Dizziness and the

Otolaryngology Point of
View
Sharmeen Sorathiaa,b, Yuri Agrawal, MD, MPH
c
,
Michael C. Schubert, PT PhDc,d,*

KEYWORDS
 Dizziness  Vertigo  Evaluation  Physical therapy  History  Examination
 Vestibular tests

KEY POINTS
 Dizziness can be classified as vertigo, lightheadedness, oscillopsia, or disequilibrium. It is
most commonly caused by peripheral vestibular disorders.
 Vertigo is an illusion of motion often caused by asymmetric stimulation of the vestibular
pathway. It is most common in benign paroxysmal positional vertigo (BPPV), Meniere dis-
ease, and vestibular neuritis.
 Evaluation of dizziness from the otolaryngology point of view includes essential compo-
nents in the history, examination, and vestibular function tests.
 Vestibular rehabilitation plays an integral role in the management of vertigo. For BPPV, the
classic treatment is canalith repositioning maneuvers.

INTRODUCTION
Dizziness and Its Types
Dizziness is a broad term used to describe several sensations that are typically cate-
gorized as vertigo, disequilibrium, lightheadedness, or oscillopsia.
It is a commonly reported symptom presenting to specialists and emergency de-
partments affecting 15% to 20% of the general adult population.1,2 It is reported to
be more prevalent in women and the elderly.1

Disclosure Statement: None of the authors have any disclosure.

a
Ziauddin University College of Medicine, 4/B, Shahrah-e-Ghalib, Block 6, Clifton, Karachi
75600, Pakistan; b Johns Hopkins University School of Medicine, 601 North Caroline Street,
Baltimore, MD 21287, USA; c Department of Otolaryngology–Head and Neck Surgery, Johns
Hopkins University School of Medicine, 601 North Caroline Street, Baltimore, MD 21287, USA;
d
Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of
Medicine, 601 North Caroline Street, Baltimore, MD 21287, USA
* Corresponding author. Johns Hopkins University School of Medicine, 601 North Caroline
Street, Baltimore, MD 21287.
E-mail address: mschube1@jhmi.edu

Med Clin N Am - (2018) -–-

https://doi.org/10.1016/j.mcna.2018.06.004 medical.theclinics.com
0025-7125/18/ª 2018 Elsevier Inc. All rights reserved.
2 Sorathia et al

It can be caused by a disturbance in multiple systems or pathways, including the

central nervous system (CNS) and the vestibular end organ, but also the visual path-
ways, the cardiovascular system, and others. It can also have an association with anx-
iety and panic disorder. Because of the symptoms being vague and the large number
of causes for dizziness, the clinical diagnosis and management can be challenging.

Common Causes
The nonspecific symptom of dizziness can have numerous causes ranging from life-
threatening to benign conditions. A critical review from 12 studies conducted on the
cause of dizziness classifies and reports the quality-adjusteda mean frequencies of
various causes, summarized in Table 1.3 The most common classifications are periph-
eral vestibular conditions followed by nonvestibular and nonpsychotic, psychiatric,
unknown, and central vestibular causes.
Vertigo is the sense of spinning or an illusion of a movement that is often described
as being objective (ie, the world is moving) or subjective (the person feels as if they are
moving). It is caused by an asymmetrical stimulation of the vestibular pathway and
thus can be due to intrinsic peripheral or central vestibular diseases or external con-
tributors that affect the pathway (ie, neurologic disease, medication). Common

Table 1
Causes of dizziness

Cause Mean Frequency (%)

Peripheral vestibular 44
Benign paroxysmal positional vertigo 16
Labyrinthitis 9
Meniere disease 5
Other (drug-related ototoxicity or nonspecific) 14
Central vestibular 11
Cerebrovascular 6
Tumor <1
Other (multiple sclerosis, migraine, or other) 3
Psychiatric 16
Psychiatric disorder 11
Hyperventilation 5
Nonvestibular, nonpsychotic 26
Presyncope 6
Disequilibrium 5
Other (anemia, metabolic, drug-related, Parkinson, and other) 13
Unknown 13

