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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.

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Presentation on theme: "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."— Presentation transcript:

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  % of people experience tinnitus  % 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 (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

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 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

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

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  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 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  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

41  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

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

53

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

56

57 Thank You


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