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124 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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The Vertigo Case History
Jay A. Gantz, Belinda C. Sinks, and Joel A. Goebel
This chapter focuses on the elements of the case history
of the dizzy patient. The diagnosis is often revealed
during the clinical interview.
magnitude of the Problem
Dizziness is a common problem seen in primary care
clinics and emergency departments and is one of the
most common symptoms referred to neurology and
otolaryngology practices (Kroenke, Hoffman, & Einstadter, 2000). Dizziness is prevalent in all adult populations and accounts for significant health care costs.
Approximately 4% of visits to U.S. emergency departments have a chief complaint of dizziness or vertigo,
and the cost of these visits in 2011 was estimated to be
$3.9 billion (Saber Tehrani et al., 2013). The prevalence
of dizziness in the elderly population is estimated at
greater than 30% (Sloane, Coeytaux, Beck, & Dallara,
2001). Dizziness is a major risk for falls; a systematic
review by Deandrea et al. (2010) demonstrated a twofold increased risk of falling when patients report dizziness. A literature review reported that 44% of patients
presenting to primary care offices, emergency rooms,
and referral clinics with dizziness complaints suffered
from peripheral vestibulopathy, whereas only 11%
of dizziness was attributed to central vestibulopathy
(Kroenke et al., 2000). While life-threatening emergencies associated with dizziness complaints are rare,
it is important to differentiate between disorders of
dizziness to ensure that permanent impairments are
avoided (Sloane et al., 2001). Patients in the emergency
department who are diagnosed with “benign” dizziness and discharged are at a 50-fold higher risk of
stroke hospitalization in the subsequent seven days
compared with propensity score-matched controls
(Atzema et al., 2016).
imPortanCe of taking
a Com
A complete history is crucial to the diagnosis and management of the dizzy patient. Although diagnostic vestibular tests quantify function within the system, which
is sometimes helpful for a differential diagnosis, an
accurate diagnosis can often be made from the history
alone if the appropriate questions are asked and time is
taken to understand the patient’s experience.
For patients complaining of symptoms of disequilibrium, unsteadiness, or lightheadedness, history taking is an important tool to evaluate for the possibility
of a disorder originating outside of the inner ear. Many
patients present to the audiologist or otolaryngologist
with complaints of vertigo but are actually experiencing something very different. Additionally, true vertigo
can be a sign of serious neurologic disease and there
are red-flag symptoms that should not be overlooked.
Some patients may have not yet discussed their symptoms in depth with any other health care worker, let
alone a specialist; a detailed history will both elicit and
identify these warning signs.
Plete history
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It is important and time efficient to have all new
patients fill out a questionnaire regarding the nature
and time course of their symptoms, past medical and
surgical history, family history, medications, and lifestyle prior to their first visit. When scheduling a new
patient with a complaint of dizziness, the questionnaire
can be mailed to the patient’s home for review prior
to his or her appointment. Depending on the patient,
the questionnaire may take up to 30 minutes to complete. If patients do not fill out the questionnaire prior
to their appointment, answers provided in the waiting
room may be rushed, poorly thought out, incomplete,
or inaccurate. This time spent may also interfere with
the timely flow of clinic. Due to advances in technology
and secure survey databases, it may also be possible to
distribute the questionnaire electronically, giving the
physician and audiologist access to the electronic version of the form as soon as it is completed.
In order to remain effective and time efficient during the office visit, it is important for the examiner to
review the questionnaire answers prior to evaluating
the patient. A complete review of the patient’s answers
will allow the examiner to direct the conversation
toward relevant aspects of the questionnaire and better
focus the specialist’s evaluation. It is also important to
clarify any questions that the patient may have found
confusing, as a lack of understanding of the questions
may affect the specialist’s review of the form. Even
though the questionnaire is extremely helpful and time
efficient, it is not a substitute for a thorough discussion
with the patient regarding his or her symptoms. It is
not uncommon for new information to arise from the
face-to-face discussion that was not made clear in the
questionnaire.
