1. Tinnitus Aurium
Dr. Vishal Sharma

2. History “Bewitched ear” in Ebers papyrus (3000 BC)
Tinnire (to ring) used by Pliny Elder, 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
% 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
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 level for 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

45. 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 months. Success rate = 80%

46. Conditioned reflex loops

47. Effect of habituation by TRT

48. Pharmacological Treatment

49. 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

50. 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

51. 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

52. 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

54. Treatment of Hyperacusis & Misophonia

55. 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

57. Thank You