The percentages add up to more than 100% due to dizziness being attributed to more than one
cause in some patients.
Data from Kroenke K, Hoffman RM, Einstadter D. How common are various causes of dizziness?
A Critical Review. South Med J 2000;93(2):162; with permission.

a
Quality adjusted: square root of the study’s quality score to enable weighting of the means of each
study.
 Dizziness and the Otolaryngology Point of View 3

peripheral vestibular diseases include benign paroxysmal positional vertigo (BPPV),

Meniere disease, and vestibular neuritis.
Lightheadedness is defined as a sensation of about to faint. Causes of lightheaded-
ness include cardiovascular disease, including cardiac arrhythmias, orthostatic hypo-
tension, hypoglycemia, and anxiety. Orthostatic hypotension is a common cause of
lightheadedness.
Disequilibrium is the impairment in balance or coordination such that
confident ambulation is disturbed. It can be due to decreased somatosensation
or weakness in the lower extremities, but also due to peripheral or central vestib-
ular disorders, multiple sensory deficits, transient ischemic attacks (TIA), or Parkin-
son disease.
Oscillopsia is defined as the illusion of motion of objects known to be stationary in
the visual surround. It is typically caused by loss of vestibular sensation.

THE CLINICAL EVALUATION OF THE VESTIBULAR SYSTEM

History
It is essential to take a thorough history of a patient presenting with a complaint of
dizziness. A detailed description could reveal the sensation to be of spinning of
one’s self or surroundings (or both), feeling of about to fall, or becoming out of balance
or experiencing motion of stationary objects in the surrounding. The vertigo can be
described by the patient as a feeling of rotating, swaying, or falling.4 Recent studies
suggest that the quality of the dizziness symptom may be less informative than the
timing, frequency, and triggers of symptoms.5
Episodes and duration
It is critical to inquire about the duration and the temporal characteristic of the vertigo
(ie, episodic or constant). Chronic episodic vertigo could indicate BPPV, Meniere dis-
ease, or vestibular migraine. BPPV episodes tend to be recurrent and typically occur
within 1 minute. In contrast, vestibular migraine and TIA tend to cause single epi-
sodes with vertigo durations from minutes to hours. Meniere’s disease typically pre-
sents with recurrent attacks (2 or more) lasting for 20 minutes to 12 hours. A severe
attack of acute spontaneous vertigo for the first time lasting 24 hours or longer
is most commonly due to vestibular neuritis. It could also be due to a cerebellar
infarct.
Position
Positional changes are distinctive of BPPV and typically occur upon lying down, rolling
over in bed, or bending over/reaching up. These patients tend to not have any vertigo
at rest. Occasionally, vestibular migraine could also manifest with positional vertigo,
although the duration is commonly longer. Orthostatic hypotension can occur when
the patient arises upright from supine or sitting positions, although this does not
tend to cause a spinning sensation. Typically, episodes of vertigo due to vestibular
migraine, Meniere disease, vestibular neuritis, and TIA occur spontaneously without
positional changes.
Association
Attacks of Meniere are classically associated with hearing loss, aural fullness, and
tinnitus, which will be located to one ear. There can also be associated nausea, vom-
iting, visual disturbance, anxiety, and/or motion sensitivity. Central pathologic condi-
tions are usually associated with severe imbalance, problems with oculomotor control,
ataxia, seizures, nausea, and other neurologic symptoms. In particular, hearing
impairment is usually caused by Meniere disease or labyrinthitis, whereas vertigo in
4 Sorathia et al

BPPV or vestibular neuritis is not associated with hearing loss. Although headaches
may or may not be prominent in vestibular migraine, motion sensitivity, photophobia,
phonophobia, aura, and nausea are common.