A structured written questionnaire serves to obtain
a thorough history, and a systematically designed survey may also prove to be a powerful tool for predicting diagnoses (see Appendix 7–A for the questionnaire
provided at the Washington University Dizziness and
Balance Center). A study assessing over 600 patients
presenting to the otolaryngology clinic with complaints
of dizziness utilized a 163-item dizziness questionnaire
to predict the ultimate clinical diagnosis (following
complete history, physical exam, and vestibular testing, when appropriate). Results from this study demonstrated that when a subset of 47 questions was used,
the model was correct in predicting the ultimate diagnosis 84% of the time (Zhao, Piccirillo, Spitznagel, Kallogjeri, & Goebel, 2011). In 2015, Roland et al. reported
a prospective multi-center study using a 32-item dizziness questionnaire (a subset of the Zhao et al. study
questionnaire) demonstrating an overall predictive
accuracy of 79% for the final diagnosis.
KEY COMPONENTS OF THE HISTORY
There are several key components of the history that
can give the examiner clues to the proper diagnosis
(Table 7–1).
Characteristic of the Sensation
It is crucial to differentiate between true vertigo, lightheadedness, presyncope/syncope, and disequilibrium.
Patients may describe these sensations in a variety of
ways, so it is important to take the time to fully understand their individual symptom experience.
Vertigo
The meaning of the word vertigo is often misunderstood, and clinical experts will even disagree on the
definition of the word (Blakley & Goebel, 2001). True
vertigo is the false sensation that the individual or
Table 7–1. Key Components of the History
Key Components
of the Interview Possible Answers
Characteristic of the
sensation
Time course of attacks Seconds
Associated events and
symptoms
Exacerbating factors Movement
Vertigo
Light-headedness
Presyncope/syncope
Disequilibrium
Minutes–hours
Hours–days
Hearing loss
Ear pressure
Drop attacks
Tinnitus
Amplification of sound
Loud noises
Atmospheric and
weather changes
Diet
Medication
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environment is moving. This is commonly described
as a “room spinning” sensation. Bisdorff, Von Brevern,
Lempert, and Newman-Toker (2009) defined vertigo as
“the sensation of self-motion when no self-motion is
occurring or the sensation of distorted self-motion during an otherwise normal head movement.” The term
dizziness can involve lightheadedness, disorientation,
or loss of balance. The term vertigo is more specific and
is defined as the illusion of movement, which can be
in the horizontal, vertical, or oblique axis (Waheeda
& Davies, 2004). Balance is dependent on multiple
sensory inputs, including visual, vestibular, and proprioceptive. Vertigo results from mismatched information between these input systems (Waheeda & Davies,
2004). When a diagnosis of true vertigo is made, it is
then important to differentiate between central and
peripheral vertigo.
Peripheral Vertigo
The peripheral vestibular system consists of the semicircular canals, the utricle, the saccule, and the vestibular nerve. Peripheral causes of vertigo are more likely
than central causes of vertigo to present with an acute
illusion of movement, nausea, and vomiting (Waheeda
& Davies, 2004). Peripheral causes of vertigo are also
more likely than central causes to produce auditory
symptoms, such as ringing, aural fullness, aural pressure, and hearing changes. Additionally, while balance
is impaired with peripheral vertigo, patients with central vertigo will often be unable to stand or walk without falling (Baloh, 1998). This inability to stand or walk
is a red flag that should not be overlooked and suggests
significant central pathology. Although patients with
acute peripheral vestibular pathology may feel too sick
or imbalanced to walk, they are capable of enough posture control to stand and ambulate.
Central Vertigo
acute vestibular syndrome (AVS; defined by NewmanToker and Edlow [2015] as “acute onset of persistent
dizziness associated with nausea or vomiting, gait
instability, nystagmus, and head-motion intolerance
lasting days to weeks”), 25% ± 15% of cases are estimated to be due to stroke (Tarnutzer et al., 2011).
Tumors. It is important to include tumor in the differ-
ential diagnosis of a patient presenting with vertigo.
Cerebellopontine angle tumors include vestibular
schwannomas, meningioma, epidermoid cysts, facial
nerve schwannomas, lipomas, trigeminal neuromas,
and metastatic tumors (Karatas, 2008). Schwannomas
of the eighth cranial nerve are the most common cerebellopontine angle tumors, accounting for 60% to
90% of cerebellar pontine angle lesions (Swartz, 2004).
Patients with cerebellopontine angle tumors can present with one or more unilateral symptoms, including
hearing loss, tinnitus, ataxia, vertigo, disequilibrium,
facial numbness, and facial weakness, all due to compression and displacement of nearby structures (Karatas, 2008).
