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12 Physiology andDiagnostic Tests oftheVestibular System
133
• Three main parameters are measured:
– Gain: Ratio of eye velocity to the head
velocity; ideally, it is equal to 1, but in reality, chair testing is normally lower since
other factors (e.g., equipment) can lead to
this reduction.
– Phase or time constant.
Time constant is measured with step
velocity and is dened as the time needed
for the peak SCEV to reduce to 37% from
peak velocity, and normal value is 10–25s.
The phase is measured with the SHA,
and it compares SCEV with the maximum chair velocity.
– Asymmetry: compares SCEV in the right
to the left side; normally, there is no asymmetry (both rotations are equal).
• Acute vestibular hypofunction (e.g. vestibular
neuritis) leads to reduced gain at all
frequencies.
• Bilateral vestibular hypofunction (typically
chronic) leads to low normal gain at high frequency and low gain at low frequencies.
• Vestibular compensation is suggested by the
absence of asymmetry.
– Pathway: Acoustic Stimuli (95–100
dBnHL) → saccule → inferior vestibular
nerve → vestibular nucleus (brainstem) → vestibulospinal tract → sternocleidomastoid muscle.
– It is generally indicated in cases of
Meniere’s disease, superior canal dehiscence, vestibular neuritis, and to evaluate
saccular and inferior vestibular nerve
function.
– In cases of third window effect (superior
semicircular canal dehiscence syndrome
and perilymphatic stula), abnormally low
thresholds are detected.
• oVEMP:
– It is the only vestibular function test that
specically tests utricle and superior vestibular nerve.
– It is a test of VOR pathway. Both air and
bone conduction stimuli can be used (in air,
contralateral response is tested, and in
bone, conduction bilateral response is
tested).
– Pathway: Acoustic stimuli → utri-
cle→superior vestibular nerve→inferior
oblique.
12.5.6 Vestibular Evoked Myogenic
potential
• It is an electrophysiological (EMG, electro-
myography) test of the otolith function.
• cVEMP (cervical) is a test of saccular and
inferior vestibular nerve function, while
oVEMP (ocular) tests the utricle and superior
vestibular nerve.
• cVEMP:
– cVEMP: VEMP measures VCR (vestibu-
locollic reex), which is a reex that acts
on neck muscles to stabilize the head based
on inputs from the vestibular system.
– It is the only vestibular function test that
specically tests the saccule and inferior
branch of the vestibular nerve.
– The test is similar to ABR where electrodes
are placed over the ipsilateral SCM; however, the response is larger (200 μV compared to 1μV for ABR).
12.5.7 Video Head Impulse Test
(vHIT)
• It is the only vestibular test that can test all the
semicircular canals (superior, lateral, and
posterior).
• It is comprised of rapid head movement
(impulses) to the right and left of small amplitude 10–20° with a velocity of 100°/s or more
while xing the eyes at certain point, usually on
the wall 1–2 m in front of the patient. Eye
movements are recorded with camera goggles.
• A peripheral disorder will result in a correc-
tive saccade. A right-sided lesion will result in
a corrective saccade to the left when the head
is turned to the right.
• The main advantage of the video head impulse
test over the clinical/bedside head impulse is
that it can detect overt (corrective saccade that
happens after the head movement stops) and
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covert saccade (which happens during head
movement). In contrast to the bedside test, it
only detects the overt saccade.
• A normal test helps to differentiate vestibular
neuritis from ischemic brainstem/cerebellar
stroke in cases of acute vestibular syndrome.
12.5.8 Computerized Dynamic
Posturography
• It is a test of postural stability at different conditions to give a functional assessment of visual,
proprioceptive, and vestibular systems.
• Sensory organization test (the main test): it
evaluates body sway under the following
conditions:
– Eyes opened: xed surface and visual
surrounding
– Eyes closed: xed surface
– Eyes opened: xed surface, sway refer-
enced visual surrounding
– Eyes opened: swayed referenced surface,
xed visual surrounding
– Eyes closed: swayed referenced surface
– Eyes opened: swayed referenced surface
and visual surrounding
• Uses include vestibular testing to detect functional vestibular impairment, evaluate
improvement in function pre- and postvestibular rehabilitation, and medico-legally
to assess malingerers.
