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A. Larem et al.
• Normal examination of the external ear canal
and tympanic membrane.
• Weber and Rinne’s tests show a positive
Rinne’s test (air conduction (AC)>bone con-
duction (BC)). Weber’s lateralized to the bet-
ter ear.
• Pure-tone audiometry (PTA) normal air-bone
gap with decreased bone conduction.
Identifying the severity of the hearing loss is
essential to determine the appropriate intervention. Hearing losses between 26 and 40dB HL
are considered mild, 41 and 55dB HL moderate, 56 and 70dB HL moderately severe, 71 and
90dB HL severe, and >91dB HL profound [1].
10.2 Etiology ofSensorineural
Hearing Loss
Etiologies of SNHL can be divided as a congenital (hereditary, non-hereditary, and idiopathic) or
acquired. Figure10.1 summarizes the most common causes.
10.2.1 Congenital
Congenital etiologies are divided into hereditary,
non-hereditary, and idiopathic.
• Hereditary (50%)
– Non-syndromic (70%): more common,
autosomal recessive (AR) in (75–80%),
autosomal dominant (AD) in (20–25%),
X-linked in (2–4%), and Mitochondrial in
<1%. GJ2B mutation (autosomal recessive) coding for the protein gap junction
beta 2 (also called connexin 26); results in
impaired Potassium (K+) exchange.
– Syndromic (30%): Divided to AR, AD,
and X-linked. Most common include Usher
and Pendred syndromes (both autosomal
recessive). Most common AD syndrome is
Waardenburg syndrome. X-linked includes
Alport syndrome.
Syndromes’ features include [2]
Waardenburg’s syndrome → White
forelock, heterochromia of iris.
Usher syndrome → Retinitis pigmentosa.
Sensorineural
hearing loss
Acquired
(75%)
Meningitis
Ototoxicity
Trauma
Nose induced
hearing loss
Mumps/measles
Recurrent
otitis/mastoiditis
Unknown
Non-syndromic (70%)
AR (75%-80%)
AD (20%-25%)
X linked (2%-4%)
Mitochondrial <1%
Fig. 10.1 Etiologies of sensorineural hearing loss
Hereditary
(50%)
AD syndromes
Waardenburg
Treacher-Collins
Stickler
Goldenhar
Syndromic
(30%)
AR syndromes
Usher
Jervell and lang-on
Pendred
Congenital
(25%)
X-Linked
syndromes
Alport
Non-
hereditary
(25%)
TORCH
Teratogenic
drugs
Neonatal
sepsis
Prematurity
Low birth weight
Idiopathic
(25%)
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113
Alport’s syndrome → Nephritis.
Pendred syndrome → Thyroid goiter.
Jervell and Lange-Nielsen syndrome →
Prolonged Q-T intervals and enlarged T
waves.
• Non-hereditary (25%)
– Malformations can be membranous
(Alexander’s Aplasia, Scheibe Deformity,
Siebenmann–Bing Dysplasia) or Osseous
and Membranous (Cochlear Hypoplasia,
Mondini, Common Cavity, Cochlear Aplasia,
Michel Aplasia, Small Internal Auditory
Canal). Mondini malformation is the most
common type of cochlear malformation.
– TORCH Infections: It includes
Toxoplasmosis, Other (syphilis, varicellazoster, parvovirus B19), Rubella,
Cytomegalovirus (CMV), and Herpes.
– Cytomegalovirus is the most common
cause of congenital viral deafness [3].
– Mumps is the most common infectious
cause of acquired sensorineural hearing
loss.
– Other perinatal factors include prematurity,
low birth weight, teratogenic drugs, maternal diabetes, hyperbilirubinemia, and neonatal sepsis.
• Idiopathic (25%)
10.2.2 Acquired
The most common causes of acquired sensorineural hearing loss are the following:
1. Presbycusis.
2. Noise-induced hearing loss.
3. Post-meningitis.
4. Cerebrovascular accident.
5. Ototoxic medication exposure.
6. Autoimmune inner ear disease (Coganʼs
syndrome, relapsing polychondritis,
Wegenerʼs granulomatosis, systemic lupus
erythematosus, Sjogrenʼs syndrome, and
rheumatoid arthritis).
