TINNITUS AND HYPERACUSIS

DEFINITIONS

 It is true that the word tinnitus originates from the Latin word
tinnire (to ring)
 McFadden’s description of tinnitus as ‘the conscious expression of a
sound that originates in an involuntary manner in the head of its
owner, or may appear to him to do so’
 though it would include the hallucinations of mental illness and
exclude tinnitus that is perceived outside the body

 sensation of hearing a sound in the absence of an external

stimulus or a sound sensation in the absence of an external
or internal acoustical source or electric stimulation.

 would still include auditory hallucinations of mental illness

as a form of tinnitus and the latter definition would exclude
some types of pulsatile tinnitus where there is an intracorporeal
sound source.
 NON-PULSATILE TINNITUS
EPIDEMIOLOGY

 The largest investigation into the epidemiology of tinnitus

was carried out in UK the prevalence of persistent
spontaneous tinnitus in the adult population was 10.1%,
 defining persistent spontaneous tinnitus as tinnitus that
arose spontaneously, not as a response to sound stimulus, and
lasted for periods of 5 minutes or more at a time
 in Italy have been reported as 14.5% of the population,
 in the US as 14.9%
 in Sweden as 15.8%
 In Egypt 5.2%, rising to 17.7% in patients over 60 years of age.
 In Japan,18.6% of people aged over 65 described tinnitus and
 in Nigeria the figure was 14.1%.
 CLASSIFICATION
 we have divided tinnitus into pulsatile and non-pulsatile.
 Pulsatile tinnitus is considered to be either synchronous or non-
synchronous, depending on whether the sound is in synchrony with
the patient’s arterial pulse ,also modified by external movements, or
altered by changes in position

 Tinnitus can also be divided into subjective only the patient is

aware of the sound or objective, the sound can be perceived by
others, either unaided, using a stethoscope or a microphone and
amplifier.

 The majority of people with tinnitus report subjective non-pulsatile

tinnitus with no specific associated pathological process other than
age-associated hearing loss: this is often referred to as subjective
idiopathic tinnitus.
simple sounds: whistling, humming, ringing buzzing or tones
complex sounds are sometimes described including voices or music
 HISTORY

 A careful and accurate history of the present illness is

crucial for tinnitus characterization and has important
implications in both diagnosis and management.
 pulsatile from nonpulsatile

 unilateral or bilateral,

 onset, duration, intensity,

 modified by external movements or position changes,

 If pulsatile tinnitus concords with their pulse or not

,
 A complete otologic history
 associated symptoms of hearing loss, otalgia, otorrhea, autophony.
vertigo, imbalance, disequilibrium
 other neurologic symptoms.
 Review of systems mood , sleep patterns
 Past medical history should include prior history of otitismedia.
 otologic or neurosurgical procedures, head trauma.meningitis,
 exposure to ototoxic medications (including antibiotics,
chemotherapeutic agents, and nonsteroidal anti-inflammatory
medications),
 history of autoimmune diseases,
 current or prior psychiatric disorders.
 family history. such as paragangliomas.
 Social history should include tobacco, alcohol. illicit drug usage, and
intake of caffeine,
 Levels of previous noise exposure.
 PHYSICAL EXAMINATION

 A complete head and neck exam should be performed,

including otoscopy , pneumatic otoscopy, and tuning fork
exam
 Patients should be monitored for torsional nystagmus
during pneumatic otoscopy (fistula test
 The patient should be questioned for vertigo induced
during pneumatic insufflation of the canal -Hennebert
 Cranial nerves should be tested.
 Additional elements of a neurotologic examination,
including cerebellar function, gait evaluation, Romberg
and Fukuda testing, and positional testing, should be
performed when appropriate
 For patients complaining of pulsatile tinnitus, palpation
of the postauricular region, mastoid, and neck should note
any thrills or vascular cords.
 Auscultation of periauricular region, neck, and chest
should note the presence of objective tinnitus as well as
the presence of any bruits, vascular hums, or murmurs.
 Light ipsilateral and bilateral neck compression should
be performed to assess the effect of decreased jugular
venous flow on presence or intensity
of the pulsatile tinnitus.
 In young patients, carotid artery compression can also be
attempted with the goal of differentiating venous from
arterial causes of pulsatile tinnitus.
 Careful exam of the temporomandibular joint and
ipsilateral pterygoid muscles should note any tenderness,
clicking, or inflammation. Palpation of the pre- and
supraauricular regions should assess for parotid
abnormalities or masses.
 Flexible fiberoptic nasopharyngoscopy should be
performed when examination of the eustachian tube
(ET) orifice is warranted or when palatal myoclonus is
suspected.
 DIAGNOSTIC EVALUATION

 puretone, word recognition scores, and tympanometry.