W. Omer and K. Abdulhadi
Take-Home Messages
• Understanding the physiology of the
vestibular system is important in understanding vestibular testing.
• Vestibular test complements history and
physical examination, and it does not
replace them.
• The vestibular tests help to identify the
site and extent of the lesion in addition
to assessing the degree of central
compensation.
References
1. Goldberg JM, Wilson VJ, Angelaki DE, Cullen KE,
Fukushima K. The vestibular system: a sixth sense.
Oxford: Oxford University Press; 2012.
2. Grill E, Heuberger M, Strobl R, Saglam M, Holle R,
Linkohr B, Ladwig KH, Peters A, Schneider E, Jahn
K, Lehnen N. Prevalence, determinants, and consequences of vestibular hypofunction. Results from the
KORA-FF4 survey. Front Neurol. 2018;9:1076.
3. Kandel ER, Schwartz JH, Jessell TM, Siegelbaum SA,
Hudspeth AJ, editors, Mack S, art editor. Principles
of neural science. 5th ed. NewYork: McGraw-Hill;
2013.
4. Iurato S.Organ of Corti. In: Submicroscopic structure
of the inner ear. Oxford: Pergamon; 1967. p.80–106.
5. Ewald JR. dizziness-and-balance.com/history/ewald.
html.
AL GRAWANY
Dizziness andVestibular Disorders
HassanHaidar andRawanH.A.Azzam
13
Key Points
• Vertigo is a common presentation in
general practice.
• A careful history is required to elicit
features of central or peripheral causes
of vertigo.
• Serious causes including stroke need to
be considered.
• Physical examination involves a neurological, cardiovascular, eye, and ear
examination.
• Treatment is specic to the cause of
vertigo.
13.1 Introduction
Dizziness is a common symptom in ENT practice
as well as primary care.
The prevalence of vertigo as a function of age
lies around 17% and rises up to 39% in those over
80years of age [1]. Most of the causes are benign,
and there are few serious causes that must be considered in diagnosis. Unfortunately, there is no
simple and reliable method to identify those
patients with serious underlying causes, further
increasing the need for a systematic approach to
evaluation.
13.2 Evaluation ofaDizzy Patient
The history and physical examination are the
critical elements in determining the underlying
cause of the dizziness (Table13.1).
In the evaluation of a patient who experiences
dizziness, our initial efforts must be directed at
determining the exact nature of the patient’s
symptoms because the pathophysiology determines the patient’s sensations.
13.2.1 History
The main goal of the history is to determine
exactly what the patient means by the term “dizziness”. There are generally three things that
patients mean by “dizziness”, and each requires a
distinct process of evaluation:
H. Haidar (*)
Hamad Medical Corporation, Doha, Qatar
ENT Department, Hamad Medical Corporation,
Doha, Qatar
R. H. A. Azzam
ENT Department, Hamad Medical Corporation,
Doha, Qatar
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_13
1. Vertigo is dened as the sensation of spin-
ning. Questions such as “does it feel like
you’re on an amusement ride” and “are you
sick to your stomach with the dizziness” suggest that they have vertigo.
135
136
H. Haidar and R. H. A. Azzam
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Table 13.1 Characteristics of major causes of dizziness
Disorder Duration Triggers Diagnosis
BPPV Seconds Turning in bed Dix–Hallpike
Vestibular Neuritis 3–5days Spontaneous, after u Unidirectional nystagmus,
Meniere’sdisease Hours Salt intake, sleep deprivation, stress Low-frequency hearing loss,
Migraine-associated
dizziness
Stroke Days to weeks Spontaneous in patients with
Orthostatic
hypotension
Anxiety Disorder Minutes to days Complex visual surround, crowds, stress Anxiety symptoms
Cerebellar ataxia Chronic Alcohol, genetic Ataxia
Minutes to days Migraine triggers (menses, seasonal
changes, sleep deprivation, specic
food, stress)
cardiovascular risk factors
Seconds Standing from sitting position Postural drop in blood
Positive head thrust test
Fluctuating
Positive family history,
association with migraine
headache and symptoms
Associated neurological
decits
pressure
2. Pre-syncope is a feeling of faintness or light-
headedness. Questions such as “do you feel
like you might pass out” or “does it feel similar to when you stand up too fast” are questions which suggest that the patient is
describing pre-syncope.