7. Sudden sensorineural hearing loss.
8. Vestibular schwannoma or meningioma.
9. Erosive inner ear disease (cholesteatoma or
chronic otitis media).
10. Trauma to inner ear.
11. Endolymphatic hydrops.
10.2.2.1 Presbycusis
It is an age-related sensorineural hearing impairment. It results from a combination of environmental and genetic factors. Males are affected
more often than females. Its features include
slow and insidious onset, lack of clarity than a
loss of volume, and tinnitus as often the presenting symptoms [4].
• Four types of presbycusis have been identied [5].
1. Sensory presbycusis, characterized by
symmetric high frequency hearing loss
with a decrease of speech discrimination.
The loss affects both hair cells and supporting cells in the basal turn of the
cochlea. Figure 10.2 demonstrates puretone audiometry with features of
Presbycusis in both ears.
2. Neural presbycusis, characterized by a
signicant loss of speech discrimination.
Loss of whole cochlear neurons.
3. Strial presbycusis, characterized by at
pure-tone audiogram with excellent speech
discrimination. Associated with atrophy of
the stria vascularis in the middle and apical
turn of the cochlea.
4. Conductive presbycusis (cochlear con-
ductive), changes affect the basilar
membrane.
Management
Hearing aids or cochlear implants are an excellent option for those who have severe to profound
hearing loss with discrimination scores below
40% in both ears [4].
10.2.2.2 Ototoxicity
Ototoxicity can be induced by any route of drug
administration (topical, drops, sprays, inhalation,
or systemic). Symptoms of ototoxicity include
hearing loss (primarily high frequency), tinnitus,
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Fig. 10.2 Pure-tone audiometry showing features of Presbycusis in both ears
A. Larem et al.
and balance impairment. The most commonly
used drugs causing ototoxicity are the aminoglycosides and platinum-containing chemotherapy
agents [4]. Hearing loss may be unilateral or
asymmetric and can progress during or after cessation of therapy. Ototoxic drugs inducing lowfrequency hearing loss include arsenic and
erythromycin. Ototoxic drugs’ effects can be permanent (aminoglycoside, cisplatin, carboplatin,
or vancomycin) or temporary (salicylates, erythromycin, or quinine). The most common ototoxic
drugs are described as follow:
• Aminoglycosides
It can be mainly vestibulotoxic
(Streptomycin or Gentamycin) damaging type
1 hair cells of crista ampullaris [6], or mainly
cochleotoxic (Neomycin, Kanamycin, or
Amikacin) damaging outer hair cells, or vestibulo-cochleo toxic (Tobramycin). The toxicity starts at the basal coil of cochlea (high
frequency) and progressing up to the apex.
Mitochondrial 12S rRNA gene mutation
increases susceptibility to aminoglycosides
ototoxicity [7]. Ototoxicity may continue even
after the stopping of aminoglycoside [4]. Risk
factors include dose, duration, liver and kidney disease, bacteremia, concomitant use of
other agents, and genetic predisposition.
• Anti-neoplastic (chemotherapy)
It includes cisplatin and carboplatin. It is
highly ototoxic. Cisplatin affects mainly outer
hair cells, while carboplatin affects mainly
inner hair cells [7]. The main cochlear damage
occurs in the basic turn within the outer hair
cells. Figures 10.3 and 10.4 show pure-tone
audiometry showing and otoacoustic emission
ndings of bilateral platinum chemotherapy
ototoxicity.
• Loop Diuretics
It includes frusemide, ethacrynic acid, and
bumetanide. It causes reversible or permanent
bilateral hearing loss. Mechanism of toxicity
occur by affecting stria vascularis which lead
to reductions of endocochlear potential [4].
• Salicylates (Aspirin)
It presents tinnitus more than a loss of hearing. It causes reversible hearing loss.
• Others
It includes industrial chemicals, Vancomycin,
Macrolides, and Quinine.
Ototoxicity can be limited and prevented by
antioxidants such as N-acetyl-cysteine and
sodium thiosulfate [8]. It is treated by the cessation of treatment and substitution by a different
agent if possible, and hearing rehabilitation can
be achieved with applying hearing aid.
