilitation exercises are designed to help the patient compen-
sate for permanent loss of vestibular function. A10  As the acute stage of nausea
and vomiting subsides, the patient should attempt to focus the eyes and to
move and hold them in the direction that provokes the most dizziness. A useful
exercise involves staring at a visual target while oscillating the head from side
to side or up and down, slow at first and then fast. The patient should try to
stand and walk, at first in contact with a wall or with an assistant, and make
slow supported turns. As improvement occurs, head movements should be
added while standing and walking.

  PROGNOSIS
Vertigo commonly resolves, either because patients become truly asymptomatic
or adjust to occasional symptoms. Among patients diagnosed with a peripheral
cause of vertigo, the 30-day risk of accidental injury is less than 0.2%, as is
the 30-day risk of stroke.15

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 CHAPTER 400  Hearing and Equilibrium
 
2565.e1

GENERAL REFERENCES
1. Lin HW, Mahboubi H, Bhattacharyya N. Self-reported hearing difficulty and risk of accidental injury
in US adults, 2007 to 2015. JAMA Otolaryngol Head Neck Surg. 2018;144:413-417.
2. Usami SI, Kitoh R, Moteki H, et al. Etiology of single-sided deafness and asymmetrical hearing loss.
Acta Otolaryngol. 2017;137(suppl 565):s2-s7.
3. Carroll YI, Eichwald J, Scinicariello F, et al. Vital signs: noise-induced hearing loss among adults—
United States 2011-2012. MMWR Morb Mortal Wkly Rep. 2017;66:139-144.
4. Cunningham LL, Tucci DL. Hearing loss in adults. N Engl J Med. 2017;377:2465-2473.
5. Sladen DP, Peterson A, Schmitt M, et al. Health-related quality of life outcomes following adult
cochlear implantation: a prospective cohort study. Cochlear Implants Int. 2017;18:130-135.
6. Walker DD, Cifu AS, Gluth MB. Tinnitus. JAMA. 2016;315:2221-2222.
7. Bauer CA. Tinnitus. N Engl J Med. 2018;378:1224-1231.
8. Phillips JS, McFerran DJ, Hall DA, et al. The natural history of subjective tinnitus in adults: a sys-
tematic review and meta-analysis of no-intervention periods in controlled trials. Laryngoscope.
2018;128:217-227.
9. Brandt T, Dieterich M. The dizzy patient: don’t forget disorders of the central vestibular system. Nat
Rev Neurol. 2017;13:352-362.
10. Nuti D, Masini M, Mandala M. Benign paroxysmal positional vertigo and its variants. Handb Clin
Neurol. 2016;137:241-256.
11. Espinosa-Sanchez JM, Lopez-Escamez JA. Menière’s disease. Handb Clin Neurol. 2016;137:
257-277.
12. Omron R. Peripheral vertigo. Emerg Med Clin North Am. 2019;37:11-28.
13. Fife TD. Dizziness in the outpatient care setting. Continuum (Minneap Minn). 2017;23:359-395.
14. Whitman GT. Examination of the patient with dizziness or imbalance. Med Clin North Am.
2019;103:191-201.
15. Atzema CL, Grewal K, Lu H, et al. Outcomes among patients discharged from the emergency depart-
ment with a diagnosis of peripheral vertigo. Ann Neurol. 2016;79:32-41.

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2565.e2 CHAPTER 400  Hearing and Equilibrium
 

REVIEW QUESTIONS 4. Which of the following would be an unusual precipitant for benign par-
oxysmal positional vertigo?
1. Which of the following would not be typical of a conductive hearing loss?
A . Turning in bed
A . Marked improvement with amplification B. Yoga class
B. Ability to hear speech in a noisy background C. Driving
C. Relatively maintained speech recognition D. Reaching for something on a high shelf
D. Loud speech is annoying. E. Working under an automobile
E. Bone greater than air conduction
Answer: C  Benign paroxysmal positional vertigo is typically triggered by
Answer: D  Patients with conductive hearing loss prefer loud speech, which movement in the vertical plane (plane of the posterior semicircular canal). It
they can understand as well as normal people can. A, B, C, and E are typical would be unusual to make such a movement while driving. The other maneu-
for conductive hearing loss. vers are common precipitating circumstances.

2. Which of the following diagnoses would be least likely to be manifested 5. Which of the following would most likely be associated with a positive
with a unilateral hearing loss? head-thrust test result?
A . Acoustic neuroma A . Meniere disease
B. Meniere disease B. Lateral medullary infarction
C. Otosclerosis C. Cerebellar infarction
D. Brain stem glioma D. Gentamicin ototoxicity
E. Otitis media E. Otitis media
Answer: D  Brain stem lesions rarely cause unilateral hearing loss unless they Answer: D  Gentamicin is remarkably selective for the vestibular system, and
involve the root entry zone of the cochlear nerve. Otosclerosis is usually bilat- the head-thrust test is useful for identifying toxicity at the bedside. The head-
eral but often begins unilaterally. The other conditions are typically unilateral. thrust test result is rarely positive with Meniere disease and would be negative
with lateral medullary infarction, cerebellar infarction, and otitis media.
3. Which of the following is least likely to be manifested with vertigo?
A . Acoustic neuroma
B. Meniere disease
C. Lateral medullary infarction
D. Migraine
E. Vestibular neuritis
Answer: A  Acoustic neuroma typically is manifested with unilateral hearing
loss or tinnitus. It compresses the vestibular nerve slowly, so central compen-
sation can occur. It rarely is manifested with vertigo. B, C, D, and E commonly
are manifested with vertigo.

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