Others including drugs, social, recent events, impact on daily life

BPPV mostly frequently occurs in the middle aged and elderly.2,6,7 Patients should
be asked if their symptoms are experienced while driving or riding in vehicles, trav-
eling with public transportation, or during the routine activities of daily life. Depres-
sion and anxiety should be addressed because unique surroundings such as
supermarkets or crowded spaces can create symptoms of dizziness and imbal-
ance. Recent medical events should be assessed. For example, the onset of an
antihypertensive medication might be causing orthostatic hypotension, or a recent
head trauma might have preceded BPPV. Alcohol, nicotine, and caffeine can all
potentially aggravate vertiginous symptoms.8,9 Current or previous use of medica-
tions should be taken into account. Aminoglycosides, furosemide, ethacrynic acid,
acetylsalicylic acid, amiodarone, quinine, and cisplatin can all lead to ototox-
icity.8,10 Sexual history should also be investigated because some sexually trans-
mitted diseases (ie, syphilis) can manifest in vestibular symptoms.8 In patients
with suspected migraine, the role of possible triggers, such as caffeine, red wine,
chocolate, cheese, and fermented foods, should be determined. Some women
with migraine have worse symptoms during the perimenstrual cycle or during
perimenopause.11,12

Examination and Clinical Testing

Important examinations and clinical tests to perform in a vertiginous patient include
the oculomotor examination, an otologic examination, positional testing for BPPV,
and a balance/gait examination.

Ocular examination
For a thorough physical examination, it is important to begin with an ocular examina-
tion including pupillary reactivity and oculomotor movements. The examiner should
check smooth pursuit, saccades, and the ability to keep the eyes stable in different
positions of gaze. Subtle oculomotor abnormalities can sometimes be the only sign
behind a cerebellar dysfunction. A fundoscopic examination can also be helpful to
identify oculomotor abnormalities such as ocular torsion. Moreover, in cases of
increased intracranial pressure, visual acuity can be normal, and only papilledema
may present on fundoscopy. A cover test is also essential to perform to identify any
misalignments in the visual axis; of particular concern is any vertical deviation. Vertical
skew deviation in the absence of an extraocular muscle abnormality is the vertical
misalignment of the eyes that can occur in both acute peripheral lesions and more
sinister central disorders, more commonly in the latter. This test is helpful to distin-
guish between the peripheral or central disorders given peripheral typically causes
recover within a week.13

Ear examination
It is further essential to perform an ear examination. The use of an otoscope can reveal
impacted cerumen or any foreign object in the ear canal, removal of which might
relieve vertiginous symptoms.8 Fluid behind the eardrum, perforation, prominent scar-
ring, and other signs of middle ear disease should also be ruled out. A bedside hearing
examination can also be performed if the patient complains of hearing impairment,
including the Weber and Rinne tests to distinguish between conductive or sensori-
neural hearing loss.
 Dizziness and the Otolaryngology Point of View 5

Nystagmus
Nystagmus is an involuntary rhythmic oscillatory movement of the eyes. It is essential
to examine any nystagmus present in a vertiginous patient. The jerk nystagmus typical
of inner ear pathologic condition includes a slow and fast component with the latter
used to name the direction of the nystagmus (ie, fast phase to the right is termed right
beating nystagmus). It is optimal to use Frenzel glasses that prevent fixation when
examining spontaneous nystagmus.
Spontaneous nystagmus is defined as nystagmus present at rest with the eyes in
primary position; the head should not be allowed to move. Spontaneous nystagmus
can appear in a patient with acute vertigo. In an acute peripheral vestibular loss (eg,
vestibular neuritis), spontaneous nystagmus is typically unidirectional and moving in
a horizontal and torsional manner, “beating” away from the pathologic ear. When ga-
zing in the direction of the fast phase, the velocity of the nystagmus will increase. The
velocity of nystagmus will also reduce with visual fixation. The inability to suppress the
nystagmus suggests a central cause.
Nystagmus from a central pathologic condition typically is direction changing
depending on gaze position, vertical (upbeat or downbeat), or even purely torsional.
However, some central causes for nystagmus can also have features similar to pe-
ripheral causes. Gaze-evoked nystagmus occurs with changes in gaze. Caution is
warranted if a symmetric horizontal nystagmus occurs with a few beats present in
each direction of gaze because this is normal and is called physiologic “endpoint”
nystagmus. Asymmetric, prolonged, or more pronounced nystagmus on changing
gaze indicates a pathologic condition. Horizontal gaze-evoked nystagmus can occur
from use of anticonvulsants, alcohol intoxication, or brainstem or cerebellar
disorders.14
Headshake nystagmus (HSN) identifies asymmetrical involvement from the vestib-
ular pathways. The examiner shakes the patient’s head back and forth vigorously,
20 cycles at the rate of 2 per second (2 Hz). At the end of the head shaking, the
eyes are examined for nystagmus with the direction of the fast phase beating toward
the healthy ear. This test is best done using Frenzel lenses in order to block visual fix-
ation. Not all patients with unilateral vestibular loss will have a positive HSN test. HSN
can also occur in cerebellar dysfunction.15,16 Those patients with symmetric vestibular
involvement will have a negative HSN test.
Positional nystagmus should be checked in every patient that reports dizziness,
to rule out BPPV. Nystagmus should be checked in both the Dix-Hallpike maneuver
and the roll test, described in detail in later discussion. It is important to first
identify any spontaneous nystagmus before proceeding with positional testing in
order to avoid the enhanced spontaneous nystagmus that often occurs when
placed in different head positions. Enhanced spontaneous nystagmus can cause
clinicians to mistakenly diagnose BPPV.