10.2.2.3 Noise-Induced Hearing Loss
It can be temporary or permanent hearing loss.
Temporary threshold shift (TTS) presents with a
brief period of hearing loss after noise exposure,
and it is reversible. Permanent threshold shift
30
dB SPL
30
8.0
Frequency (kHz)
10 Sensorineural Hearing Loss (SNHL)
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Fig. 10.3 Pure-tone audiometry showing nding of bilateral platinum chemotherapy ototoxicity
115
25
20
15
10
5
0
-5
-10
-15
-20
-25
-30
0.5 1.0 2.0 3.0 3.5 4.5 5.5 7.0
0.75 1.5 2.5 3.2 4.0 5.0 6.0 8.0
25
20
15
10
5
-5
0
dB SPL
-10
-15
-20
-25
-30
0.5 1.0 2.0 3.0 3.5 4.5 5.5 7.0
0.75 1.5 2.5 3.2 4.0
Fig. 10.4 Otoacoustic emission in left and right ears with platinum ototoxicity
(PTS) hearing loss does not return to the previous
hearing level [4]. The natural resonance of external auditory canal is from 3 to 5kHz which may
be the reason for a “noise notch” at 4 kHz.
louder than 85dB for an 8-h period, with each
5-dB increase that must cut exposure into half.
Hearing rehabilitation can be achieved by apply-
ing hearing aid.
Figure10.5 demonstrates a pure-tone audiometry
of patient with noise-induced hearing loss.
Acoustic trauma can occur from exposure to
intense trauma and lead to immediate hearing
loss. The hypothesis of metabolic changes leads
to TTS, while the hypothesis of structural changes
leads to PTS [9].
10.2.2.4 Sudden Sensorineural
Hearing Loss
It is dened as a unilateral hearing loss of at least
30 dB in at least three contiguous frequencies
occurring within 3days. It can be bilateral in 2%.
It is of unknown etiology, possible underlying
viral or vascular (ischemic) etiology [10]. Pure-
Management
Workplace restriction and prevention is better
than cure, and measures must be taken for work
environments that expose patients to sounds
tone audiometry and MRI should be considered
to rule out vestibular schwannoma or other intracranial causes such as multiple sclerosis and
small vessel ischemic changes. The prevalence of
Frequency (kHz)
5.0
6.0
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Fig. 10.5 Pure-tone audiometry of patient with noise induced hearing loss
A. Larem et al.
acoustic neuroma among patients with sudden
SNHL is less clear, although estimates range
from 0.8% [11].
Management
Most recent clinical practice guidelines recommend oral or intratympanic steroids as the rstline treatment, and oral prednisone typically is
given at 1mg/kg/day (up to 60mg) for 7–14days
and then taper dose over the similar period of
time. Intratympanic steroid injection can be used
as an initial or salvage treatment [12].
As an adjunct to oral steroids, hyperbaric oxygen and antivirals may be offered. Prognosis is
worse with a greater degree of hearing loss, vertigo, advanced age, poorly controlled diabetes,
hypertension, and hyperlipidemia [10].
10.2.2.5 Auditory Neuropathy/
Dys-Synchrony
It is dened as an abnormal/absent neural transmission in the auditory but evidence of normal
outer hair cells function (cochlear microphonic
and otoacoustic emissions normal), thought to be
caused by abnormal central auditory temporal
processing in response to a stimulus. Typically
seen in young children, it is mostly related to a
genetic cause and has a frequent association with
other developmental delays. It may have relatively good pure-tone thresholds but poor speech
understanding and auditory development. It
exhibits variable response to amplication and/or
cochlear implants [13].
10.2.2.6 Autoimmune Inner Ear
Disease (AIED)
It is characterized by a subacute progressive uctuating bilateral sensorineural hearing loss that
responds to steroids. One ear is frequently
involved initially and worsens before the development of hearing loss in the contralateral side.
Patients often describe aural fullness as well as
tinnitus [4].
