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11 Tinnitus andHyperacusis
123
The effect of the surrounding stimuli on
the tinnitus; it is exacerbating or inhibiting the tinnitus.
The effect of the tinnitus on the patient like
anxiety, depression, or sleep deprivation.
– Different standardized questionnaires can
detect tinnitus severity and the disability
that can occur on the individual [3].
– Audio tympanogram [3].
– Other tests like:
Measurement of loudness and pitch of
the tinnitus: it is often not accurate
[12].
Minimal masking level: the intensity of
sound needed to mask the tinnitus [13].
Residual inhibition: the length of time
where the tinnitus is absent or decreased
after being exposed to one minute of
masking [14].
– MRI: especially for unilateral tinnitus [3].
• Management:
• Different devices, medications, and psychotherapy techniques were used to treat tinnitus;
some of these methods are:
– Counseling and reassurance which are con-
sidered the key step in management [15].
– Hearing aid: hearing amplication can
decrease tinnitus. Patients with associated
hearing loss can benet from hearing aid in
treating this condition [16].
– Sound therapy: by utilizing specic
devices, sound can be used for tinnitus
masking or distraction [17].
– Combination treatment modalities (called
tinnitus retraining therapy (TRT)), in which
combination of counseling and sound ther-
apy is used [18].
– Cognitive behavioral therapy (CBT) [19].
– Some other techniques were used to treat
tinnitus like relaxation technique, acupunc-
ture, and some herbal medicines [3].
– Electromagnetic stimulation [20].
– Certain medications were used like
Tricyclic antidepressants, selective sero-
tonin reuptake inhibitors (SSRI), and ben-
zodiazepine. Local anesthesia like
lidocaine can suppress tinnitus, but the
effect is short term [3].
– Intratympanic injection of steroid or local
anesthesia [21, 22].
– Dietary supplements, like vitamins and
minerals, were used to treat tinnitus.
Vitamin B was found to offer ear protection
against noise trauma [3].
– Lasers [3].
– Surgery: stapedectomy was found to treat
tinnitus caused by otosclerosis [23]. Also,
cochlear implantation was found to
improve tinnitus in those patients with pro-
found hearing loss [24].
11.2.2 Objective Tinnitus
• It can be pulsatile or non-pulsatile. Look at
Table11.3 [2].
11.2.3 Non-pulsatile Objective
Tinnitus
• Caused by otoacoustic emission or patulous
Eustachian tube.
• Patulous Eustachian tube:
Table 11.3 Objective tinnitus
Pulsatile
– Arteriovenous
malformation or
stula
– Persistent stapedial
artery
– Primary vascular
abnormality
– Carotid artery
stenosis
– Atherosclerosis of
external carotid
subclavian artery
– Paraganglioma
– Hyperdynamic
circulation like
pregnancy and
hyperthyroidism
– Pseudotumor
cerebri
– Jugular bulb
anomaly
– Venous hum
Nonsynchronous
– Palatal
myoclonus
– Tensor
tympani/
Stapedial
myoclonus
Non-pulsatileSynchronous
– Otoacoustic
emission
– Patulous
Eustachian
tube
124
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A. Larem et al.
– Tuba aperta is another name [3].
– There are two types:
Patulous ET: in which the ET remains
anatomically open [3].
Semi-patulous ET: in which the ET may
open at exercise due to low resistance to
airow [3].
– Symptoms: autophony, hearing loss, a sen-
sation of pressure in the ear, and tinnitus
synchronized to breathing [7].
– Causes: weight loss (causing loss of
Ostmann’s fat pad), radiation, injury to cranial nerve V, or iatrogenic injury to tensor
veli palatini muscle during surgery to cleft
palate [7].
– Diagnosis: through history and physical
examination. Movement of the tympanic
membrane with respiration is diagnostic,
but it is not always seen. Tympanogram
with reux delay can help in diagnosis but
needs an intact TM.Tympanometry can be
utilized for diagnosis, and it helps in differentiating between patulous ET and
obstructive ET [3].