Cerebellar tumors can produce similar symptoms
to cerebellopontine angle tumors, including ataxia,
nystagmus, headache, and vertigo. Common cerebellar
tumors include astrocytomas, ependymomas, medulloblastomas and hemangioblastomas, and metastatic
tumors (Karatas, 2008).
Ataxia. Ataxia presents as difficulty coordinating vol-
untary movements and unsteadiness. Some forms of
ataxia can present with vertigo if there is involvement
of the vestibular nerve. Multiple hereditary ataxias
exist, but the most common is Friedreich ataxia (Karatas, 2008). Friedreich ataxia is a slowly progressive
disease with deficits due to degeneration of the spinal cord and cerebellum. The disease process can also
cause degeneration of the vestibular nerve, likely leading to symptoms of vertigo (Delatycki & Corben, 2012).
The central vestibular system consists of the vestibular
nuclear system, the cerebellum, brainstem, spinal cord,
and vestibular cortex. This chapter focuses on peripheral causes of vertigo, but it is important to note that
central vertigo may be associated with potentially lifethreatening conditions that require immediate medical attention, such as stroke, vascular dissection, and
tumors. Central disorders can involve other neurologic
signs and symptoms, such as facial weakness, difficulty talking, and difficulty ambulating, but only 20%
of stroke cases that present with vestibular symptoms
have focal neurologic signs (Tarnutzer, Berkowitz, Robinson, Hsieh, & Newman-Toker, 2011). In patients with
Multiple Sclerosis. Multiple sclerosis (MS) is an auto-
immune demyelinating disorder that affects the central nervous system. Patients with MS can present with
dizziness or vertigo as their initial complaint, or these
symptoms can be experienced later during the course
of this progressive disease. Symptoms can be acute or
prolonged, making it difficult to differentiate MS from
other diagnoses based on the history alone. The dizziness of MS is caused by demyelination, similar to the
mechanism of some forms of ataxia. MS plaques, which
represent areas of active demyelination, can be located
on the vestibular nerve or near the vestibular nuclei
(Pula, Newman-Toker, & Kattah, 2013).
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Cerebrovascular. The vertebrobasilar system sup-
plies the inner ear, brainstem, cerebellum, and occipital lobes. A disruption of blood flow to these areas
can result in weakness, clumsiness, ataxia, disequilibrium, and/or vertigo. It is important to remember that
transient symptoms, such as intermittent clumsiness,
weakness, dysarthria, and even drop attacks, can be a
sign of transient brainstem ischemia (Troost, 1980).
Disequilibrium
Disequilibrium is another form of dizziness that is
commonly encountered in the otolaryngology clinic.
Disequilibrium is defined as imbalance or unsteadiness without the illusion of motion or vertigo. Patients
usually report that symptoms are worse with standing
or navigating within their environment due to uncoordinated movements. It can be caused by an abnormality in multiple organs, including the vestibular system,
musculoskeletal system, and cerebellum (Karatas,
2008). Usually this sensation is thought to be caused by
neurological deficits; however, bilateral or uncompensated unilateral vestibular disorders can also present
with disequilibrium.
Presyncope and Syncope
Presyncope is the feeling of lightheadedness, blurred
vision, and/or muscular weakness that is experienced
immediately before fainting. Syncope is defined as a
transient decrease in blood flow to the brain and temporary loss of consciousness, followed by full recovery
(Hilz, Marthol, & Neundorfer, 2002). Patients report
symptoms such as weakness, headache, changes in
vision, nausea, and vomiting prior to fainting (Karatas, 2008).
Categories of syncope and presyncope include
cardiovascular, neurologic, and neurocardiogenic.
These disorders can be dangerous, and it is important to differentiate these potentially life-threatening
causes of dizziness from inner ear causes. Presyncope
and syncope can be distinguished from vertigo by the
absence of true motion sensation (Karatas, 2008).
Cardiovascular causes of presyncope and syncope include structural heart disease, coronary heart
disease, and arrhythmias (Karatas, 2008). These conditions can be dangerous and can even precede sudden
cardiac death.
Neurologic causes of presyncope/syncope include
orthostatic hypotension and postural orthostatic tachycardia syndrome (POTS) (Karatas, 2008). Orthostatic
hypotension is defined as an abnormal decrease in
systolic blood pressure when changing body position.