The diagnostic criteria include bilateral sensorineural hearing loss >30 dB at any frequency
and progression in at least one ear on two serial
audiograms <3months apart [14]. The hallmark
of the disease is the responsiveness of the hearing
loss to steroids or cytotoxic drugs [4].
Cogan syndrome is a rare disease of young
adults, characterized by triad of autoimmune keratitis, vertigo, and SNHL [4]. Around 15% of
cases are associated with other systemic autoimmune diseases including multiple sclerosis, rheumatoid arthritis, and inammatory bowel
disease.
Investigations that help to diagnose AIED
include an audiogram and MRI of the internal
auditory canal if asymmetric hearing is present.
Lab work including anti-HSP-70 (= 68-kDa antigen) can be considered, but it has limited sensitivity and specicity. If other autoimmune
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117
diseases are suspected with presence of ndings
such as arthritis, ocular disease, skin lesions, and
kidney disease, a further rheumatological investigation might be required.
Management
It includes a trial of prednisone 60mg daily for
4–6weeks, with a close audiological follow-up
by repeating PTA frequently. If the patient
responds to steroid, then continue until a plateau
is reached in the hearing gain, and then a maintenance dose for steroid should be continued for at
least 6months. Regarding non-steroid responders, taper immediately. Methotrexate is used for
patients who cannot tolerate steroids or in cases
where weaning steroids cause a decline in hearing [15]. Cyclophosphamide and etanercept are
considered as a second line. In case profound
bilateral SNHL is developed, cochlear implantation is an excellent modality for the restoration
of auditory function for this type of pathology.
10.3 Hearing Aids andAuditory
Rehabilitation
Hearing aids provide a major role in auditory
rehabilitation, where it amplies the sound to
make speech more audible without being uncomfortable. It is mainly indicated for patients with
sensorineural hearing loss (SNHL), and it also
has a role in the management of conductive hearing loss (CHL), particularly for patients who are
not amenable to surgical intervention. Multiple
options are available depending on the patient
factors, type of hearing loss, unilateral or bilateral, cosmetic appearance, batteries type, and
electronic issues. Hearing aids can be either conventional or implantable.
Hearing aid is composed of a microphone,
amplier, receiver, battery, and volume control
(see Fig.
10.6).
Hearing aids can be conventional or implantable. The conventional type is more affordable
and less invasive but has limitations when it is
compared with implantable hearing devices
which include insufcient amplication, acoustic
feedback, non-linear sound distortion, occlusion
effects, poor auditory transduction, and cosmoses. The implantable hearing aids include
osseointegrated bone-conducting hearing prostheses and middle ear implants.
1. Conventional Hearing Aid:
It can be categorized to analogue, analogue/digital hybrid, and digital hearing aids.
Analogue hearing aid is less common as it has
less exibility than the digital one. The analogue/digital hybrid hearing aids are characterized by digital memory and the ability to
control the analogue circuit digitally which
makes it more exible in adjusting gain and
acoustic output. The digital hearing aids are
computer- controlled devices, via Digital signal processing (DSP) chip, and they have the
highest exibility with improved speech rec-
Fig. 10.6 Hearing aid
components and
function. EAC external
auditory canal
Input acoustic
signal
Acoustic to
mechanical
Microphone Amplifier
Mechanical to
electrical
Output acoustic
signal to EAC
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Boost the
electrical
signal
Electrical to
acoustic
Receiver
118
A. Larem et al.
Table 10.1 Advantages and disadvantages of hearing
aids by type
Type of
hearing aid Advantages Disadvantages
Body
Hearing
Aids
Behind the
Ear (BTE)
In the Ear
(ITE)
In the Canal
(ITC)
Completely
in the Canal
(CIC)
Low feedback with
high level output,
easy to manage.
It can be used for
severe and
profound hearing
loss, large case ts
larger batteries
allows for more
amplication and
battery life.
For moderate-tosevere hearing loss,
better cosmetically
appealing, superior
ability to amplify
on high-frequency
sounds.
More cosmetically
appealing and
allows for normal
acoustics provided
by the pinna,
superior ability to
amplify on
high-frequency
sounds, helps
localization of
sound
Most cosmetically
appealing,
maximizes pinna
and concha effects
greater highfrequency gain.
