Tinnitus, defined as the perception of sound without an external source, has many underlying causes and pathophysiologies. It is a symptom with diverse presentations rather than a single disease. Treatment aims to manage comorbidities, reduce distress, and promote habituation to the phantom sounds through counseling, sound therapy, and in some cases medication. Future therapies continue to explore modulating neural activity and neurotransmitter systems involved in central tinnitus generation and perception.

1. DR. SHUBHANGI

2. TINNITUS
From Latin, tinnire, to ring
and was introduced
by Pliny the Elder

3. DEFINITION
Tinnitus may be defined variously, as 'a sound
perceivedfor more than five minutes at a time, in the
absence of any external acoustical or electrical
stimulation of the ear and not occurring immediately
after exposure to loud noise‘,'phantom auditory
perception,or 'head noise'.

4. THE MANY SOUNDS OF TINNITUS
 Ringing
 Hissing
 Roaring
 Whistling
 Swishing
 Buzzing
 Chirping
 Clicking
 “It goes along with my
heartbeat.”(Intermittent / Constant) [One
tone / Multiple tones]

5. COMMON AUDIOLOGICAL CAUSES
 Hearing loss
 Cerumen accumulation/occlusion
 Eustachian tube blockage
 Otitis media
 Exposure to loud noise
 Ototoxic
chemicals(aspirin,quinine,aminoglycosides)
 Otosclerosis - frequently
 Meniere’s Disease (episodic tinnitus along with
hearing loss, dizziness, and aural fullness)
 Acoustic neuroma – Even when the tumor is
removed, 50% of pts continue to experience tinnitus
(Benson et al., 2009)

6.  Only the patient perceives
head noise
 This is the more common
form
 Head noise is audible to the
patient and to the professional
 Relatively rare
 Also called as Somatosound
 Originates in the ear, head, or
neck
 Muscular or vascular etiology
 Myoclonus is found in pts with
degenerative
diseases(Neuromuscular
control loss due to CVA,
Parkinson’s Disease,Multiple
sclerosis, Huntongton’s
Disease, myasthenia gravis)
Subjective Tinnitus
Objective tinnitus
TYPES OF TINNITUS

7. SOMATOSOUNDS
 Vascular causes-
-Arteriovenous fistulas/malformations
-paragangliomas
-carotid artery stenosis
-atherosclerotic disease
-arterial dissection
-persistent stapedial artery
-intratympanic carotid artery
-vascular compression of eighth cranial nerve
-jugular bulb anomalies,venous hum,pseudotumor cerebri
 Non-vascular causes- palatal myoclonus,tensor
tympani/stapedius myoclonus,vascular neoplasms of skull base
PULSATILE NON-PULSATILE

8. MYOCLONUS
Abnormal rhythmic activity of muscles adjacent to the
auditory system could be a basis for myogenic
somatosounds.
-perceived by patients, usually as unilateral, regular or
irregular 'twitching', or 'clicking‘ sound.
- The most common forms are palatal and less
common middle ear muscles, tensor tympani and
stapedial myoclonus.

9. OTHER CAUSES OF “CLICK” TINNITUS
 Jaw joint misalignment
 i.e. the tempero-mandibular
joint (TMJ)

10. PATULOUS EUSTACHIAN TUBE
 associated with mucosal atrophy or muscular dysfunction of the
Eustachian tube
 leads to to-and-fro movements of the tympanic
membrane,synchronous with nasal respiration
 perceived as 'blowing' sound or their own voice reverberation.
 observed at otoscopy and demonstrated by tympanometry as
fluctuation in the tracing. The findings can be enhanced by
forced respiration with mouth and contralateral nostril closed.
 Nasal congestion, due to compression, may alleviate the
problem.
 Conservative treatment, including local application of potassium
iodine solution and conjugated oestrogen, and surgical
procedures, can be applied with variable success.

11. RISK FACTORS
•Age
•Cardiovascular/cerebrovascular disease
•Drugs
•Ear infections/inflammation
•Head/neck trauma
•Thyroid abnormalities
•Loud noise exposure
•Meniere’s disease
•Otosclerosis
•Sudden deafness
•Vestibular schwanoma
• anxiety
•Depression
•Familial inheritance

12. The intrusiveness of tinnitus depends on psychological
state and emotional response.
It has been suggested that patients suffering from
depression are vulnerable to developing distress at a
relatively low degree of tinnitus, while stress-tolerant
individuals can endure higher degrees of tinnitus before
seeking help.
Factors that play role –
Psychologic factors
Attentional mechanisms
Who complains of tinnitus?