3. Disequilibrium is the feeling of being
unsteady on one’s feet. Typically, this
improves quite a bit when there are other sensory cues (such as the ability to touch things)
and is much worse when the patient’s vision is
blocked, or when the surface on which they
are walking is very uneven. Questions such as
“does it only happen when you’re on your
feet” and “does it get much better if you touch
things” are very useful. Additionally, disequilibrium is probable if the patient notes that the
sensation is substantially worse in the dark or
when they are in the shower.
Other important points to look after during
history taking are:
• The timing of the dizziness whether it appears
constantly or in attacks.
• Any associated symptoms (such as hearing
change, nausea, etc.).
• The duration of the attacks.
• Provocative causes (such as movement, loud
noise, or pressure changes).
The most essential question is whether any
neurologic symptoms are present. As there are
several potentially dangerous causes of dizziness,
one must always maintain a high degree of suspicion (cerebellar hemorrhage or ischemia, brainstem hemorrhage or ischemia, vertebral artery
dissection).
One should ask about any weakness or change
in sensation of the limbs or face, slurred speech,
vision changes, memory loss, or ataxia. These
symptoms are indicative of a central insult.
Although rare, compromise of the posterior
cerebral circulation may manifest with neck pain
(from trauma or vertebral artery dissection) and
associated dizziness and requires prompt neurosurgical consultation.
13.2.2 Examination
The examination should focus on the cardiovascular system (cardiac rhythm and orthostatic
blood pressure measurements) on the neurologic
system (oculomotor function and balance) and
the ear examination (vestibular system and
hearing).
• Spontaneous nystagmus
Spontaneous nystagmus indicates an
imbalance within the vestibular system (central or peripheral). A unidirectional horizontal
AL GRAWANY
13 Dizziness andVestibular Disorders
137
spontaneous nystagmus is characteristic of an
acute peripheral vestibular insult. Spontaneous
vertical, pure torsional nystagmus indicates a
central lesion.
• Gaze-evoked nystagmus
Unilateral vestibular lesion can result in
gaze- evoked nystagmus that only occurs in
one direction.
Central lesions typically lead to gazeevoked nystagmus that is “multidirectional”.
• Head Thrust Test
The head thrust test is used to assess the
vestibulo- ocular reex (VOR).
In patients with normal vestibular function,
the VOR results in movement of the eyes in
the direction opposite to the head movement.
In peripheral vestibular insult, impairment
of the VOR is identied where the eyes move
off the target and a voluntary saccade (socalled rexation saccade or catch-up saccades) is observed bringing the patient’s eyes
back to the target after the head thrust test.
• Positional testing
Positional testing can trigger peripheral or
central nystagmus.
The Dix–Hallpike test is used to diagnose
the posterior semicircular canal in benign paroxysmal positional vertigo (BPPV). The head
is turned 45° to the side in the sitting patient,
and then he/she is moved to the head-hanging
position. If the patient has debris moving in the
posterior canal, this will lead to a burst of
upbeat-torsional nystagmus lasting about 15s.
Pure vertical nystagmus, particularly persistent
downbeat nystagmus, suggests a central lesion,
usually involving the midline cerebellum.
• Gait and balance testing
The patient is observed while walking normally, while walking in tandem, and in the
Romberg position with eyes opened and
closed. Impaired gait and balance can accompany dizziness of any cause.
Severe gait impairment suggests a neurologic disorder.
Patients with peripheral vestibular lesions
are off-balance but usually can walk with
assistance and their imbalance gets exacerbated once they close their eyes.
13.3 Vertigo
Vertigo, the illusion of movement, is due to
imbalances of signals to the central vestibular
apparatus. This can either be due to peripheral or
central causes. Signs and symptoms can usually
distinguish peripheral from central causes of vertigo (Table13.2).
