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 (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

Subjective vs. Objective tinnitus

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

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

Otological subjective tinnitus

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, anti-

histamines

Psychogenic: anxiety, depression

Vascular Causes

of Objective Tinnitus

Arterio-venous shunts: congenital arterio-venous

malformation, acquired AV shunt, carotico-

cavernous 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

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

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