Tinnitus - The Medical Post

Report
Tinnitus Aurium
Dr. Vishal Sharma
History

“Bewitched ear” in Ebers papyrus (3000 BC)

Tinnire (to ring) used by Pliny Elder, 23-79 AD

Joseph Toynbee died in 1866 due to chloroform
+ prussic acid vapour inhalation as tx for tinnitus

Fowler (1941): performed frequency matching,
loudness matching & tinnitus masking
Definition

Conscious experience of a sound that
originates in an involuntary manner in owner’s
head with no corresponding external acoustic
or electrical stimulus (McFadden, 1982)

Must persist for > 5 min at a time (Scott-Brown)

Due to aberrant spontaneous activity arising
from altered state of excitation or inhibition
within auditory system
Incidence

6 - 17 % of people experience tinnitus

3 - 7 % of people seek help for their tinnitus

0.5 - 2.5 % report severe effects of tinnitus

Tinnitus present in: deafness (60-85%), sudden
SNHL (50%), NIHL (50-90%), presbyacusis (70%),
acoustic neuroma (70%), Meniere’s attack (100%)
Subjective vs. Objective tinnitus

Subjective (true) tinnitus: heard by patient only

Etiology = otological & non-otological

Objective (pseudo) tinnitus or somato-sounds:
heard by patient & examiner with stethoscope

Etiology = vascular & non-vascular
Other associated Dysacusis

Hyperacusis = hypersensitivity to sound due to
increased abnormal gain within auditory system

Phonophobia or Misophonia = hypersensitivity +
fear toward sound stimulus due to abnormal
excitation of limbic & autonomic nervous system
Otological subjective tinnitus
Conductive causes
Cochlear causes
 Impacted wax
 Presbyacusis
 Impacted foreign body
 Noise induced
 Otitis externa
 Meniere’s disease
 Otitis media
 Ototoxicity
 Otosclerosis
 Temporal bone trauma
 Labyrinthitis
Otological subjective tinnitus
Retro-cochlear causes
Central causes
 Acoustic neuroma
 Multiple sclerosis
 Other CPA lesions
 CVA
 Vascular compression
 CNS tumors
of 8th nerve
 Hydrocephalus
Non-Otologic Causes
of Subjective Tinnitus
Temporo-mandibular joint disorders
Cardiovascular: anemia, hypertension, Hypotension
Metabolic: hypoglycemia, hypothyroidism,
hyperthyroidism, hyperlipidemia
Neurologic: epilepsy, migraine, meningitis
Withdrawal: alcohol, caffeine, anti-depressants, antihistamines
Psychogenic: anxiety, depression
Vascular Causes
of Objective Tinnitus
Arterio-venous shunts: congenital arterio-venous
malformation, acquired AV shunt, caroticocavernous fistula
Arterial bruits: aberrant ICA, aneurysm / stenosis
of ICA, persistent stapedial artery
Venous hum: dehiscent jugular bulb, Hypertension
Paragangliomas: glomus jugulare / tympanicum
Objective Tinnitus
(non-vascular causes)

Patulous Eustachian tube

Myoclonus: palatal, stapedial, tensor tympani

Clicking temporo-mandibular joint

Live foreign body in external auditory canal

Spontaneous oto-acoustic emissions
Models for
Mechanisms of
Tinnitus
Conductive tinnitus model
Lack of ambient noise masking leads to
enhancement or revealing of:

Sensori-neural tinnitus

Non-otological subjective tinnitus

Somato-sounds or objective tinnitus
Cochlear tinnitus model

Cochlear pathology  abnormal spontaneous
rate or rhythm of activity in cochlear nerve

Spontaneous oscillations of outer hair cells

Glutamate neuro-transmitter excito-toxicity

Enhanced sensitivity of receptors to glutamate &
endogenous opioid peptides dynorphins
Neural Tinnitus Model

De-myelinization of cochlear nerve fibres 
cross-talk b/w nerve fibres  distortion of
resting state of discharge in nerve fibres

Lack of efferent auditory pathway inhibition
(pathway dysfunction or GABA down regulation)

Calcium channel dysfunction  ed intracellular
calcium  ed activity in cochlear nerve
Central tinnitus model