Although it can be asymptomatic in some people, it is
also associated with increased mortality (Ong, Myint,
Shepstone, & Potter, 2013). Postural orthostatic tachycardia is a more serious form of orthostatic hypotension caused by dysfunction of the autonomic system.
The symptoms of presyncope occur in the upright
position and are associated with a marked rise in heart
rate. Symptoms will then decrease when lying flat. The
disorder is most commonly seen in women and can be
brought on by trauma, infection, stress, exertion, heat,
or food ingestion. Behavioral changes as well as pharmacological treatments can treat both orthostatic hypotension and POTS (Mathias et al., 2012).
Neurocardiogenic syncope is also known as vasovagal syncope. Vasovagal syncope is often seen with
emotional or stressful situations, or prolonged standing (Karatas, 2008). While the exact cause of vasovagal
syncope remains uncertain, it is thought that venous
pooling in the lower extremities contributes to the phenomenon. Symptoms include decreases in vision and
hearing as well as nausea and a feeling of impending
doom (Waheeda & Davies, 2004). Vasovagal syncope is
the most common abnormal response to upright posture and has been known to occur in all age groups.
For most patients, vasovagal syncope can be treated
with increased intake of salt and fluids and education
regarding the condition (Bloomfield, 2002).
Lightheadedness
The feeling of lightheadedness, without the illusion
of motion, has many possible causes. The dizziness
associated with psychiatric disorders is often reported
as lightheadedness, floating, or being removed from
one’s body (Karatas, 2008). While panic attacks with
dizziness can be accompanied by fear, palpitations,
chest pain, and sweating, anxious patients with dizziness usually describe their symptoms as fogginess,
lightheadedness, and/or motion sickness (Staab, 2008).
Other psychiatric disorders, such as post-traumatic
stress disorder (PTSD), obsessive compulsive disorder,
and social and specific phobias, have been found to
be associated with somatic syndromes, such as unexplained dizziness (Gupta, 2013). Psychiatric disorders
associated with dizziness do not present as ataxia or
true vertigo and symptoms slowly decline over minutes to hours. It is also important to note that anxiety
and depression are more common in patients with neurotologic disease than in the general population, which
can make diagnosis of dizziness more complicated.
Psychiatric patients with vestibular dysfunction and
true vertigo likely suffer from a coexisting neurotologic
disorder (Staab, 2008).
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Metabolic disorders, when untreated, can also
lead to a feeling of lightheadedness. Patients with glucose abnormalities from diabetes or diabetes-related
treatment can experience lightheadedness from hypoglycemia. Blood glucose levels should always be
checked in diabetic patients if they present with new
dizziness symptoms. Similarly, patients with electrolyte abnormalities or untreated hypertension can experience dizziness.
Time Course of Attacks
The time course of dizziness symptoms can give the
clinician several clues toward the diagnosis. It is important to note that patients may exaggerate or fail to recall
the exact time course of their dizziness due to the severity of their symptoms. Additionally, it is important to
determine the time course of true vertigo. Attacks of
vertigo may be followed by prolonged disequilibrium
or unsteadiness and the two symptoms should be distinguished from one another as much as possible.
Seconds
Vertigo with a duration of less than a minute is most
consistent with benign paroxysmal positional vertigo
(BPPV). BPPV is the most frequent form of peripheral
vestibular disorder (Strupp & Brandt, 2013) and is characterized by brief attacks of vertigo with nystagmus.
BPPV is a mechanical disorder of the inner ear due to
movement of inappropriately free-floating otoconia
and is elicited by the influence of gravity during head
movements (Parnes & McClure, 1992). A common history of patients with BPPV is sudden onset of shortduration vertigo with rapid head movements, such
as those elicited from rolling or turning over in bed,
from turning one’s head abruptly while driving, or
from looking up or down to pick something up. The
free-floating otoconia settle most commonly in the posterior semicircular canal due to the effects of gravity.
This phenomenon is known as canalithiasis. The term
cupulolithiasis describes particles that become adherent to the cupula of the affected semicircular canal.