 Other audiologic tests, including immittance testing,
auditory brainstem responses, otoacoustic emissions, and
high-frequency audiograms,
 Testing for vestibular function,

 imaging studies may be indicated for certain patients

 SUBJECTIVE NONPULSATILE TINNITUS
Etiology
 Chronic otitis media. cholesteatoma, canal occlusion, and otosclerosis
can cause a conductive hearing loss that ultimately may result in
tinnitus.
 Noise-induced hearing loss, presbyacusis, ototoxic medications,
labyrinthitis, herpes zoster oticus, Meniere's disease, and genetic
hearing losses cause inner ear hair cell damage resulting in hearing
loss, which can lead to nonpulsatile tinnitus.
 Lesions that affect the cochlear nerve and central
nervous system (CNS) such as acoustic neuroma, meningioma,
multiple sclerosis, and Charcot-Marie-Tooth disease
can also induce tinnitus
 Other primary causes of tinnitus include pharmacologic or dietary
stimulants, head trauma, and psychiatric disorders.
 Drugs or stimulants which increase neural firing, such as aspirin,
nomteroidal anti-inflammatory medication, nicotine. ethanol, and
caffeine. can cause or exacerbate nonpulsatile tinnitus
CENTRAL MECHANISMS
 Increased spontaneous firing
 Increased central neural synchrony
 Reorganization of the cortical auditory map

PERIPHERAL MECHANISMS
 Discordant damage of cochlear hair cells
 Calcium channel dysfunction
 Glutamate receptors
 RISK FACTORS
 socioeconomic class, smoking, alcohol consumption
 previous head injuries,
 cardiovascular disease and hypertension.
 Specific otological conditions including Ménière’s disease,
otosclerosis and vestibular schwannoma are associated with an
increased risk of tinnitus: such cases are sometimes referred to
as cases of ‘syndromic tinnitus’.
 Numerous drugs have been cited as possible triggers for the
development of tinnitus. salicylates, quinine, aminoglycoside
antibiotics, and some antineoplastic agents, particularly the
platinum based drugs.
 tinnitus development may have a small genetic predisposition.
 certain personality types such as type D personality
 dietary factors
 DIETARY FACTORS
 The authors subdivided tinnitus into persistent, transient and
bothersome subtypes and investigated the association of the subtypes
with reported consumption of common food groups.
 An increased report of persistent tinnitus was associated with fruit,
vegetable and bread consumption and dairy avoidance.
 Reduced reporting of persistent tinnitus was associated with
consumption of fish and caffeinated coffee and avoidance of eggs.
 Transient tinnitusreports increased with dairy avoidance and
decreased with caffeinated coffee and brown bread consumption.
 Bothersome tinnitus reports decreased with consumption of whole
meal, whole grain bread.
 TINNITUS HAS SEVERAL COMORBIDITIES
 Depression and anxiety are seen with tinnitus and in many instances
it is impossible to determine whether these neuroses have
precipitated the emergence of tinnitus or vice versa.
 Temporomandibular joint dysfunction.
 Disorders of sound tolerance are commonly seen in association with
tinnitus: 40% of people with tinnitus report some degree of
hyperacusis and, when this association is reversed,
 86% of people reporting hyperacusis also report tinnitus
 TINNITUS QUESTIONNAIRES
Tinnitus Handicap Inventory (THI),
Tinnitus Handicap Questionnaire,
The Mini Tinnitus Questionnaire
Tinnitus Functional Index

others
Hospital Anxiety Depression Scale
Insomnia Severity Index

VISUAL ANALOGUE SCALES

Tinnitus Handicap Inventory
the most popular one
It is a self-administered test that otolaryngologists ,
audiologists and other clinicians use to help determine the
degree of distress suffered by the tinnitus patient.
It is widely used in medical offices and in clinical trials to
determine the effectiveness of a given therapy
 INVESTIGATION

 BASIC AUDIOMETRY
 TINNITUS-SPECIFIC AUDIOLOGICAL
MEASUREMENTS
 loudness discomfort levels,

 tinnitus pitch matching,

 tinnitus loudness matching and

 minimal masking levels.

IMAGING
 Patients with unilateral tinnitus,
 an asymmetrical sensorineural hearing loss or
 associated neurological symptoms or signs require
imaging to exclude the presence of a retrocochlear
pathology such as a vestibular schwannoma.