Dix-Hallpike test
This maneuver is the gold-standard test for diagnosing the most common location for
BPPV (the posterior canal) and confirms the displacement of otoconia (calcium car-
bonate crystals) into the semicircular canals (SCC). It is a quick and easy bedside
test that positions the head in a manner for gravity to cause displaced otoconia to
move and reproduce the patient symptoms while the examiner looks for nystagmus.
The direction of nystagmus along with the vertigo symptom (and sometimes nausea)
indicates which SCC is involved (Table 2).
To check for posterior canal BPPV, the most common location, the patient sits up-
right on a flat examination table wearing Frenzel glasses. Throughout the test, the
6 Sorathia et al

Table 2
Types of nystagmus with each affected semicircular canals

Semicircular Canal Type of Nystagmus

Posterior SCC Cupulolithiasis Persistent upbeating nystagmus torsional toward the
affected ear
Canalolithiasis Transient upbeating nystagmus torsional toward the
affected ear
Horizontal SCC Cupulolithiasis Persistent ageotropic
Canalolithiasis Transient geotropic
Superior SCC Cupulolithiasis Persistent downbeating nystagmus torsional toward the
affected ear
Canalolithiasis Persistent downbeating nystagmus torsional toward the
affected ear

patient has to keep their eyes open. The examiner moves the patient’s head 45 to one
side and brings the patient to the supine position with head hyperextended 30 below
the horizon (head can be held hanging over the edge of the table). The typical BPPV
nystagmus begins after a latent period of a few seconds and then reduces within
1 minute. The test should be performed for each side. Alternatively, examiners can
perform this test with the head rotated 45 , but the patient lies on their side with no
hyperextension of the neck.17 It is the side of the head facing the ground that is
being tested each time.

Roll test
A supine roll test should be performed to evaluate horizontal SCC BPPV. The patient is
initially supine with head elevated w30 . Next, the head is rotated 90 to one side while
nystagmus and vertigo are assessed. Once the direction of the nystagmus is deter-
mined, the head is then returned to the neutral supine position. After any further eli-
cited nystagmus has subsided, the head is then turned 90 to the opposite side,
and the eyes are once again observed for nystagmus. In horizontal SCC BPPV, the
nystagmus may be described as either geotropic or apogeotropic when in the roll
test. Geotropic is horizontal nystagmus beating toward the undermost ear (toward
the earth). Ageotropic is horizontal nystagmus beating toward the uppermost ear
(away from the earth).