– Treatment: conservative (it is often self-
limited in children). Medical treatment like
nasal estrogen drops or oral administration
of iodide to induce swelling to the opening
of ET [3, 25]. Surgical treatment, for example, grommets insertion was seen to help in
alleviating the symptoms [26], and another
example is augmentation tympanoplasty
with cartilage or tuboplasty [3].
11.2.4 Pulsatile Tinnitus
• It can be divided into synchronous and nonsynchronous [3].
11.2.4.1 Synchronous Pulsatile
Tinnitus
• It means it synchronizes with the patient’s
heartbeats.
• Etiology [2].
– Arterial causes:
Arteriovenous malformation or stula.
Persistent stapedial artery.
Primary vascular abnormality.
Carotid artery stenosis.
Atherosclerosis of external carotid subclavian artery.
Paraganglioma.
Hyperdynamic circulation like pregnancy
and hyperthyroidism.
– Venous causes:
Pseudotumor cerebri.
Jugular bulb anomaly.
Venous hum.
• Investigation:
– If retrotympanic mass is found during otos-
copy, then order CT temporal bone [27].
– If atherosclerosis of the carotid is sus-
pected, then ask for duplex carotid US [3].
– If idiopathic intracranial hypertension is
suspected, then referral to ophthalmology
should be done along with LP for the measurement of CSF pressure [3].
• Treatment:
– If no pathology is found, then reassurance
is recommended.
– If pathology is found, treat the underlying
condition [3].
11.2.4.2 Non-synchronous Pulsatile
Tinnitus
• It is not synchronized with the patient’s
heartbeat.
• Causes:
– Palatal myoclonus: it is caused by myoclo-
nus of the palate leading to rapid clicking
tinnitus [28].
– Tensor tympani/Stapedial myoclonus:
leading to low-frequency tinnitus exaugurated by external sound [29].
• It is essential to differentiate between middle
ear myoclonus and palatal muscle myoclonus,
with the latter presenting with involuntary
movement of the soft palate and suprahyoid
muscles. Palatal myoclonus is often associated with CNS lesions so that brain MRI
should be done [30].
• Treatment: first conservative and support-
ive therapy should be tried like relaxation
therapy, biofeedback, and tinnitus masking.
Certain medications can be used like carba-
AL GRAWANY
11 Tinnitus andHyperacusis
125
mazepine and benzodiazepine. If these trials failed, then surgical therapy can be
offered, which includes the division of both
tensor tympani and stapedial muscles [3]
(Figs.11.1 and 11.2).
Fig. 11.1 Otoscopic view of aberrant carotid artery
11.3 Hyperacusis
• Dened as unusual tolerance to ordinary envi-
ronmental sounds [7].
• It is considered a central phenomenon and
should be distinguished from recruitment,
which is a peripheral phenomenon.
Recruitment is not considered part of hyperacusis as the patients will experience rapid
growth of loudness upon increasing the tone
level [2].
• Prevalence: 8–15% [3].
• Both hyperacusis and tinnitus often occur
together [3].
• Most of the cases of hyperacusis have no
known pathology. There are some medical
conditions that can lead to hyperacusis: look
at Table11.4 [7].
• Pathophysiology is thought to be by GABA
central pathways as patients with
Benzodiazepine withdrawal experience this
phenomenon [31].