Table 13.2 Common signs and symptoms differentiating central vertigo from peripheral vertigo
Central vertigo Peripheral vertigo
Onset Gradual, slow Sudden
Intensity Mild Severe
Duration Weeks to months Intermittent episodes:
Fatigability Does not fatigue Fatigues, adaptation
Associated symptoms Weakness, numbness, falls more likely Nausea, hearing loss, sweating
Eye closure Symptoms better with eyes closed Symptoms worse with eye closed
Nystagmus Vertical, bilateral Horizontal
Latency of nystagmus Short (<5sec) Longer (>20sec)
Ocular xation No effect or enhances nystagmus Suppresses nystagmus (may not suppress
Effect of head position Little change, associated with more
than one position
<1min for BPPV
Continuous lasting for hours or days for
vestibular neuritis
during acute phase)
Worsened by position, often single critical
position
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H. Haidar and R. H. A. Azzam
13.3.1 Peripheral Vertigo
It relates to damage of the inner ear receptors or
to the vestibulocochlear nerve. There may be
auditory symptoms. There should be no other
signs of damage to the nervous system. The
patient is likely to experience nausea or “motion
sickness”.
The nystagmus is unidirectional either hori-
zontal or rotary.
Head thrust can provide important information. Usually, individuals are able to maintain
good focus if the inner ears are intact since the
head thrust activates the VOR.Inability to maintain xation when doing this indicates damage to
the inner ear.
13.3.2 Central Vertigo
Central causes include damage to the central nervous system mainly the brain stem. Central vertigo is typically milder than peripheral. The
amount of nystagmus is usually greater than the
patient’s symptoms. Additionally, the nystagmus
may be in multiple directions or possibly in a vertical direction. There are often other abnormalities of the central nervous system found by
examination.
13.4 Vestibular Disorders
13.4.1 Vestibular Neuritis
Vestibular neuritis is an inner ear disease characterized by a sudden drop in ipsilateral vestibular
function and acute onset of severe vertigo without any neurologic decits.
Epidemiology: Vestibular neuritis accounts
for 5–10% of all cases presenting with vertigo,
with an annual incidence of approximating 3.5
cases per 100,000 persons. Common age is
between 30 and 50years [2, 3].
Physiopathology: Herpes viral infectious
process affecting “Scarpa’s” ganglion or the vestibular nerve might be responsible.
The superior vestibular nerve, which supplies
the utricle, superior, and horizontal semicircular
canals, is more likely to be involved in cases of
vestibular neuritis because of the increased
length, reduced diameter, and increased bony trabeculae of the bony canal housing it as compared
with the inferior vestibular nerve [4–7].
Benign paroxysmal positional vertigo (BPPV)
is more common in patients who have suffered
from vestibular neuritis because the utricular otoconia might be loosened with the initial neuritis
and oat into the posterior canal innervated by
the superior vestibular nerve which stays functional in the majority of vestibular neuritis
patients as evidenced by normal VEMP studies
(saccular nerve is branch of superior vestibular
nerve).
Clinical manifestations: It is characterized
by the acute onset of vertigo with associated nausea, vomiting, and generalized imbalance. The
acute phase is often severe and can last from a
few hours to several days, while a more subtle
sense of imbalance and unsteadiness may linger
for weeks. Auditory symptoms are absent.
Patients with accompanying hearing loss are
believed to have a slightly different pathophysiological entity termed acute labyrinthitis.
Physical examination: Patients with vestibular
neuritis may sway toward the side of the involved
ear while standing, but an inability to stand without assistance is indicative of a central lesion.
It is characterised by Spontaneous horizontorotatory nystagmus that beats to the contra-lateral
side and improves with xation.
Head thrust testing toward the affected ear
will often demonstrate catch-up saccades indicating a peripheral vestibular insult.
Diagnosis: History and physical examination
alone are usually adequate for diagnosis and no
need for imaging.
Management of the acute phase of vestibular
neuritis is primarily medical, while long-term
treatment is designed to improve vestibular
compensation.
The early administration of steroids may
improve the rate and extent of recovery of vestibular function.
AL GRAWANY
13 Dizziness andVestibular Disorders
139
Early exercise is encouraged, and patients are
instructed on various vestibular exercises
designed to enhance ocular stability and improve
the tolerance of various head and body
movements.
The degree of compensation is somewhat variable and likely depends on a number of factors,
including patient age, underlying functional status, and degree of initial vestibular injury. While
many patients may be able to compensate with
the help of home vestibular exercise programs,
others may require formal vestibular
rehabilitation.