Head thrust test

The head thrust test (also called the head impulse test) is performed to evaluate the
vestibulo-ocular reflex (VOR). The patient is asked to fix their gaze at a near target
point (typically the examiners nose about an arm’s length away). The head is moved
in an unpredictable direction by 10 to 20 with a small-amplitude (5 –15 ), high-
acceleration (3000 –4000 /s2), and moderate velocity (w200 /s) angular rotation.18
A normally functioning VOR ensures the eyes remain fixed on the target. However,
in vestibular hypofunction, the eyes move with the head rotation, and upon ceasing
the head rotation, make a quick refixation saccade to position bring the eyes back
to the target. In horizontal SCC hypofunction, the corrective saccades occur when
the head is moved toward the lesioned ear. If there is bilateral vestibular hypofunction,
the head impulse test may be abnormal on both sides. This test is more sensitive in
patients with complete loss of function of the labyrinth of one side as compared
with incomplete hypofunction.19,20
 Dizziness and the Otolaryngology Point of View 7

Romberg test
In the Romberg test, the patient is made to stand on a firm surface with feet
together and arms folded against the chest. This test is performed first with the
eyes open and then closed. Inability to maintain a straight posture or occurrence
of sway with both eyes open and closed suggests a pathologic condition, although
this test cannot locate where. Abnormal test results may be due to peripheral neu-
ropathy, cerebellar pathologic condition, or vestibular hypofunction among other
causes. If the sway is present only with the eyes closed, then the patient may
have difficulty using vestibular information. Next, the test is repeated while the pa-
tient stands on a 20-cm-thick foam cushion, which alters the proprioceptive input.
In bilateral vestibular loss, there is commonly an inability to maintain an upright po-
sition standing on foam with eyes closed. The Romberg test is not diagnostic for
vestibular hypofunction.

Vestibular Function Testing

Electronystagmography/videonystagmography
Electronystagmography/videonystagmography (ENG/VNG) involves the use of elec-
trodes/video to measure eye motion and examine oculomotor function as well as
nystagmus. It is a helpful tool for evaluating vestibular disorders; however, it is more
sensitive and specific for central vestibular diseases than peripheral.9,21

Caloric testing
The caloric test is one component of the ENG/VNG and considered the gold-standard
measure of unilateral vestibular hypofunction (UVH). It is the only test that measures
each labyrinth separately. Cold and warm water or air is flushed into the external audi-
tory canal leading to creation of a temperature gradient. This gradient causes endo-
lymphatic flow in the horizontal SCC. In addition, the eighth cranial nerve is directly
stimulated due to the gradient-induced flow, causing nystagmus (and sometimes
nausea). The slow components of the induced nystagmus from each stimulation are
compared to identify the side of lesion.

Rotational chair testing

Another useful test for vestibular hypofunction is the rotatory chair test, a gold-
standard test for bilateral vestibular hypofunction because it measures function
from the combined inputs of each labyrinth. The patient is secured to a chair that ro-
tates in different speeds and directions while eye movements are measured. To
determine the extent of the pathologic condition, the velocity and position of the
resulting eye rotations are compared with the chair rotation. The metrics are also
compared with healthy controls. This test can be helpful in measuring vestibular
function in pediatric and disabled populations, although it involves expensive
equipment.

Vestibular evoked myogenic potentials testing

The otolith end organs can be stimulated with sound or bone-conducted vibration,
which generates a myogenic potential that can be recorded. It has recently gained sig-
nificant clinical importance and is now considered a standard test. Two methods are
offered: the cervical vestibular-evoked myogenic potentials record surface electromy-
ography (EMG) from the sternocleidomastoid muscles and assess the saccular otolith
organ; the ocular vestibular-evoked myogenic potentials version records surface EMG
from the inferior oblique extraocular muscle and assesses the utricular otolith organ.
Patients with vestibular hypofunction may have absent VEMPs on the side of the
lesion.
8 Sorathia et al

PATHOLOGIC CONDITIONS OF THE PERIPHERAL VESTIBULAR SYSTEM

Unilateral Vestibular Hypofunction
Pathologic conditions that are typically included under the umbrella of UVH include
vestibular neuritis, labyrinthitis, unilateral Menieres disease, and perilymphatic fistula.
Vestibular neuritis can be caused by viral, autoimmune causes, or vascular mecha-
nisms. Labyrinthitis can be caused due to bacterial infection of labyrinthine fluids. Both
clinically present as an acute onset of imbalance and rotary vertigo, with nausea and a
spontaneous horizontal nystagmus. It is diagnosed with a reduced or absence of
response in the horizontal SCC when ENG and caloric tests are performed. Hearing
loss is present with labyrinthitis, which distinguishes it from vestibular neuritis.
Menieres disease typically presents with an acute episode of hearing impairment,
tinnitus, and vertigo lasting for hours. The pathogenesis putatively involves an increase
in endolymphatic fluid that causes distention of the membranous tissues. The diag-
nosis is confirmed using audiogram, ENG (caloric test), or a high-resolution MRI of
the inner ear after injecting gadolinium.15