• In hyperacusis, patients experience physical
discomfort upon exposure to moderate or
weak sound stimuli, which generally will not
cause any discomfort in a normal person.
ab
Fig. 11.2 (a) Right ear otoscopic image of the typical
bluish appearance of the prominent high jugular bulb
(asterisk) visible through the tympanic membrane (b)
coronal CT-reconstruction of a right ear, showing a promi-
nent jugular bulb (JB), protruding in into the hypotympanic cavity up to the level of the round window recess
(black arrow). Tympanic aerator (white arrow) inserted
through a thin tympanic membrane
126
A. Larem et al.
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Table 11.4 Medical conditions that can lead to
hyperacusis
Tinnitus
Bell’s palsy
Ramsay hunt syndrome
Lyme disease
Stapedectomy
Perilymphatic stula
Translabyrinthine excision of a vestibular schwannoma
Head injury
Migraine
Depression
Addison disease
Williams syndrome
• Hyperacusis can have a negative psychological impact on patients. It can lead to misophonia (which means the patient will dislike
sounds) or phonophobia (in which patients
will have fear from exposure to sounds). In
severe cases, patients can become housebound [7].
• Investigation: hyperacusis questionnaires can
be utilized. Measurement of loudness discomfort level can be used, but some claim that it is
not reliable [3].
• Treatment: Gradual desensitization can be
used to treat this condition. Tinnitus retraining therapy (TRT) and cognitive behavioral
therapy (CBT) can also be used [32, 33]. It
is important to note that in those patients,
they may use earplugs as a defense from
their increased perception of loudness.
However, these earplugs can aggravate the
hyperacusis by increasing the central nervous system gain [34].
Take-Home Messages
• Tinnitus is divided into subjective and
objective.
• Subjective has different subtypes.
Examples are hearing loss subtype,
somatic tinnitus, typewriter tinnitus,
musical tinnitus, intrusive, and associated with affective disorder.
• Hearing loss subtype includes noiseinduced hearing loss and presbycusis.
The somatic subtype is modulated
through physical stimulation like eye
movements, leg movement, and pressure on the temporomandibular joint.
Usually, they respond to acupuncture
therapy. Typewriter tinnitus has staccato
quality and can respond to
Carbamazepine therapy.
• History is vital during the evaluation of
patients with tinnitus. An audio tympanogram can be ordered. Ask for MRI in
cases of unilateral tinnitus.
• Counseling and reassurance are an
essential step while managing patients
with tinnitus. Different methods were
used to treat the condition like hearing
aid, sound therapy, tinnitus retraining
therapy, and cognitive behavioral
therapy.
• Objective tinnitus can be pulsatile or
non-pulsatile.
• Non-pulsatile tinnitus includes otoacoustic emission and Patulous
Eustachian tube.
• Patulous Eustachian tube can be caused
by weight loss, radiotherapy, and injury
to CN V and tensor veli palatini muscle.
It presents with autophony, hearing loss,
a sensation of pressure in the ear, and
tinnitus that is synchronized to
breathing.
• Objective non-pulsatile tinnitus can be
synchronous or non-synchronous to the
patient’s heartbeat.
• Synchronous pulsatile objective tinnitus
has different etiologies and is usually
caused by vascular pathology.
• Non-synchronous pulsatile objective
tinnitus is caused by either palatal
myoclonus or tensor tympani/stapedial
muscle myoclonus. Palatal myoclonus
is often associated with CNS lesions so
that brain MRI should be done.
AL GRAWANY
11 Tinnitus andHyperacusis
• Hyperacusis is a different pathology in
which the patient has unusual tolerance
to ordinary environmental sounds. It is
believed that a central phenomenon
causes it.
• Hyperacusis usually coincides with tinnitus. It usually results in a negative psychological effect on the patients.
Tinnitus retraining therapy (TRT) and
cognitive behavioral therapy (CBT) can
be used in treating this condition.
Acknowledgment Authors of the chapter would like to
appreciate the help of Dr. Adham Aljariri, an ENT resident in Hamad medical corporation, for his help and effort
in editing the chapter.
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.2014.893377. Epub 2014 Mar 31.
