Tinnitus - The Medical Post

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Transcript Tinnitus - The Medical Post

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

Impacted wax

Impacted foreign body

Otitis externa

Otitis media

Otosclerosis Cochlear causes

Presbyacusis

Noise induced

Meniere’s disease

Ototoxicity

Temporal bone trauma

Labyrinthitis

Otological subjective tinnitus

Retro-cochlear causes

Acoustic neuroma

Other CPA lesions

Vascular compression of 8 th nerve Central causes

Multiple sclerosis

CVA

CNS tumors

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, 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

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