13.4.2 Meniere’s Disease
Meniere’s disease (MD) is a clinical syndrome
characterized by episodic spontaneous vertigo,
uctuating hearing loss, aural pressure, and
tinnitus.
13.4.2.1 Epidemiology
The incidence of MD varies between 4.3 and
15.3 per 100,000 [8, 9].
Affected individuals are usually between the
fourth and sixth decades of life, with a female/
male ratio of 1.3:1. Bilateral MD at presentation
was seen in 11%, with another 14% of unilateral
MD becoming bilateral MD.
13.4.2.2 Physiopathology
Endolymphatic hydrops (ELH) is felt to be the
underlying histopathologic correlate in MD.
Histopathological studies in human temporal
bones have found ELH in most patients with MD
[10, 11] .
3T MRI (3 Tesla MRI)with gadolinium chelate showed ELH in 93% of ears with symptoms
attributable to MD [12].
Electrophysiologic studies showing increased
SP/AP ratios suggest the presence of ELH [13].
The cause of ELH is multifactorial. Several
intrinsic (genetic, anatomic, autoimmune, or vascular) or extrinsic (allergic, viral, or trauma) factors can cause disturbance in the mechanisms
involved in the regulation of endolymphatic uid
homeostasis.
13.4.2.3 Diagnosis
History, physical examination, and audiometry
alone are enough to establish the diagnosis of
MD:
• Two or more spontaneous episodes of vertigo
each lasting 20min to 12h.
• Low- to medium-frequency sensorineural
hearing loss in one ear, dening the affected
ear on at least one occasion before, during, or
after one of the episodes of vertigo.
• Fluctuating aural symptoms (hearing, tinnitus,
or fullness) in the affected ear.
• Not better accounted for by another vestibular
diagnosis.
13.4.2.4 Electrophysiologic Studies
Several diagnostic tests have been proposed to
study the presence of ELH and complement the
clinical diagnosis of MD.Two electrophysiologic
tests merit discussion: electrocochleography
(ECoG) and VEMPs.
• Electrocochleography
It is an evoked potential in response to a
click or tone burst stimuli recorded by an intratympanic or extra tympanic electrode. The SP
and AP of the eighth nerve are recorded.
An increased SP/AP ratio (greater than 0.4)
and/or a widened AP width (greater than 3ms)
are considered to be signicant for ELH.The
sensitivity is 70–90%.
• The cervical VEMP (cVEMP)
The cVEMP is a recording of the vestibulo-
collic reex generated in the saccule, carried
via the inferior vestibular nerve. It consists of
an inhibitory potential of the ipsilateral sternocleidomastoid muscle (SCM) muscle
evoked by a brief and loud (>85dB) monaural
click or tone burst stimuli.
Patients with MD were shown to have
increased cVEMP thresholds or absent reex
compared with controls.
• Caloric Testing and Head-thrust Testing
Signicant caloric weakness is present in
42–73% of patients with MD.
Caloric testing is useful in: (1) assessment
of contralateral function before an ablative
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H. Haidar and R. H. A. Azzam
procedure, (2) assessment of residual function
after an ablative procedure, and (3) assessment of ipsilateral function; if residual function is good, we favor a non-destructive
procedure.
13.4.2.5 Management
The initial management of MD includes a lowsalt diet and avoidance of caffeine derivatives and
alcohol.
• Diuretics and low-sodium diet are effective in
controlling the symptoms of MD in most of
patients.
• Intratympanic dexamethasone can control
vertigo in more than 90% of patients. Although
more than half of the patients responded to
one or two injections, some patients may
require more than four injections.
• Intratympanic gentamicin is a destructive
treatment that results in chemical labyrinthectomy. Gentamicin is a selective vestibulotoxic aminoglycoside antibiotic that causes
apoptotic cell death of the vestibular dark
cells, resulting in partial or complete ablation
of peripheral vestibular function. Hearing
deterioration occurs in 10–35% of patients
and depends on host genetic susceptibility to
aminoglycosides affect. When hearing is
poor, it is a reasonable option that offers
effective vertigo control with minimal morbidity; however, in patients with serviceable
hearing, many physicians feel reluctant to
use it.
• Endolymphatic sac surgery: The efcacy of
sac surgery has been, and continues to be,
debated. There is no evidence of its superiority to natural history of the disease.