Noticeable, poor
sound localization,
clothes, and body
may rub against the
microphone.
Cosmesis,
inadequate induces
feedback, cannot be
used with auricular
anomalies.
Limited gain,
feedback problems.
Gain sufcient for
no more than
moderate hearing
loss, requires
dexterity to insert,
small size limits
output/response
controls, venting
options limited.
Requires certain
tting criteria, only
for moderate
hearing loss, small
size limits output/
response controls,
venting options
limited, venting
options very limited
ognition, sound quality, and comfort via different mechanism, that is, digital noise
reduction, digital feedback, and control spectral enhancement. Different types of conventional hearing aid are available which are
described in Table10.1.
Bineural Versus mononeural hearing aid:
the general rule is that binaural amplication
is the arrangement of choice, unless signi-
cant contraindication is present. The main
advantages of binaural amplication include
better sound localization, speech discrimination, intelligibility in noise, and release from
masking, and it also eliminates head shadow
effects which reduce high-frequency cues
[16]. In addition, patients with binaural hearing loss can have temporary and perhaps a
permanent decrease in the auditory function in
the unaided ear which can be minimized by
tting a bilateral hearing aid.
Contralateral routing of signal (CROS): it is
used in case of single-sided deafness with
normal hearing in the other ear. Microphone is
tted on the impaired side and transmitted to
a good ear. Bilateral CROS hearing aids also
amplify sound to the better hearing ear.
2. Implantable Hearing Aid:
Numerous implantable devices are options for
hearing rehabilitation in patients with conductive
hearing loss who cannot use a conventional hearing aid.
(a) Bone-anchored hearing aids (BAHA):
They are indicated in cases of chronic otitis media patients with chronically discharging ears, or the presence of a large
mastoid bowl or meatoplasty, and they are
also indicated in case of congenital anomalies (external ear deformity, aural atresia,
and canal stenosis) as well as for singlesided deafness [17].
Contraindications: Age<5years, emotional instability, drug abuse, development
delay, average bone conduction threshold
(500, 1000, and 3000Hz) of the indicated
ear worse than 45 dB HL, and if maximum speech discrimination of the indicated ear below 60% [17].
(b) Middle-ear Implants (MEIs): There are
two basic types of transducers used in
middle ear implantable hearing aids:
piezoelectric and electromagnetic. They
are used in cases of bilateral moderate-tosevere sensorineural. Its advantages
include the elimination of feedback and
occlusion effects [18].
10 Sensorineural Hearing Loss (SNHL)
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Take-Home Messages
• Most common prenatal cause of hearing
loss is intrauterine infection (CMV).
• Common causes of perinatal hearing
loss are hypoxia, hyperbilirubinemia,
infection, and medication toxicity.
• The most common postnatal cause of
hearing loss is meningitis.
• Fluctuating hearing loss is seen in perilymphatic stula, Meniere disease,
syphilis, autoimmune induced, sarcoidosis, multiple sclerosis, and migraineassociated hearing loss.
3. Cochlear implant.
Acknowledgment Authors of the chapter would like to
appreciate the help of Dr. Rani Salim Hammoud, an ENT
resident in Hamad medical corporation, for his help and
effort in editing the chapter.
References
1. Baiduc RR, Poling GL, Hong O, Dhar S. Clinical
measures of auditory function: the cochlea and
beyond. Dis Mon. 2013;59(4):147–56. https://doi.
org/10.1016/j.disamonth.2013.01.005.
2. Toriello HV, Reardon W, Gorlin RJ.Hereditary hearing loss and its syndromes. 2nd ed. Oxford, UK:
Oxford University Press; 2004.
3. Fowler KB, Boppana SB.Congenital cytomegalovirus (CMV) infection and hearing decit. J Clin Virol.
2006;35:226.
4. Flint PW, Haughey BH, Lund V, etal. Sensorineural
hearing loss in adults, Chap 150. In: Cummings
otolaryngology: head & neck surgery. 6th ed.
Philadelphia: Elsevier; 2015. p.2319–35.
5. Schuknecht HF. Pathology of the ear. 2nd ed.
Philadelphia: Lea & Febiger; 1993.
