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Tinnitus Aurium

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

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Tinnitus Aurium

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  1. Tinnitus Aurium Dr. Vishal Sharma

  2. 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

  3. Definition

  4. 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

  5. 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%)

  6. 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

  7. 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

  8. 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

  9. Otological subjective tinnitus Retro-cochlear causes Central causes  Acoustic neuroma Multiple sclerosis  Other CPA lesions CVA  Vascular compression CNS tumors of 8th nerve Hydrocephalus

  10. Non-Otologic Causes of Subjective Tinnitus

  11. 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

  12. Vascular Causes of Objective Tinnitus

  13. 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

  14. 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

  15. Models for Mechanisms of Tinnitus

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  21. Neuro-physiological model for tinnitus Proposed by Pawel Jastreboff in 1990

  22. Conditioned reflex loops

  23. 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

  24. 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

  25. History taking in Tinnitus patient

  26. 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

  27. 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

  28. 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

  29. Investigations

  30. 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

  31. 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

  32. Psycho-acoustical measurement • Pitch or frequency matching of tinnitus • Loudness matching of tinnitus • Minimal masking levelfor tinnitus • Residual inhibition: temporary suppression or elimination of tinnitus following its masking

  33. 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

  34. 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 ?

  35. Prevention / Avoidance of: • Viral infections • Noise induced hearing loss • Ototoxic drugs • Chocolate, cheese, tea, coffee, red wine • Rapid withdrawal of addictive substances

  36. Tx of causative factors • Impacted wax • Otitis media • Meniere’s disease • Anemia • Hypertension & hypotension • Diabetes mellitus & hypoglycemia • Hypothyroidism & hyperthyroidism

  37. 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.

  38. 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

  39. 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

  40. 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

  41. 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”

  42. Ideal masking intensity

  43. 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

  44. Based on neuro-physiological model of tinnitus • Blocks tinnitus-related neuronal activity from reaching cerebral cortex (where it is perceived) & from activatinglimbic & autonomic nervous systems • Uses combination of low level, broad-band sound therapy & psychological counseling to achieve habituationof tinnitus. Tinnitus never masked in TRT. Retraining takes 12 -18 months. Success rate = 80%

  45. Conditioned reflex loops

  46. Effect of habituation by TRT

  47. Pharmacological Treatment

  48. 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

  49. 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

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