BPPV can technically be caused by either of these conditions (Parnes, Agrawal, & Atlas, 2003). Vertigo and
nystagmus result from the abnormal stimulation of the
affected semicircular canal caused by movement of the
head. BPPV may be underestimated in the population,
as many patients have spontaneous resolution. Primary
or idiopathic BPPV is responsible for the majority of
cases, approximately 50% to 70% (Parnes et al., 2003).
However, trauma as well as other vestibular conditions
have been found to be associated with BPPV (Mucha,
Fedor, & DeMarco, 2018).
Minutes to Hours
Vertigo attacks lasting minutes to hours frequently are
seen with Ménière’s disease. The most recent international consensus definition of Ménière’s disease states
that the condition is characterized by vertigo, ringing/
roaring (tinnitus), fluctuating low-frequency sensorineural hearing loss, and the sensation of aural pressure
or fullness (Goebel, 2016; Lopez-Escamez et al., 2015).
One theory of the pathophysiology of Ménière’s disease
is that impaired resorption of endolymph by the endolymphatic sac results in endolymphatic hydrops, which
contributes to the symptoms of the disorder. Other possible hypotheses include infectious, vascular, or immunologic etiologies (Strupp & Arbusow, 2001). Although
vertigo attacks are intermittent due to progressive loss
of vestibular function from attacks, patients can experience general imbalance even between vertigo episodes
(Wipperman, 2014).
Another cause of episodic vertigo with symptoms
lasting between minutes and hours includes vertigo
associated with perilymph fistulas. These abnormal
connections allow leakage of perilymph and the abnormal transfer of pressure (Strupp & Arbusow, 2001).
Fistulas may be caused by trauma, cholesteatoma, or
idiopathic dehiscence in bone. A specific variant of
abnormal perilymph movement is superior semicircular
canal dehiscence (SSCD). As the name implies, this syndrome is caused by a defect of the bone overlying the
superior semicircular canal, which can often be seen
on high-resolution CT scan images. The dehiscence
allows for formation of a movable third window. In
SSCD, stimuli that cause a change in middle/inner ear
or intracranial pressure can induce vertigo symptoms
(Minor, Solomon, Zinreich, & Zee, 1998).
A concerning neurologic form of vertigo with an
intermediate duration is transient ischemic attacks
(TIAs). TIAs of the vertebrobasilar circulation can present with intermittent vertigo events. Symptoms can last
for up to 20 minutes with complete resolution. If other
neurologic changes occur with vertigo events, the diagnosis of TIA should be seriously considered.
Hours to Days
Peripheral causes of vertigo do not usually have attacks
of long duration compared with central disorders.
However, vestibular neuritis, a common peripheral
vestibular disorder, has a prolonged course without
resolution for up to hours or days from the time of
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onset. Vestibular neuritis is described as an acute-onset
vertigo with nausea/vomiting, which is described as
very severe. Even after the acute phase has resolved,
balance abnormalities may persist for weeks. Auditory
symptoms are rare with the acute, initial attack (Goddard & Fayad, 2011). Patients will often report that
they will lie completely still for hours in an attempt to
decrease the vertigo. Due to the severity of symptoms,
patients with vestibular neuritis often present to the
emergency department.
The pathophysiology of vestibular neuritis is controversial. The two leading hypotheses for the cause
of the disorder are inflammatory and ischemic (Strupp
& Brandt, 2009). Viral inflammation is a popular theory due to findings of herpes simplex virus DNA and
anatomic observations (Goddard & Fayad, 2011). Anatomic studies have shown that the superior division
of the vestibular nerve is more commonly involved
in vestibular neuritis than the inferior division. This
effect may be explained by anatomic differences in the
nerve divisions, as the superior division has a longer
and narrower bony channel than the inferior division,
increasing the risk for damage, entrapment, and ischemia following viral inflammation (Gianoli, Goebel,
Mowry, & Poomipannit, 2005).
The vertigo experienced with vestibular migraine
has a variable time course. Patients report symptoms
of vertigo and dizziness for durations ranging from
minutes to days (Reploeg & Goebel, 2002). The etiology of vertigo with migraine headaches is not completely understood. One explanation is the parallel
activation of cranial nociceptive and vestibular pathways (Furman & Balaban, 2015). The afferent fibers
of the vestibular and nociceptive pathways intersect
in brainstem structures like the parabrachial nucleus,
the raphe nuclei, and the locus coeruleus. Vestibular
migraines are considered to be central causes of vertigo
(see detailed discussion of this in Chapter 22).