Abnormal central processing of peripheral neural
activity mediated by neuro-transmitters
glutamate, glycine & acetylcholine

Extra-lemniscal auditory activation by somato-
sensory, somato-motor & visual-motor systems

Tonotopic reorganization of auditory cortex
Trigger factors for tinnitus

Psychological stress (serotonin & adrenaline)

Noise exposure

Head injury, TM joint injury, neck injury

Ear syringing

Changes in atmospheric pressure

Surgical operations
Neuro-physiological
model for tinnitus
Proposed by
Pawel Jastreboff
in 1990
Conditioned reflex loops
Conditioned reflex loops

CRL develop b/w limbic system, ANS,
subcortical pathways & auditory cortex

Concern & fear toward tinnitus  negative
reinforcement  make CRLs strong

Once strong CRLs develop, peripheral auditory
signals not necessary for tinnitus perception

Role of tinnitus retraining therapy: break these
CRLs by natural habituation
Points in favour of
Neuro-physiological model
1. Significant damage to auditory system not
required for tinnitus to develop as 30% pt with
tinnitus have normal hearing
2. 30% pt with hearing loss don’t have tinnitus
3. Tinnitus associated with emotional distress,
sleep problems, anxiety & negative emotions,
suggesting involvement of limbic system & ANS
History taking
in Tinnitus patient

Sleep disturbance / emotional upset

Pulsatile or persistent tinnitus

Does tinnitus get masked by ambient noise?

Deafness / vertigo / hyperacusis / phonophobia

Trauma: head / cervical spine / noise

Ototoxicity / withdrawal from drugs

Anxiety / depression

DM / HTN / thyroid disease / epilepsy / migraine
General Examination

Auscultation: for objective tinnitus

Pallor / hypertension / hypotension

Effect of neck turning on tinnitus

Effect of jugular vein compression on tinnitus

Temporo-mandibular joint mobility for clicks
E.N.T. examination
1. Otoscopy:  for EAC pathology
 for spontaneous movement of T.M.

Synchronous with pulse: vascular somatosound

Synchronous with breathing: patulous E.T.

Synchronous with soft palate twitch: myoclonus
2. Tuning Fork Tests: conductive vs. SNHL
Investigations

Pure Tone Audiometry: to assess hearing
threshold & rule out hyperacusis

S.I.S.I. & A.B.L.B.: for cochlear deafness

T.D.T.: for retro-cochlear deafness

Impedance audiometry: Rule out otosclerosis
Large fluctuations in compliance with respiration
= patulous Eustachian tube

Otoacoustic emissions: for cochlear function

B.E.R.A.: for retro-cochlear pathology

CT scan with contrast: for CPA & CNS tumours in
unilateral tinnitus

Angiography: for vascular malformations,
glomus tumours

Functional MRI & PET scan: tinnitus activates
primary auditory (temporal) cortex, associative
auditory (temporo-parietal) cortex, hippocampus,
prefrontal-temporal network & limbic system
Psycho-acoustical measurement

Pitch or frequency matching of tinnitus

Loudness matching of tinnitus

Minimal masking level for tinnitus

Residual inhibition: temporary suppression or
elimination of tinnitus following its masking
Other Investigations

CBP with ESR

Sugar profile: FBS, PPBS, RBS

Thyroid profile: T3, T4, TSH

Lipid profile: TG, LDL, HDL

Circulating auto-antibodies

Syphilis serology
Treatment Protocols

Prevention

Pathological conditions to be treated

Psychotherapy

Prosthetic: H.A., C.I., T.R.T., tinnitus maskers (?)

Pharmacological (?)

Surgery (?)