14. Deklerck AN, Degeest S, Dhooge IJM, Keppler
H.Test-retest reproducibility of response duration in
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Speech Lang Hear Res. 2019;62(9):3531–44. https://
doi.org/10.1044/2019_JSLHR-H-18-0514. Epub
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15. Henry JA, Loovis C, Montero M, etal. Randomized
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16. Searcheld GD, Kaur M, Martin WH.Hearing aids as
an adjunct to counseling: tinnitus patients who choose
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17. Vernon JA, Meikle MB.Masking devices and alprazolam treatment for tinnitus. Otolaryngol Clin N Am.
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18. Henry JA, Schechter MA, Zaugg TL, etal. Outcomes of
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19. Grewal R, Spielmann PM, Jones SE, Hussain
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31. Richardson M, Flint P, Haughey B, Lund V,
Niparko J, Robbins K, Regan Thomas J, Lesperance
M. Cummings otolaryngology, head and neck surgery. 5th ed. Philadelphia: Elsevier; 2010.
.
32. Hazell JWP, Sheldrake JB, Graham RL. Decreased
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AL GRAWANY
Physiology andDiagnostic Tests
oftheVestibular System
WalidOmer andKhaledAbdulhadi
12
12.1 Introduction
• The vestibular system can be regarded as the
sixth sense [1].
• Its main functions are to stabilize gaze, posture, and gait during movement (balance
inlocomotion).
• Usually, the vestibular system input is not
consciously perceived, except in abnormal
conditions.
• Any disturbance in vestibular input can lead to
vertigo (illusion of movement at rest), imbalance (mainly on uneven surfaces and dark
areas), and difculty in reading signs while
moving (oscillopsia) [2].
12.2 Anatomy oftheVestibular
System
The vestibular system consists of two main
organs in the inner ear (Fig. 12.1):
• Otolithic (Otoconial) organs (two on each
side):
– Saccule and utricle.
– Responds to linear acceleration and gravity
(tilt).
W. Omer (*) · K. Abdulhadi
Hamad Medical Corporation, Doha, Qatar
e-mail: Womer@hamad.qa; Khadi@hamad.qa
– Saccule (oriented vertically) is more sensi-
tive to vertical acceleration, while the utricle (oriented horizontally) is more sensitive
to horizontal acceleration.
– The sensory neuroepithelium in the oto-
lithic organs is called the macula.
– The macula consists of hair cells and sup-
porting cells.
– The hair cells have apical hair bundles
that project into a gelatinous material
(otolithic membrane) covered by millions of calcium carbonate crystals
(Otoconia) [3].
– Bending of hair bundle happens after head
tilt (by the otoconia as a result of gravity)
[3, 4].
Depolarization: Once the bundle is bent
in the direction of a hair cell’s axis of
polarity.
Hyperpolarization: when tilting the
head to the opposite direction, the same
cell hyperpolarizes and inhibits the
afferent ber.
• Semicircular canals (three on each side)
gure.
– Horizontal (Lateral), Anterior (superior),
and Posterior.
– Responds to rotational acceleration.
– Senses head rotation in three-dimensional
space.
© 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_12
129
130
Stationary
substance
Endolymp
Hair cells
Supporting
cells
Head upright Head bent forward
Ampullae
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Semi-
circular
canals
Crista ampullaris
Utricle
Saccule
W. Omer and K. Abdulhadi
Maculae
Cupula
Sensory
nerve fibers
Direction of
h
Crista
ampullaris
Crista ampullaris of
lateral semicircular canal
head
rotation
Endolymph
lags behind
due to inertia
Cupula is pushed
Stereocilia are bent
Rotating
over and
stimulates
hair cells
The maculae of the
Fig. 12.1 Figure illustrating the anatomy and physiology of the vestibular system
– When the head rotates to one side, endo-
12.3 Vestibular Reexes
lymph moves, relative to the skull, to the
opposite side.
– Deection of the cupula by endolymph,
which in turn bends the hair cells
(Stereocilia) in the crista ampullaris (sensory organ of rotation).
– Depending on the direction of endolym-
phatic uid and the semicircular canal
stimulated, activation or inhibition of nerve
ring happens:
Ampullopetal: toward ampulla (excitatory to the horizontal canal and inhibitory to superior and posterior canal).