A concerning disorder presenting with acute vertigo lasting for hours to days is acute stroke or cerebrovascular event. Ischemic strokes of posterior circulation
can cause central vertigo. Again, neurological deficits
beyond dizziness are clues toward a diagnosis of a
cerebrovascular event.
Associated Events and Symptoms
Hearing Loss
Hearing loss in the setting of vertigo is commonly associated with Ménière’s disease. In addition to fluctuat-
ing hearing loss and vertigo, Ménière’s patients often
present with aural fullness and/or tinnitus (Goebel,
2016; Lopez-Escamez et al., 2015). The diagnosis can be
challenging, as the symptoms are episodic. The hearing
loss associated with Ménière’s disease is initially a lowfrequency sensorineural hearing loss but can progress
to hearing loss in all frequencies (Wipperman, 2014).
Sudden sensorineural hearing loss accompanied
by acute vertigo can be associated with symptoms similar to vestibular neuritis. When hearing loss occurs with
symptoms of vestibular neuritis, usually acute labyrinthitis is suspected. Patients will complain of acuteonset vertigo with sudden unilateral hearing loss and
tinnitus. Patients may report a viral illness preceding
the event.
Hearing loss is also a complaint in some patients
presenting with signs and symptoms of SSCD (Yew
et al., 2012). Audiograms for these patients can show
an air–bone gap, suggesting a conductive hearing loss
(Brantberg, Ishiyama, & Baloh, 2005). This hearing loss
is likely due to the third window effect where the air
conduction signal is attenuated by hypercompliance of
the inner ear.
It is also important to note that acute-onset vertigo
accompanied by hearing loss can be present in patients
with cerebrovascular events involving the posterior
circulation, as the vertebrobasilar system provides
blood supply to the inner ear. When weakness, dysarthria, confusion, or other neurological signs are present
with acute onset of vertigo and hearing loss, a cerebrovascular event should be suspected and addressed
immediately.
Ear Pressure
Ménière’s disease is associated with feelings of increased
aural pressure or fullness. Patients complain that this
symptom often coincides with times of hearing loss.
This symptom is episodic and may also correspond
with weather and barometric pressure changes.
Drop Attacks
Drop attacks in Ménière’s patients were first described
in 1936 (Tumarkin, 1936). The attacks are thought to
be otolithic crises due to sudden changes in endolymphatic fluid pressure. The fluctuation in pressure
contributes to stimulation of inappropriate reflexes.
Patients report feeling the sensation of being pulled
down (Ozeki, Iwasaki, & Murofushi, 2008). Although
patients do not lose consciousness from the drop attack
alone (an important distinguishing feature from syn-
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cope), unexpected falls lead to an increased risk of
injury for these patients.
Drop attacks have also been seen in patients with
SSCD. These attacks have reportedly improved after
surgical correction (Brantberg et al., 2005). The exact
process of these attacks in SSCD is unknown but may
have an explanation similar to the drop attacks in
Ménière’s disorder, as SSCD patients can also experience sudden changes in endolymphatic pressure.
The above causes of drop attacks are peripheral
causes of vertigo; central causes of dizziness and vertigo may also present with episodes similar to drop
attacks. Orthostatic hypotension and vasovagal syncope can result in fainting with loss of consciousness.
Syncopal events always require additional investigation to rule out dangerous cardiac abnormalities. Ataxia
and disequilibrium may also result in frequent falls.
Tinnitus
As mentioned previously, tinnitus often coincides
with Ménière’s disease attacks. Interestingly, the tinnitus experienced by Ménière’s patients can change in
character during an actual vertigo attack and become
louder, or change in pitch (Wipperman, 2014).
Patients with labyrinthitis will also complain of
tinnitus associated with their hearing loss. Labyrinthitis is thought to be caused by an infectious process and
is associated with vertigo, sudden hearing loss, and tinnitus (Beyea, Agrawal, & Parnes, 2012).