 The modality of choice is MRI

 The presence of non-compatible medical devices such
as pacemakers or the presence of metal foreign bodies
may still preclude MRI, in which case CT may be
utilized
 EXPLANATION AND REASSURANCE
 An explanation of the condition and reassurance is a key
initial step in the management of any patient with
tinnitus.
 Reports such as ‘the doctor told me
that I would have it forever and nothing can be done’ are
all too common. This negative counselling is damaging
for patients with tinnitus and should always be avoided.
 HEARING AIDS
 As there is an association between tinnitus and hearing loss,
it would make sense that providing hearing amplification
would in part ameliorate a patient’s symptoms.
 Hearing amplification may amplify external sounds and
mask
tinnitus, but indirect effects, such as improving
communication, may reduce stress and anxiety that may be
exacerbating the patient’s symptoms.
Currently, when supplemented with education and advice,
hearing amplification is considered to be the primary
intervention for a patient
with tinnitus and aid-able hearing.
 SOUND THERAPIES
 used at very low levels just below the perceived level of the
tinnitus. is supposed to facilitate the habituation process
 There are three methods of providing wearable sound
therapy:
 patients may wear hearing aids that produce masking
 small ear level devices that generate wide-band sound
(known as tinnitus maskers, sound generators, white noise
generators
 combination devices
 An alternative to a wearable device is to use an appliance
that produces sound in the patient’s immediate environment.
This is referred to as environmental sound enrichment and
can be delivered by devices such as electric fans, wind
chimes, water features,
 TINNITUS RETRAINING THERAPY
 TRT is based on the concept that habituation to the unpleasant
stimulus can minimize the reactions that these patients
experience
 TRT does not seek to reduce production of the tinnitus sound
but instead attempts to change the linkage between the
tinnitus perception and autonomic and limbic systems using
extensive counseling and sound therapy.
 Counseling attempts to reclassify tinnitus as a neutral
stimulus and is felt to be necessary to allow habituation.
 Sound therapy decreases abnormal neural activity causing
tinnitus and can also be an effective means to decrease
hyperacusis via exposure and habituation.
 Studies have shown that completion of a 12-month course
ofTRT can decrease scores on the Tinnitus Handicap Index. a
validated scale of tinnitus severity, by up to 80%
 NEUROMONICS

 device usessound therapy , extensive tinnitus education, and

cognitive therapy to treat patients with tinnitus.
 Patients begin their therapy by listening to preprocessed mixed
"calming music· combined with noise mixed by proprietary
algorithm for 2 to 4 hours daily.
 The sound spectrum of this noise is shaped according to
patient's audiogram to compensate for hearing loss.
 Over 6 to 24 months, the noise sounds are gradually decreased.
lead to gradual desensitization
 Following completion of therapy. up to 77% of patients
report improvement of their tinnitus (33).
 REGIONAL DRUG TREATMENTS
 Botulinum toxin has been shown to be beneficial through
non-paralytic effects for conditions such as neuropathic
pain and migraine.
 With respect to migraine, botulinum toxin is thought not only
to block acetylcholine but also to inhibit the release of other
neurotransmitters and neuropeptides involved in the
autonomic pathway.
 Botulinum toxin A has been trialled in a small study of 26
tinnitus patients with the drug injected into soft tissues
around the ear.
 Benefit was demonstrated in the treatment arm as compared
to the control arm but, due to the small number of patients
recruited, no statistical significance was demonstrated.
 INTRATYMPANIC DRUG TREATMENTS

 It has been theorized that trans tympanic administration allows

direct labyrinthine drug absorption which may offer improved
labyrinthine metabolism and hence reduction of tinnitus in
those patients who have tinnitus with cochlear pathology.

 Events within the ear such as sudden sensorineural hearing

loss, acute noise trauma or acute otitis media can trigger
tinnitus and it has been suggested that there is a small
therapeutic time window between the pathological event in the
ear in these cases and the development of permanent changes
in the central auditory system that produce troublesome
tinnitus
 in patients with sudden onset of tinnitus, there might be a short
period when intratympanic treatments could be efficacious.
Various agents have been delivered into the middle ear,
either by single transtympanic injections, through
perforations and grommets, or via an implanted
micropump , including
 steroids,

 local anaesthetic agents,

 anticholinergic drugs,

 glutamate antagonists

 antioxidant compounds1
SYSTEMIC DRUG TREATMENTS
 tricyclic antidepressant
 Benzodiazepines

 selective serotonin reuptake inhibitor

 Antiepileptic

 antispasmodic

 vasodilators

 diuretics

 Betahistine

 anesthetic agents (IV lidocaine),

OTHERS

 LASERS
 ULTRASOUND

 ELECTROMAGNETIC STIMULATION
 SURGERY
 certain conditions such as otosclerosis when stapedectomy is
reported as improving or eradicating tinnitus in 80–88.%
 When tinnitus is associated with profound hearing loss,
tinnitus suppression has been demonstrated as a secondary
benefit of cochlear implantation. up to 86%
There is no good evidence to support cochlear implantation for
the sole purpose of tinnitus suppression and it would be
ethically difficult to propose cochlear implantation for
someone with significant residual hearing.
 Vascular compression of the vestibulocochlear nerve is highly
controversial.
 Destructive surgical procedures including VIIIth nerve neurectomy
or selective cochlear neurectomy have been tried
 endolymphatic sac decompression of Ménière’s disease are generally
aimed at control of vertigo and few trials have explored the effect on
tinnitus.