Benign Paroxysmal Positional Vertigo

BPPV is characterized by recurrent episodes of positional vertigo lasting seconds to
minutes. The widely accepted theory of pathophysiology creating BPPV is canalithia-
sis. This mechanism involves otoconia freely floating inside the lumen of the SCC, hav-
ing become displaced from the utricle. When patients change head position, an
atypical stimulation of the SCC results in nystagmus and vertigo in the plane of the
affected SCC.22 The otoconia may attach to the cupula of the affected SCC and cause
a persistent positional nystagmus (termed cupulolithiasis). In both types, posterior
SCC is most commonly affected (w75%) followed by horizontal SCC (w20%). Rarely
does BPPV affect the anterior SCC, although multiple SCC BPPV, including bilateral
BPPV, can occur.21,23,24 The types of nystagmus with the affected semicircular canals
have been mentioned in Table 2.
A diagnosis for posterior canal BPPV is made when vertigo associated with
torsional, upbeating nystagmus is provoked by the Dix-Hallpike maneuver. Horizontal
canal BPPV is diagnosed with a horizontal nystagmus in the supine roll test.

THE PHYSICAL THERAPY MANAGEMENT OF VESTIBULAR DISORDERS

There has been moderate to strong evidence that vestibular rehabilitation is an effec-
tive and safe modality in UVH and BPPV.25–27 It has been recorded that patients after
resection of an acoustic neuroma recover balance earlier than if not treated.28 Like-
wise, patients suffering from acute unilateral vestibular neuritis have shown normaliza-
tion of postural sway within a significantly shorter time course than those without
treatment.29 Physical therapy has also improved symptoms in patients with vestibular
migraine.30,31 The goal is for patients to develop a home exercise program addressing
their limitations while safely improving function and symptoms.

Unilateral Vestibular Hypofunction

Vestibular exercises are prescribed to treat the gaze and gait instability experienced
by patients with vestibular hypofunction. The exercises promote CNS compensation
based on repeated exposure to specific stimuli under different conditions. The goals
of the therapy include demonstration of improved gaze stability during head move-
ment, decreased sensitivity to motion, improvement in static and dynamic postural
stability, and the return to normal activities of daily life. It is essential for patients to
be aware of the approximate 6 to 12 weeks of recovery time required, dependent
 Dizziness and the Otolaryngology Point of View 9

on the extent of hypofunction. Patients benefit most when reinforced about compli-
ance with the exercises.

Gaze stability exercises

These exercises aim to reduce the instability of gaze during head movement that oc-
curs when the VOR is impaired. This type of exercise exposes the patient to retinal slip,
which implies visual images move off the fovea of the retina (during head motion) and
cause a blurring of vision. Repeated stimuli of the retinal slip improve the CNS adap-
tation.32 Patients are instructed to avoid excessive retinal slip and ensure their focus
remains stable on the target during head motion.
Generally, these exercises are progressed in difficulty from sitting to standing and
then during ambulation. Difficulty can also be increased by using a distracting back-
ground around the target and varying distance from the target. Surface supports can
also be adjusted, such as standing on a solid surface, grass, a foam pad, or in sand.

Postural stability exercises

Most patients suffering from vestibular disorders have balance dysfunction too. The
aim of postural stability exercises is to improve balance. Exercises should be safe,
within the limitations of the patient’s abilities, and challenging to perform as part of
a home exercise program. These exercises are generally progressed in terms of diffi-
culty. Some examples include the following:
1. Stand with feet shoulder-width apart, arms across the chest. Progress to bringing
feet closer together, then close eyes or stand on foam.
2. Attempt to walk with heel touching toe on a firm surface. Progress to now walk on
carpet.
3. Practice walking 5 steps and turning 180 (left and right). Progress to making
smaller turns and closing eyes.
4. Walk and move the head side to side, up and down. Progress to counting back-
ward from 100 while doing so.