Amplification of Sound
SSCD patients often complain of abnormal amplification of sounds such as their own voice, heartbeat, joint
movement, or eye movements. This amplification is
often attributed to the mostly low frequency conductive hearing loss seen in these patients (Crane, Carey,
& Minor, 2010). The bone conduction is often suprathreshold (<0 dB HL) at low frequencies due to the
third-window phenomenon (Yew et al., 2012).
sodes must present with a concurrent migraine feature,
such as localization to one side, pulsations, photophobia, phonophobia, visual aura, moderate to severe
pain, or worsening with physical activity. Patients will
report variable time frames of symptoms, and the vertigo may be spontaneous or induced by movement or
visual stimuli (Lempert et al., 2012). The International
Headache Society adopted these criteria in 2018 for
the third edition of the International Classification of
Headache Disorders (IHS, 2018).
Exacerbating Factors
Movement
In BPPV patients, an abnormal vestibular response
is thought to be caused by inappropriate movement
of otoconia during head motion. Patients will often
describe their vertigo attacks as occurring when they
roll over in bed, look up or down suddenly, or are driving and look over their shoulder while switching lanes.
Patients may be able to identify the laterality of their
disease based on the direction of head movements that
stimulate a response for them. Due to this phenomenon, diagnosis can often be made by asking patients to
recall the direction of head movements that preceded
their attacks or reliving the experience through maneuvers in the office.
With peripheral pathology, uncompensated unilateral vestibular pathology will also present with symptoms during head movement. The incongruent output
from each vestibular system can lead to instability.
Neurologic and neurocardiogenic dizziness can
also be influenced by movement or positional factors.
However, these movements are not specifically stimulating the peripheral vestibular system; for example,
orthostatic hypotension is often stimulated by standing up quickly from a seated position, and neurocardiogenic or vasovagal dizziness is often preceded by
prolonged standing.
Headaches
Vestibular migraine is a common diagnosis, with a
prevalence of 1% of the population affected by the disorder (Neuhauser et al., 2006). Patients with vestibular
migraine are defined as those with current migraines
or a history of diagnosed migraines and at least five
episodes of vestibular symptoms lasting between 5 min
and 72 hr. In order to meet criteria of the vestibular
migraine diagnosis, at least half of the vestibular epi-
Loud Noises, Pressure Changes
Patients with SSCD often complain that loud sounds
cause vertigo or disequilibrium. Although well before
SSCD was first described, this phenomenon was known
as the Tullio phenomenon and was first reported in
1929 (Tullio, 1929). Activities that produce changes
in middle ear or intracranial pressure, such as straining, nose blowing, and increasing pressure in the
external ear canal, can also cause vertigo (Minor, 2000).
132 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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This is due to the abnormal communication between
the middle fossa and vestibule, or the third-window
effect, resulting in sensitivity to sounds transmitted
through bone and intracranial pressure changes (Yew
et al., 2012).
Atmospheric, Weather, and Lifestyle Changes
Atmospheric and weather changes have been shown to
be associated with the onset or worsening of Ménière’s
symptoms (Mizukoshi et al., 1995). Many patients will
attribute variations in symptoms to sudden changes in
the weather. Additionally, Ménière’s disease is thought
to be heavily influenced by dietary intake. This is due
to the fact that episodes are often preceded by ingestion of certain foods, including salt, caffeine, alcohol,
and nicotine. In fact, primary treatment for Ménière’s
disease includes dietary changes.
Similar to Ménière’s disease, vestibular migraine can
also be affected by weather and diet. Migraine headaches are commonly triggered by environmental stimuli,
stress, and dietary changes (Fraga et al., 2013). Furthermore, stress, as measured by the Hospital Anxiety and
Depression Scale (HADS), is significantly increased
in patients with chronic dizziness and higher HADS
scores are associated with more prolonged dizziness
symptoms (Roh, Kim, Kim, & Son, 2017) (Table 7–2).
Past mediCal and surgiCal history
It is always important to elicit a complete past medical and surgical history during an interview. Even
though the questionnaire can help focus the questions
about past medical and surgical history, the patient’s
responses to inquiries about the sensation, associated
symptoms, and exacerbating factors may lead this
portion of the interview in multiple directions. It is
important to consider the patient’s description of the
sensation and rule out any concerning diagnoses. For
example, if the patient reports presyncope or syncopal
events, a thorough past medical and family history of
cardiac disease must be taken. Similarly, if the patient
reports any neurological signs at the time of vertigo
attacks, stroke and risk factors for stroke should be
considered.