13. DEMOGRAPHIC FEATURES
Tinnitus prevalence is a positive function of age:
38 percent
of patients < 40 years and 62 percent of patients >
40 years
present with tinnitus.
 Population statistics suggest that females are
more affected than males

14. RELATION TO HEARING IMPAIRMENT
In about 50 percent of the population with self-
reported
tinnitus, hearing has been judged (by patients) as
Normal.
Tinnitus prevalence rises with increasing hearing
l0ss, with 74 percent of patients complaining of hearing
loss (of unspecified type) having tinnitus.
The reports on profoundly deaf individuals, those
undergoing cochlear implantation who have
tinnitus,vary between 27 and 81 percent.

15. Laterality of tinnitus
In general, a greater prevalence of patients with
tinnitus,affecting the left ear more than the right, has
been reported although in some studies, no significant
difference between the two ears has been found.
Socioeconomic status
An overwhelming preponderance of patients in a tinnitus
clinic comes from the higher socioeconomic
groups.However, an increasing prevalence of tinnitus in
unskilled,in comparison with the professional classes,
has been noted.

16.  Tinnitus is a symptom, NOT a disease.
 The pathology causing tinnitus may be
outside of the scope of audiologists.
 The actual “cause” of tinnitus depends on
pathophysiology.

17. PATHOPHYSIOLOGY
 The most recent pathophysiologic theory suggests that
the central nervous system is the source or
‘‘generator’’ of tinnitus .
 Positron emission tomography (PET) scanning and
functional magnetic resonance imaging(fMRI) studies
indicate that a loss of cochlear input to neurons in the
central auditory system (such as occurs in cochlear
hair cell damage or a lesion of the vestibulocochlear
nerve) can result in abnormal neural activity in the
auditory cortex. This activity is linked to the perception
of tinnitus.

18. PATHOPHYSIOLOGY
 In addition, there is also a loss of
suppressionof the neural feedback loops
which help tune and reinforce auditory
memory in the central auditory cortex.
Disruption of this feedback loop leads to the
disinhibition of normal synapses and the
creation of uncontrolled alternative neural
synapses which lead to the abnormal
auditory perception of tinnitus

20. Sites in which these processes take place-
 24% cases - abnormalities within the otoacoustic periphery (i.e.
inner ear and the vestibulocochlear nerve)
 35% from the acoustic pathways
 41% within supratentorial structures .
A decrease in inhibition and/or increase in excitation - excitatory-
inhibitory imbalance causing neuronal hyperexcitability in these
regions - the perception of tinnitus .
However, neuronal excitability can be modulated by different
neurotransmitters and neuromodulators that act on voltage- or
ligand-gated channels, thus providing potential pharmacologic
targets

21. DIAGNOSIS
Pulsatile tinnitus requires an individual approach and should
include the following.
• A detailed history- provide information on the synchrony of
tinnitus with the pulse, effects of neck movements or
compression, effect of respiration,etc.
• Physical examination, include-
- palpation and light compression of the jugular vein may
diminish tinnitus of venous origin (a similar effect can be
achieved by the Valsalva manoeuvre,during which an
increased intrathoracic pressure and decreased venous return,
may also reduce tinnitus);
- auscultation of the neck and cranium for the presence of
carotid bruit or blood turbulance dueto arteriovenous
malformation;

22. • Tympanometry may demonstrate myoclonic
activity and patulous Eustachian tube.
• Pure tone audiometry may indicate
conductivehearing loss secondary to vascular
lesions affectingthe middle ear.
- otoscopy/otomicroscopy may reveal glomus
tumours or tympanal haemangioma;
- oropharyngeal. examination could reveal
contraction of the soft palate in palatal myoclonus.

23. • Imaging - gadolinium-enhanced computed tomography
(CT) and magnetic resonance imaging (MRI) is
necessary in most cases.
• Imaging usually starts with a CT of the temporal bones,
skull base,brain, calvaria and overlying soft tissue, as
some(bony) abnormalities are better visualized
(e.g.otosclerosis, or to delineate the anatomical extent of
glomus tympanicum) by this type of imaging.
However, MRI –soft tissue lesions (e.g. glomus jugulare
or vascular loops compressing the VIIIth cranial nerve).
Magnetic resonance angiography (MRA) and ultrasound
(e.g. duplex carotid) may help in identifying an
abnormality in selected cases

24. HOW IS TINNITUS QUANTIFIED?
 To assess the degree of distress or handicap that
tinnitus causes-inventories have been developed
1. Tinnitus Handicap Inventory
2. Tinnitus Effects Questionnaire
3. Tinnitus Handicap Questionnaire
4. Tinnitus Severity scale
5. Tinnitus Coping Style Questionnaire
6. Tinitus Functinal Index

25. HOW IS TINNITUS QUANTIFIED?
 The Tinnitus Handicap Inventory
 Self-report measure
 Validated in 1996
 Measures how tinnitus affects daily life
Functional, Emotional, and Catastrophic
subscales
Includes 25 items.