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6. Rybak LP, Ramkumar V. Ototoxicity. Kidney Int.
2007;72:931.
7. Schacht J, Talaska AE, Rybak LP.Cisplatin and aminoglycoside antibiotics: hearing loss and its prevention. Anat Rec (Hoboken). 2012;295(11):1837–50.
https://doi.org/10.1002/ar.22578.
8. Sheth S, Mukherjea D, Rybak LP, Ramkumar
V. Mechanisms of cisplatin-induced ototoxicity and
otoprotection. Front Cell Neurosci. 2017;11:338.
https://doi.org/10.3389/fncel.2017.00338.
9. Lim DJ.Effects of noise and ototoxic drugs at the cellular level in the cochlea: a review. Am J Otolaryngol.
1986;7(2):73–99.
10. Kuhn M, Heman-Ackah SE, Shaikh JA, Roehm
PC. Sudden sensorineural hearing loss: a
review of diagnosis, treatment, and prognosis.
Trends Amplif. 2011;15(3):91–105.
org/10.1177/1084713811408349.
11. Shaia FT, Sheehy JL. Sudden sensori-neural hearing
impairment: a report of 1,220 cases. Laryngoscope.
1976;86:389.
12. Chandrasekhar SS, Tsai Do BS, Schwartz SR,
Bontempo LJ, Faucett EA, Finestone SA, Hollingsworth
DB, Kelley DM, Kmucha ST, Moonis G, Poling GL,
Roberts JK, Stachler RJ, Zeitler DM, Corrigan MD,
Nnacheta LC, Sattereld L. Clinical practice guideline: sudden hearing loss (update). Otolaryngol Head
Neck Surg. 2019;161(1_Suppl):S1–S45.
13. Rance G. Auditory neuropathy/dys-synchrony
and its perceptual consequences. Trends Amplif.
2005;9(1):1–43. Review.
14. Mijovic T, Zeitouni A, Colmegna I. Autoimmune sensorineural hearing loss: the otology–rheumatology
interface. Rheumatology. 2013;52(5):780–89.
15. Sismanis A, Thompson T, Willis HE. Methotrexate
therapy for autoimmune hearing loss: a preliminary
report. Laryngoscope. 1994;104:932.
16. Morera C, Manrique M, Ramos A, Garcia-Ibanez
L, Cavalle L, Huarte A, Castillo C, Estrada
E.Advantages of binaural hearing provided through
bimodal stimulation via a cochlear implant and a conventional hearing aid: a 6-month comparative study.
Acta Otolaryngol. 2005;125(6):596–606.
17. Kraus EM, Shohet JA, Catalano PJ. Envoy esteem
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https://doi.
AL GRAWANY
Tinnitus andHyperacusis
AishaLarem, Ma’inAliAl Shawabkeh,
andWalidOmer
11
11.1 Introduction
Tinnitus is dened as a perception of sound with
no external stimulus [1]. It is considered chronic if
it lasts more than 3 months. Tinnitus is divided
into two entities: Subjective tinnitus in which
only the patient can hear it, and Objective tinni-
tus, where others can detect it by either a stethoscope or ear canal microphone [2, 3]. Objective
tinnitus can be pulsatile or non-pulsatile.
Hyperacusis is considered a central phenomenon
that is dened as an unusual tolerance to ordinary
environmental sounds. Most of the cases of hyperacusis have unknown pathology. Hyperacusis and
tinnitus can coexist with each other.
11.2 Tinnitus
11.2.1 Subjective Non-pulsatile
Tinnitus
• Half of the patients have tinnitus in both ears.
In those who have it unilateral, it is more common on the left side [3].
A. Larem (*) · M. A. Al Shawabkeh · W. Omer
Hamad Medical Corporation, Doha, Qatar
e-mail: alarem@hamad.qa; MAIGhshoum@hamad.qa;
Womer@hamad.qa
• The prevalence increases with age [4].
• Risk factors: age, male sex, lower education
and annual income level, more than 15h per
week of noise exposure at work, poor health
condition, obesity, hypertension, diabetes,
cardiovascular diseases, head trauma, smoking, and alcohol [1, 5].