Motion sensitivity (habituation) exercises

When continual dizziness symptoms persist, patients may be provided habituation ex-
ercises. These exercises reduce the response to a provocative movement by
repeating the movement. Over time, the provoking stimuli are less provocative. The
clinician must determine the provoking position in order to decide the exercises for
the patient. The patient should be guided that symptoms generally reduce within
2 weeks from initiation.

Benign Paroxysmal Positional Vertigo

The goal of treatment in BPPV is the resolution of nystagmus and associated symp-
toms, but also includes a rapid return to regular daily activities. New guidelines for
the management of BPPV suggest that medications are rarely needed and expensive
vestibular function tests are unnecessary.23 Clinicians should educate patients about
the impact of BPPV on their safety and the chances for disease recurrence and
emphasize follow-up.
Many different maneuvers exist for the treatment of BPPV. Two treatments are dis-
cussed. Before the physical therapy maneuvers for BPPV are performed, the patient
should be warned of symptoms during and after the procedures. The patient may
feel vertigo, nausea, and disorientation during the maneuvers that can be slightly dis-
tressing. After the treatment, sometimes symptoms are reported to subside immedi-
ately. In many cases, mild instability and motion sickness might persist for a few hours.
10 Sorathia et al

Canalith repositioning maneuver for treatment of the posterior semicircular canal

BPPV (also known as the Epley maneuver)
The patient is made to sit in an upright position with the head turned 45 toward the
affected ear (as diagnosed by Dix-Hallpike test). The patient is then brought to the su-
pine position with head extended 20 . This position is then maintained until the
nystagmus and vertigo stops. Next, the head is turned 90 toward the unaffected
side (while extension is maintained) and held until the nystagmus and vertigo stop.
From here, the patient rolls onto the unaffected side (lateral decubitus) and waits until
the nystagmus and vertigo stop. To complete the maneuver, the patient is brought
back to the upright sitting position.
Liberatory/Semont maneuver for treatment of the posterior semicircular canal BPPV
The patient is made to sit in the sitting upright position with head turned horizontally
45 away from the affected side. The patient is brought quickly to the side lying posi-
tion of the affected side (lying on the affected ear), and the head will be turned up to-
ward the ceiling. The patient remains in this position for 1 minute. Next, the patient is
moved quickly 180 such that the patient is now lying on the unaffected side with the
head faced down. This position is held for about 1 minute. The patient is slowly moved
back to the sitting upright position.

VESTIBULAR MIGRAINE

Vestibular migraine is characterized by vestibular symptoms (ie, vertigo, imbalance,

nausea) with or without a headache. To make this diagnosis, the patient should
have at least 5 episodes with vestibular symptoms of moderate or severe intensity,
lasting for 5 minutes to 72 hours and current or previous history of migraine with or
without aura according to the International Classification of Headache Disorders.33
In addition, they should have one or more migraine features in at least 50% of vestib-
ular episodes and other vestibular or migraine causes not accounted for.
Vestibular migraine can be inherited in an autosomal dominant pattern. There are
various theories behind the mechanism of this disease, including spreading cortical
depression, pathologic channels that affect different neurotransmitters, and vascular
anomalies.34
In most cases, vestibular migraine is well managed with diet and medication. Un-
controlled migraine can worsen with physical therapy and may be contraindicated
for it. Patients with migraine can have significant improvement in functional outcomes
after vestibular rehabilitation. However, with vestibular hypofunction also present in
the patient, there is often a poor response.
The vestibular rehabilitation in patients with migraine generally follows the principles
described above, including BPPV treatments given the 2 to 3 times increased inci-
dence that can occur in vestibular migraine. Vestibular rehabilitation should be
attempted when chronic, lingering symptoms of head motion induce dizziness, ver-
tigo, or imbalance. The rehabilitation will not stop the migraine episodes, but can
ameliorate the interictal symptoms.

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