26. TREATMENT
There is currently no single Food and Drug
Administration (FDA) or European Medicines Agency
(EMEA) approved drug in the market
Current treatment strategy is aimed at controlling
underlying disorders and symptomatically
suppressing the perception of tinnitus.
 The primary goal has thus been improvement in
quality of life rather than absolute cure.

27.  Comprehensive management of tinnitus
includes
 assessment of hypertension, blood lipids,
thyroid function,allergies
 informing patients of factors that aggravate
tinnitus, such as stress, caffeine, nicotine,
and aspirin

28.  Treatment of comorbidities may involve procedures
suchas
-embolization or ligation for vascular abnormalities such
as arteriovenous malformations.
-Hearing aids for presbycusis,
-cochlear implants for sensorineural hearing loss
-cessation of any offending medications

29.  Pharmacologic: Treat symptoms related to tinnitus,
such as depression and anxiety.
 Nortriptyline (50 mg): Most effective drug,
although it causes dry mouth and takes 3-4
weeks to build up summative effect for benefit.
 SSRIs
 Paroxetine (10 mg) AKA Paxil
 Sertraline (50 mg/d) AKA Zoloft: Reduced tinnitus
severity, as well as symptoms of depression and
anxiety
 Benzodiazepines: Treats tinnitus as an anxiety
disorder BUT should not use these if depression
is present (and often it is).
 Antiepileptics-Gabapentin

30. ELECTRICAL STIMULATION
 Transcutaneous Electrical Stimulation
 Overall, mixed success
-A hand held probe ---to deliver electrical
stimulation to approximately 20
arbitrarily selected points on the external
pinna and tragus of each ear
-Stimulation may only be effective during
stimulus presentation

31. REPETITIVE TRANSCRANIAL MAGNETIC
STIMULATION (RTMS)
Electromagneti
c coil
positioned near
the patient’s
head emits
magnetic
pulses that
creates
electrical
activity that
alters neuronal
activity.

32. NON-TRADITIONAL TREATMENT
Homeopathic Therapy
 Ginko Biloba: Antioxidant that inhibits
platelet aggregation  promotes
circulation to small blood vessels such as
those that supply the cochlea.
 Niacin: May provide smooth muscle
relaxation and promote circulation to
small blood vessels.
Pts may report that Niacin reduces
severity of tinnitus

33.  Tinnitus retraining therapy (TRT)
 masking
 biofeedback
 cognitive behavioral therapy.
NON TRADITIONAL
TREATMENT

34. NON-TRADITIONAL TREATMENT
 Biofeedback
 Commonly used for the management of pain
 Pt monitors involuntary bodily processes
such as heart rate, blood pressure, and
muscle tension through electromyography
(EMG) and electroencephalography (EEG) .
 Goal is to reduce anxiety and/or stress that
may aggravate tinnitus
 Conducted by a psychologist
 <80% of pts report reduction in tinnitus
symptoms

35. TINNITUS RETRAINING THERAPY (TRT)
 based on bypassing or overriding abnormal
auditory cortex neural connections.
 It is based on the principle that all levels of the
auditory pathways play essential roles in tinnitus, and
induces habituation to the
tinnitus signal.
 The goal is to reach a stage in which patients are
unaware of their condition unless they consciously
focus on it.
 This habituation is achieved by
-directive counseling, combined with low-level noise
generated by wearable generators and environmental
sounds.

36. MASKING
 Masking devices are designed to produce
low-level sounds that reduce the perception
of tinnitus.
 not successful in all patients and some
patients have even reported a worsening of
their tinnitus

37. COGNITIVE BEHAVIOURAL THERAPY
aims to motivate patients to learn to alter their
psychological response to tinnitus by identifying and
reinforcing coping strategies, distraction skills and
relaxation techniques.

38. FUTURE THERAPY
 Currently, there are only a small number of drugs in
development for the treatment of tinnitus
1.Neramexane, a non-competitive, voltage-dependent
NMDAantagonist which also blocks nicotinic cholinergic
receptors expressed on hair cells in the inner ear .
2.LidoPAIN TV is a non-sterile patch delivering lidocaine,
which is applied to the periauricular skin region.
3.Vesitipitant is a novel antagonist of the neurkinin-1 receptor
which binds substance P. Neurokinin receptors are present
in the inner ear, representing a potential therapeutic target
for tinnitus