As previously discussed, clues from the medical
or surgical history may help in understanding the etiology of peripheral vertigo. Head trauma can predispose
patients to BPPV and SSCD. Similarly, prior surgery for
cholesteatoma can put patients at risk for perilymphatic
fistulas. A recent illness or surgery may have complications related to the patient’s vertigo. The past medical
and surgical history can be very valuable in putting
together such clues regarding a patient’s dizziness.
Medication
It is always important to evaluate a patient’s prescription medications, specifically any recent changes in medications or dosages that may have preceded a change
in symptoms. Medications that affect blood pressure
can cause lightheadedness, presyncope, and syncope.
Additionally, medications that affect the central nervous
system can lead to dizziness or disequilibrium. Common medications causing dizziness include treatments
for depression (Kikuchi, Suzuki, Uchida, Watanabe, &
Mimura, 2013) and pain. Polypharmacy, particularly in
older patients and those on multiple medications for
hypertension, has been found to be associated with an
increased frequency of dizziness (Shoair, Nyandege, &
Slattum, 2011). Polypharmacy can also occur with other
classes of drugs, including sedatives, antihistamines,
and muscle relaxants. Additionally, there are multiple
medications that are known to damage the inner ear and
contribute to vertigo or disequilibrium. These medications include antibiotics used for aggressive treatment
of infection, as well as chemotherapy agents. These
medications may have been taken in the distant past by
patients, so it is important to inquire about prior hospitalizations and severe illnesses.
Vestibular Contributions to
autonomiC regulation
We often see patients with dizziness symptoms that
can be attributed to neurologic or neurocardiogenic
presyncope. While it is easy to assume that these symptoms are unrelated to the inner ear, it is also possible
for otolith organs to play a role in orthostasis, blood
pressure, and pulse changes. The vestibular system
contributes to respiratory and cardiovascular control, and studies of vestibular injuries in animals have
resulted in an inability to control blood pressure during
position changes (Yates, Bolton, & Macefield, 2014). It
is important to note that patients usually recover and
compensate quickly after vestibular injury, making the
pathophysiology of vestibular-autonomic reflexes difficult to study (Yates & Bronstein, 2005).
Possibility of multiPle diagnoses
Significant effort can be put into making an accurate
diagnosis of vertigo, but many patients may be difficult
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Table 7–2. Common Peripheral Vertigo Disorders
Superior
Semicircular
Canal
Dehiscence
Time course
Seconds
BPPV
✓
Ménière’s
Disease
Vestibular
Neuritis Labyrinthitis
Minutes to hours
Hours to days
Associated symptoms
Hearing loss
Ear pressure
Drop attacks
Tinnitus
Amplification of
sound
Exacerbating factors
Movement
Loud noises
Atmospheric and
weather changes
Diet
✓
✓ ✓
✓ ✓ ✓
✓
✓ ✓
✓ ✓
✓
✓
to classify into only one category. In fact, multiple diagnoses are often given to complicated patients.
Vestibular Migraine and BPPV
Vestibular migraine and BPPV are often diagnosed
together in the clinical setting. A prospective study found
that patients with migraines met criteria for BPPV more
than any other diagnosis of vertigo (Neuhauser et al.,
2001). Patients with migraines may become more susceptible to BPPV due to damage to inner ear structures
from ischemia or vasomotor changes responsible for the
migraine disorder (Ishiyama, Jacobson, & Baloh, 2000).
Vestibular Neuritis and BPPV
The association of vestibular neuritis and BPPV has been
reported in the literature and is a common combination
✓ ✓
✓
✓
of diagnoses seen in the clinical setting. Vestibular neuritis may be an inciting event for the development of
BPPV. Vestibular neuritis is thought to affect the superior vestibular nerve, which innervates the utricle. Following the damage of vestibular neuritis, otoconia from
the utricle may be able to migrate to the semicircular
canals and cause BPPV (Balatsouras et al., 2014; Gianoli
et al., 2005; Goebel, O’Mara, & Gianoli, 2001).
Ménière’s Disease and BPPV
Ménière’s disease is another diagnosis that is often
found in BPPV patients. Studies report variable rates of
coinciding diagnoses, but the pathophysiology of the
relationship remains unclear. It is possible that similar to vestibular neuritis, Ménière’s disease may cause
damage to the utricle through the chronic disease process, rendering the inner ear more susceptible to displaced otoconia and BPPV (Balatsouras et al., 2012).
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