Ampullofugal: away from the ampulla
(excitatory to the superior and posterior
canal and inhibitory to horizontal canal).
– Planes of the semicircular canals (func-
tional pairs):
Horizontal: left and right horizontal
SCCs.
• Sensory input from the eyes (visual), proprioception (somatosensory), and the ears
(vestibular) is integrated in the Brainstem
(Vestibular Nuclei), which in turn sends
afferents compromising the main vestibular
reflexes:
– Vestibulo-ocular reex: stabilizes gaze dur-
ing active head rotation (xation of the
retina on the target by acting on the extraocular muscles), when the head moves to
one direction, the eyes move to the opposite direction equally (i.e. head movement
to the right of 20° leads to eyes move to the
left of 20°).
– Vestibulospinal reex: Stabilizes posture
(acting on the antigravitational muscles).
– Vestibulocollic reex: stabilizes the head
on the trunk (acting on the neck
musculature).
RALP: right anterior and left posterior.
LARP: left anterior and right posterior.
Otoliths
(ear stones)
Sensory
hairs
Hair cells
urticle
Gel-like
AL GRAWANY
12 Physiology andDiagnostic Tests oftheVestibular System
131
12.4 Nystagmus: Involuntary
Repetitive Rhythmic Eye
Movement
Alexander law: It is described in individuals with
Nystagmus and refers to increase in the amplitude
of nystagmus when the eyes move to the direction
of the fast phase (the direction of nystagmus is typically named toward the fast phase, and in cases of
acute vestibular loss, the fast phase is usually
toward the healthy ear) and become slower when
looking at the direction of the slow phase.
Ewald’s three laws:
• “A stimulation of the semicircular canal
causes a movement of the eyes in the plane of
the stimulated canal”.
• “In the horizontal semicircular canals, an
ampullopetal endolymph movement cases a
greater stimulation than an ampullofugal one”.
• “In the vertical semicircular canals, the reverse
is true” [5].
12.5 Vestibular Diagnostic
Studies
History taking (the most fundamental part), physical examination, and vestibular function tests are
key elements in reaching the correct diagnosis
and designing the best management plan.
Vestibular function tests conrm the diagnosis
that is suspected by history taking and bedside
examination. It is also done to identify three main
components in the management of dizzy patient:
1. Identifying the site of the lesion (Central vs.
Peripheral)
2. Extent of the lesion (Unilateral vs. Bilateral)
3. The degree of compensation (hence asses the
need for vestibular rehabilitation)
12.5.1 Videonystagmography (VNG)/
Electronystagmography (ENG)
• It consists of oculomotor testing (smooth pur-
suit, saccade, optokinetic, and gaze stabiliza-
tion testing), positional and positioning
testing, and caloric test.
• Videonystagmography refers to recording of the
eye movement using infrared cameras, which
detect actual eye movements. While ENG (old
systems) recodes corneo-retinal potentials.
• It answers two main questions:
– Is it peripheral or central
– Localizes the ear
12.5.2 Oculomotor Testing
• Gaze testing: Holding the gaze at the primary
gaze and then eyes movement to 30° up, down,
right, and left. It tests eye stabilization on the
target and is regarded as abnormal in case the
eyes move away or off the target. It can be a
sign of central dysfunction, and also in acute
vestibular dysfunction, gaze stability can be
abnormal.
• Smooth Pursuit: It is a system that is activated
to x moving targets on the fovea (it prevents
retinal slippage of the images). It is tested by
asking the subject to follow a moving target
(which is moving smoothly in a sinusoidal
pattern on the screen). The smooth pursuit is
usually active at targets which are moving at
low velocity (less than 60° per second).
Abnormal smooth pursuit is indicative of central pathologies.