• Possible etiologies:
– Certain otologic diseases can present with
tinnitus (called syndromic tinnitus). For
example, Otosclerosis, Meniere’s disease,
and vestibular schwannoma [3].
– Certain medications can cause tinnitus like
salicylates, aminoglycosides, quinine, and
platinum-based antineoplastic medication [3].
– Tinnitus is associated with depression and
anxiety [6].
– Look at Table11.1 for some medical con-
ditions that can lead to tinnitus [7].
• Pathophysiology:
– Any pathology that can damage the audi-
tory system can lead to tinnitus like:
Damage to outer hair cells [8].
Disturbance of intracellular calcium
level (can be caused by specic medication and noise) [8].
Damage to the inner ear can cause the
downregulation of the inhibitory pathway leading to spontaneous ring of
nerves [9].
• Subtypes:
• Look at Table11.2 [2].
© 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_11
121
122
A. Larem et al.
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Table 11.1 Some medical conditions that can lead to
tinnitus
– Sensorineural hearing loss: Sudden sensorineural
hearing loss, Meniere’s disease, vestibular
schwannoma, noise-induced hearing loss, and
presbycusis.
–
Conductive hearing loss: otitis media, ossicular
dislocation, and otosclerosis.
Endocrine: pregnancy and thyroid disease.
–
–
Metabolic: Vitamin deciencies and hyperlipidemia.
Medications: salicylates, aminoglycosides, quinine,
–
platinum-based antineoplastic medication, and
antihypertensive medication.
Head trauma.
–
–
Neurological diseases like meningitis, multiple
sclerosis, and stroke.
Temporomandibular joint (TMJ) syndrome.
–
–
Depression and anxiety.
Table 11.2 Subjective tinnitus subtypes
Hearing loss subtype
Somatic tinnitus subtype
Typewriter tinnitus
Musical tinnitus
Intrusive
Associated with affective disorder
induced injury to the cochlea, metabolic
injury, and vascular injury. Taking in consideration other comorbidities that become
more prevalent by aging like diabetes, which
can affect the cochlear function [2].
11.2.1.2 Somatic Tinnitus Subtype
• It means the tinnitus in which somatic stimulation can modulate the loudness and pitch of
the tinnitus [10].
• Examples:
– The tinnitus that occurs after the removal
of vestibular schwannoma. In some of
those patients, tinnitus can be modulated
by exaggerating eye movement, leg
movement, or cutaneous stimulation of
the hand [2].
– Another example is tinnitus that can occur
with the temporomandibular joint disorder.
Jaw movement and pressure over the joint
can modulate the tinnitus in some of these
patients [2].
• Somatic tinnitus can be responsive to acupuncture treatment or electrical stimulation of
the ear and scalp [2].
11.2.1.1 Hearing Loss Subtype
• Mainly includes noise-induced hearing loss
(NIHL) and presbycusis.
• NIHL:
– The prevalence of tinnitus in NIHL is
50–70%.
– Intense sound exposure causes a reduction
in blood ow to the cochlea leading to
reactive oxygen and nitrogen molecules,
which have a damaging effect on the cells.
– Certain medicines like Vitamin E, salic-
ylates, and N-acetylcysteine have antioxidant effects and can give some
neuroprotection [2].
• Presbycusis:
– The prevalence of tinnitus in NIHL is
70%.
– In those patients, hearing loss is not only
attributed to the age, but in fact, it is a combination of the cumulative effect of noise-
11.2.1.3 Typewriter Tinnitus
• It is chronic intermittent and has staccato
quality [2].
• It is believed that it is caused by vascular compression of the ipsilateral auditory nerve [11].
• It can be misdiagnosed by objective tinnitus
caused by muscular origin [2].
• It can be responsive to Carbamazepine therapy [11].
• Other types of subjective tinnitus include
musical tinnitus, intrusive, and associated
with affective disorder [2].
• Evaluation:
– Identify the features of the tinnitus from
history like:
The laterality.
Continuous or intermittent.
Pulsatile or not, the tone.
Is it hissing, humming, sizzling, buzzing,
or roaring.
AL GRAWANY
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