• Vestibular nerve sectioning: Selective section-
ing of the vestibular nerve performed via retrosigmoid approach offers more than 95%
control of vertigo. It is an excellent option in
patient with refractory vertigo and serviceable
hearing.
• Labyrinthectomy: When conservative procedures fail to control vertigo, the treating otolo-
gist needs to consider neural or labyrinthine
destructive procedures to ablate all residual
vestibular function in the hope of controlling
the ongoing vestibulopathy.
13.4.3 Benign Paroxysmal Positional
Vertigo
Benign paroxysmal positional vertigo (BPPV) is
the most common peripheral vestibular endorgan disease and is typied by a sudden, transient vertigo which is accompanied by
characteristic nystagmus.
13.4.3.1 Epidemiology
BPPV is the most common vestibular disorders
with an estimated lifetime prevalence of 2.4% in
the general adult population. More than 30% of
patients attending a dizzy clinic are diagnosed
with BPPV.
Although this disorder affects people across
their lifespan, it tends to affect individuals aged
50–70years.
13.4.3.2 Pathophysiology ofBPPV
The otoconia from the utricle dislodge and settle
within one of the three semicircular canals,
changing the uid-lled canal dynamics from
detecting rotation of the canals to detecting gravitation forces on the head.
The debris may be found within the long arm
of the canal (canalithiasis) or in the short arm of
the canal or attached to the cupula
(cupulolithiasis).
The reasons for detachment are many but
include increasing age, trauma, and infection.
95%of BPPV cases involve the PSC, and 5%
involve the lateral semicircular canal (LSC).
13.4.3.3 Diagnosis andTreatment
ofPSC-BPPV
The diagnosis of BPPV is based on history and
ndings on positional testing. Patients who complain of vertigo with rolling in bed or getting out
of bed are most likely to have BPPV.
AL GRAWANY
13 Dizziness andVestibular Disorders
141
• Dix–Hallpike diagnostic maneuver is the
diagnostic maneuver. During this maneuver,
the patient’s head is turned 45° to one side
while he is seated. The patient is then moved
quickly to a supine position with the neck
slightly extended and the head remaining
turned. The diagnostic criteria for posterior
canal BPPV are vertigo associated with the
characteristic nystagmus—ipsidirectional torsional and up beating nystagmus is seen when
the undermost ear is affected. With a latency
of 30–45s before onset and a duration of less
than 60s.The nystagmus is noted to reverse
direction when thepatient isbrought back up
to a sitting position. The nystagmus diminishes with repeated positional testing in the
same sitting.
• Epley therapeutic maneuver is canalith reposi-
tioning maneuver described by Epley and consists of a series of four head positions designed
to use the effects of gravity to treat canalithiasis. With each head position, the debris settles
to the lowest portion of the canal, moving the
debris away from the ampulla, into the common crus, and then into the utricle.
Repeating the maneuver2–3 times is signicantly more effective than performing it
once.
There is no need for postintervention postural and activity restrictions.
It is effective in more than 90% of cases.
• The Semont therapeuticmaneuver is another
PSC canalith repositioning maneuver whereby
the patient is rapidly moved from lying on one
side to lying on the other. The Semont maneuver is less effective and not currently favored
because the high velocity which is anxiety
provoking. Practically, it is often tried when
Epley maneuver fails.
13.4.3.4 Diagnosis andTreatment
ofLSC-BPPV
LSC-BPPV can be diagnosed with supine positional testing (head centered supine, right ear
down, and then left ear down). This maneuvre
provokes a bidirectional/bipositional horizontal
nystagmus.The identication of the involved ear
in LSC-BPPV can be especially difcult because
the canals are coplanar, and nystagmus is seen in
both positionsregardless of the involved ear.
Two distinct subtypes of LSC-BPPV exist
based on nystagmusdirection during supinepositional testing:
• Geotropic LSC-BPPV
It is caused by canaliths moving within the
long arm of the LSC.
During supine positional testing, nystagmus is horizontal andbeats toward theground
and is worse with the affected ear down. The
nystagmus has a short latency and prolonged
duration with poor fatigability.