• Saccade testing: The target here rapidly shifts
(jumps) from one place to another on the
screen, and the subject moves his eyes so that
the target is kept on the fovea. It is testing by
rapidly moving target 20° right, left, and center. Abnormal saccade test (dysmetria, slow
saccadic velocity, and deconjugate saccades)
is indicative of a central pathology.
• Optokinetic test: it is activated to x images on
the retina (not only the fovea) when looking at a
moving eld (not a specic target like in smooth
pursuit or saccade). The subject is tested, while
more than 80% of the eld of vision is lled with
a moving series of objects (example colored
strips). Both central and peripheral pathologies
can lead to abnormal Optokinetic test.
• Spontaneous nystagmus.
132
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12.5.3 Positional andPositioning
(Dix–Hallpike) Testing
• Positional: relates to maintaining the head at
the provoking position and is done in the
absence of visual xation where eye movement is recorded at three positions: Supine,
head right, or head left.
• Positioning tests: relates to the action of mov-
ing the head, and the classical positioning test
is Dix–Hallpike, which is Diagnostic of
Posterior canal-BPPV.It is done by recording
of the eye movement and the resulting nystagmus after positioning the patient.
12.5.4 Caloric Test
• Caloric response was rst described by Robert
Barany in 1906. For his nding, Barany
received a Nobel Prize in 1914.
• It is part of ENG/VNG test battery.
• It tests the function of the lateral semicircular
canal only.
• It tests each labyrinth separately (independent
of the other canal), which makes it ideal for
determining the side of the weakness.
• It is done using warm and cold stimuli with
water or air. The degree and symmetry (between
both ears) of responsiveness to these stimuli are
recorded.
• Method—Patient lying supine and the head is
elevated 30° (bringing the horizontal semicircular canal to the vertical plane). Irrigation
with warm and cold water or air is done, and
the resulting response (Nystagmus) is
recorded. Water irrigation (for 30s) is done at
a temperature of 44°C for warm and 30°C for
cold. Air (for 60s) is done at a temperature of
49–50°C for warm and 24°C for cold (waiting time between each irrigation is 2–3min).
• Water irrigation gives a more robust response
compared to air. Ice water caloric irrigation
(ice calorics) is indicated in cases of absent
response or when poor irrigation is suspected.
• The mnemonic COWS: cold opposite, warm
same describes the resulting direction of the
fast phase of nystagmus.
W. Omer and K. Abdulhadi
•
Outcome Measure in Caloric test.
– Canal paresis (reduced vestibular
response): it compares the response from
one side to the other using “Jongkee’s formula” RVR = (RC+ RW − LC− LW)/
TR. Differences 25–27% or more usually
considered signicant.
– Unilateral canal paresis is usually a sign of
peripheral vestibular pathology, that is,
vestibular neuritis. Less commonly is canal
paresis with central vestibular pathologies,
for example, lesions of the vestibular nerve
root-like multiple sclerosis and lateral
brainstem infarction.
– Directional preponderance (DP):
Preference of the response (beating of the
nystagmus) toward one direction.
Generally, 35% or more is usually considered abnormal. The direction preponderance has limited diagnostic value. Both
central and peripheral dysfunctions can
lead to DP. In peripheral lesions, DP is usually away from the side of the lesion.
12.5.5 Kinetic Rotatory Chair
• It is another part of the vestibular test battery
which evaluates vestibulo-ocular reex (VOR)
function.
• Its main indications include:
– Bilateral vestibular hypofunction (BVH; it
is the goal standard for testing BVH).
– The extent of vestibular compensation.
– Testing in children.
• Method: Patient seated on the chair and
strapped for safety with eye movements
recorded during rotation. Rotations are horizontally (to right and left).
• Two main subtypes of kinetic rotatory chair
are as follows:
– Step velocity: the chair accelerates to pre-
specied velocity (80–240°/s) and keeps
rotating at this speed and then suddenly
stops (eye recording is done per-rotation
and post-rotation).
– Sinusoidal harmonic acceleration.
AL GRAWANY
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