Stimulation ?: electrical, magnetic, electromagnetic

Others: Ginkgo biloba ?, acupuncture ?, yoga ?
Prevention / Avoidance of:

Viral infections

Noise induced hearing loss

Ototoxic drugs

Chocolate, cheese, tea, coffee, red wine

Rapid withdrawal of addictive substances
Tx of causative factors

Impacted wax

Otitis media

Meniere’s disease

Anemia

Hypertension & hypotension

Diabetes mellitus & hypoglycemia

Hypothyroidism & hyperthyroidism
Psychotherapy

Cognitive behavioral therapy aims at removing
negative emotions due to tinnitus perception
(cognitive therapy) & modification of tinnitus
motivated avoidance behavior (behavior therapy)

Bio-feedback displays electro-myographic
evidence of frontalis muscle tension due to
tinnitus. Awareness helps in its removal.
Hearing aids & Cochlear Implants
They help in pt with deafness + tinnitus by:

Reducing awareness of tinnitus by amplification
of ambient sounds

Improved auditory input enhances central
mechanism of habituation & promotes central
adaptive plasticity
Tinnitus Maskers

Synonym: white noise generators

Complete masking: tinnitus becomes inaudible due
to higher intensity of masking noise. Not used.
Partial masking: provides low intensity
background noise against which loudness of
tinnitus gets reduced. Preferred technique.

Tinnitus masker + hearing aid = tinnitus instrument
Facts about tinnitus masking

total suppression (total masking) of tinnitus
prevents tinnitus habituation

partial suppression (partial masking) does not
prevent tinnitus habituation

activation of limbic & autonomic nervous
systems by too loud or unpleasant sounds,
enhances tinnitus & prevents habituation
Facts about tinnitus masking

low-level noise masking also enhances tinnitus
(stochastic resonance )

stochastic resonance range = 20 dB, beginning
from –5 dB below threshold of tinnitus detection

Ideal masking intensity = b/w stochastic
resonance & total masking called “mixing point”
Ideal masking intensity
Tinnitus characteristics

Conductive: low-pitch, masked at auditory
threshold

Cochlear: high-pitch (except Meniere’s disease),
masked at auditory threshold

Retro-cochlear: high-pitch, masked well above
auditory threshold

Central: high-pitch, resistant to masking

Based on neuro-physiological model of tinnitus

Blocks tinnitus-related neuronal activity from reaching
cerebral cortex (where it is perceived) & from activating
limbic & autonomic nervous systems

Uses combination of low level, broad-band sound
therapy & psychological counseling to achieve
habituation of tinnitus. Tinnitus never masked in TRT.
Retraining takes 12 -18 months. Success rate = 80%
Conditioned reflex loops
Effect of habituation by TRT
Pharmacological
Treatment
Anti-depressants:

Amitryptiline = 25 mg TID for 3 weeks

Fluoxetine = 20 mg BD for 3 weeks
G.A.B.A. analogues:

Alprazolam = 0.25 – 0.5 mg OD  BD for 3 weeks

Clonazepam = 0.5 – 1.0 mg OD  BD for 3 weeks

Gabapentin = 300 mg OD  TID for 3 weeks

Baclofen = 10 mg BD  25 mg BD for 3 weeks
Calcium blocker: Nimodipine = 30 mg BD X 3 wk
Glutamate blocker: Caroverine infusion
Antiepileptics:

Carbamazepine = 100 mg BD  200 mg TID (3 wk)

Na Valproate = 200 mg TID  500 mg TID X 3 wk

Lamotrigine = 50 mg OD  100 mg BD X 3 wk
Prostaglandin: Misoprostol = 200 μg QID X 3 wk
Lignocaine: IV & trans-tympanic application
Surgical treatment

Surgical removal of vascular malformations

Surgical division of cochlear nerve

Micro-vascular decompression of anterior inferior
cerebellar artery loop around auditory nerve
Results of surgery for tx of tinnitus are poor & may
actually worsen tinnitus
Stimulation of cochlea (?)

Electrical: by round window or cochlear implant

Magnetic: by magnet placed in E.A.C.

Electro-magnetic: increases blood flow
Spontaneous OAE suppression (?)

Aspirin

Quinine
Treatment of
Hyperacusis &
Misophonia
Hyperacusis treatment

Attenuation of environmental sounds by ear
plugs: temporary solution only for anticipated NIHL.
Persistent use enhances hyperacusis

Hyperacusis desensitization therapy: using sound
with higher frequencies removed (pink noise) give
short exposures to moderately loud sound

Sound retraining therapy: like TRT
Misophonia treatment: listening to music
Thank You

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