Treatment of geotropic LSC-BPV consists
of 360° log roll maneuvers toward the unaffected ear at 90° increments every 30–60 s,
beginning with the patient in the supine position and laterally rotated toward the affected
ear. Repositioning treatments can alleviate
symptoms in 75–100% of patients
• Apogeotropic LSC-BPPV
It is very rare and iscaused by otoconial
debris that adheres to the cupula of the lateral
canal (cupulolithiasis) or otoconia trapped in
the proximal segment of the lateral canal.
During supine positional testing, the nys-
tagmus beating is away from the undermost
ear. Nystagmus is usually worse with the
affected ear uppermost.
Treatment of apogeotropic LSC-BPPV
consists of the Lempert 360° roll maneuver
toward the unaffected ear. The efcacy of
canalith repositioning for apogeotropic LSCBPPV is less than 50%.
13.4.3.5 Surgical Treatment ofBPPV
If repositioning therapy is not successful, surgery
is an option for PSC-BPPV. Plugging of the
involved semicircular canal has been used in
cases of resistant PSC-BPPV.
However, this treatment has been more difcult for LSC-BPPV because of the difculty
inlocating the correct side.
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H. Haidar and R. H. A. Azzam
13.4.4 Migraine-Associated Vertigo
Migraine-associated vertigo (MAV) is dened as
vertigo or dizziness caused by migraine.
13.4.4.1 Prevalence
Ten percent of the population has migraine headaches [14],and 1/3 of them experience dizziness
[15]. It affects women approximately three times
more frequently than men. MAV is 10 times more
common than Meniere’s disease.
13.4.4.2 Clinical Manifestations
• The most common symptoms of MAV are
rotational vertigo, intolerance of head motion
or visual motion, sensation of motion sickness, oating, rocking, tilting, walking on an
uneven surface, and lightheadedness.
• The onset of symptoms could be gradual or
abrupt and usually, but necessarily, associated
with migraine symptoms like headache, photophobia, phonophobia, nausea, and/or aura.
• MAV is usually triggered by migraine triggers: menses, sleep deprivation, fasting, dehydration, change of season, caffeine (or change
in the pattern of caffeine intake), chocolate,
alcohol, aged cheeses, nitrites…
• The duration of symptoms is usually few
hours but may range from minutes to days.
13.4.4.3 Diagnosis
It is based on the identication of the following
three clinical criteria:
1. Episodic vestibular symptoms of at least mod-
erate severity.
2. History of migraine, or migrainous symptoms
during some attacks of vertigo, or migraine
triggers of vertigo in more than 50% of
attacks.
3. Other causes are ruled out by appropriate
investigations. The most useful tests include
audiometry (to exclude Meniere’s disease or
labyrinthitis) and videonystagmography (to
exclude peripheral vestibular hypofunction).
In cases where doubt remains, brain imaging
is warranted.
13.4.4.4 Treatment
MAV is managed similarly to migraine:
• Trigger avoidance.
• Pharmaceutical Prophylactic is favored when
attacks are frequent or severe. Three groups of
medications can be employed: anticonvulsants, antihypertensives, and antidepressants.
In our practice, treatment most commonly
starts with the antidepressant, venlafaxine,
followed by the anticonvulsant, topiramate,
and then b-blockers (e.g. propranolol).
Benign paroxysmal vertigo of childhood
(BPVC) is a vertiginous disorder of childhood
attributable to migraine and has a prevalence of
3%. It typically occurs in children 3–8years old.
Attacks are sudden in onset and are typically
brief, lasting only a few seconds to minutes. The
affected child may remain still, refusing to move,
or may grab onto something for support, and nystagmus is often noted during the attack. There is
often associated anxiety, pallor, nausea, sweating, and occasionally vomiting. At the completion of the attack, the child usually resumes
normal activity. Physical examination and all
imaging studies typically are normal. After a few
years, the episodes of BPVC cease. Children
affected with BPVC may develop classic
migraines later in life [16–18].
13.4.5 Superior Canal Dehiscence
Syndrome
Typical symptoms include hyperacusis for boneconducted sounds with autophony, and vertigo
induced by loud sounds (Tullio phenomenon) or
increased pressure in the middle ear (Hennebert
sign) or intracranial space (e.g. during strenuous
activities) (see Chap.13).
13.4.6 Perilymph Fistula
Perilymphatic stula results from a small leak
between the inner ear and the air-lled middle
AL GRAWANY
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