TINNITUS & HYPERACUSIS.pptx

Tinnitus and hyperacusis made easy

1. TINNITUS & HYPERACUSIS PRESENTOR–DR FALAQ FAIYAZ MODERATOR-DR PANKAJ KUMAR VERMA

2. TINNITUS Defined as sound perceived for more than 5 mins at a time , in absence of any external acoustical / electrical stimulation of ear & not occuring imme . After exposure to loud noise It is also defined as auditory perception due to aberrant spontaneous activity , arising from altered state of excitation/ inhibition wihthin auditory system. Tinnitus is further div into subjective (heard only by pt) or objective (audible to examiner as well)

3. Auditory hallucination Tinnitus differs from auditory hallucinations by absence of organization of its content (repetitive words or musical themes ) MC seen in elderly pts and psychiatric pts or by subjects suffering from alcoholism. Also seen in CNS disorders ( tumours , vascular lesions & epilepsy) acc PET & MRI middle & sup. Temporal cortex are involved.

4. Hyperacusis Intensity related dysacusis defined as reduced tolerance to noise, or increased sensitivity to sounds in levels that would not cause discomfort in normal individual. Characterized by increased growth in loudness ie - complaint of excessively loud perception of ordinary environmental sounds.(common in 6-7 % ppl ) Associated with tinnitus usually preceding it in (40-79% cases)

5. Pathophysiology of hyperacusis Lack of adaptive (inhibitory)mechanisms, which normally limit sound input & prevent overstimulation of auditory system . In bells palsy & stapedotomy hyperacusis is explained as disorder of stapedial reflex & tone which normally reduce acoustic input . In myasthenia gravis it is bcoz of reduced efficacy of stapedial reflex and olivocochlear reflex , 2˚ to reduced ACH production which mediates these reflexes.

6. Cont.. In william syndrome 95% ppl suffer from hyperacusis as fMRI shows significant reduced activation in temporal lobe forming central cause for hyper acusis . Music related sound exposure seems to be a significant aetiological factor in occurrence of hypersensitivity to sound reported by 51 % of pts. Hypothetical explanation- frequent exposure to noise alters subcortical & cortical tonotopic organization with decrease in GABA- nergic inhibition

7. Evaluation of hyperacusis Hyperacusis is judged clinically by measuring loudness discomfort level ( ldl ) which is considerably lower in pts with hyperacusis (> 70 dB in 500-4000Hz range) than in normal subjects . Alternate biaural loudness balance (ABLB)

8. Epidemiology of tinnitus Prevalence of tinnitus in general population is about 14.5% however only 7.2% have clinical tinnitus. Asso . Of otologic conditions with tinnitus- 85% of otosclerosis pts,83 % in vestibular schwannoma & 3 % in multiple sclerosis. Demographic variation – 38 % in <40 yrs & 62 % in > 40yrs of age more common in female than in males.

9. Cont…. Tinnitus prevalence rises with increasing hearing loss of unspecified type There is no corelation b/w melanin content in inner ear and tinnitus production . Greater prevalence of left ear laterality of tinnitus is has been reported. Preponderance of tinnitus is more in higher socio-economic class.

10. Aetiology of tinnitus Not a single well defined disease,but a symptom of many pathologies,one pt may have several pathological mechanisms. Mc conditions responsible for tinnitus are SNHL- NIHL , menieres ds,acoustic neuroma & intoxication

11. Ototoxic drugs and tinnitus Mc ototoxic drugs asso . With tinnitus are salicylate & quinine. According to studies done on pt with rheumatoid arthritis on salicylate drugs prevalence of tinnitus was higher . In salicylate toxicity (suicide attempts)50 g aspirin ,100-300 mg/L plasma conc. / prolong cont. usage is usually asso . With transient tinnitus & hearing recovery with 2 days. Both drugs influence active process of transduction in which OHC are involved daily dose of aspirin 3.9g & quinine 325mg can abolish OAE.

12. Objective tinnitus- SOMATOSOUNDS SOMATOSOUNDS- heard by both pt and examiner,may originate from diff. sources adjacent to auditory system due to variety of pathologies. Aetiopathologies - vascular somatosounds - arterial/venous producing turbulent blood flow leading to pulsatile somatosounds . Vascular tumours - glomus tympanicum / jugulare , hemangioma . Vascular malformation- AV malformation,aneurysm,fistulae,carotid artery stenosis

13. Contd.. Increased ICP- venous hum ,transmitted cardiac murmur , hyperdynamic vascular states- pregnancy , hyperthyroidism,anemia . Vascular loop- ant. Inf. Cerebellar artery causes compression/ irritation of acoustic nerve. Myogenic somatosounds - abnormal rhythmic activity of muscles adjacent to auditory system ,perceived by pts as unilateral regular/irregular twitching/ clicking sound, Mc forms- palatal > ME muscles (tensor tympani & stapedial myoclonus )

14. Patulous ET Mucosal atrophy or muscular dysfunction of ET , leads to to & fro motion of TM ,synchronous to nasal respiration Perceived as blowing sound / reverbration of their own voice. Observed on otoscopy & demonstrated on tympanometry ,nasal congestion due to compression relieves symptom Treatment is local applicaton of potassium iodide & conjugated oestrogen .

15. Contd … Temporomandibular joint abnormality- causes audible vibratory sound arising from jaw clenching. Spontaneous otoacoustic emissions- high level SOAE ,exceeding level of audibility such that it can be heard at a distance of 1.25-2 m Usually heard by others and not perceived by pt him self , it may be present in a perfectly healthy individual Diagnosis- synchrony of tinnitus with pulse,effect of neck movts,effect of respiration.

16. Contd.. Effect of valsalva during which intrathoracic pressure increased & decreased venous return . Auscultation of neck & cranium for presence of carotid bruit / blood turbulence due to AV malformation . Oropharyngeal examination for palatal clonus . Tympanometry – patulous ET . Imaging – gadolinium enhanced CT ,MRI ,ultrasound (duplex carotid).

17. PATHOPHYSIOLOGY OF TINNITUS Auditory feedback system – mainatined by complex feed back mechanism involves afferent ascending,efferent descending pathways. Linked with extra auditory systems such as reticular- srotonergic , somatosensory , hypothalamic & limbic systems in integration with CNS. Afferent pathway – provides input to proximal structures of auditory system (excitatory) while efferent pathway modulates acoustic information (inhibitory).

18. Mechanism underlying tinnitus Assumed that alteration in spontaneous activity leading to tinnitus arises from changes in balance b/w excitation & inhibition within auditory system through diff. underlying mechanisms. Abnormal afferent excitation at cochlear level – Mechanical tinnitus- spontaneous cochlear oscillation Glutamate neurotoxicity Modulation (enhanced sensitivity) of NMDA & non-NMDA receptors. Abnormal calcium channel dysfunction

19. Contd.. Efferent dysfunction /reduction of GABA effect Alteration of spontaneous activity & tonotopic reorganization Stress/psychological disorders. Abnormal afferent excitation at cochlear level – Spontaneous emissions – SPOAE- direct cause of tinnitus,it has been demonstrated that aspirin can abolish both SOAE & ass. Tinnitus.

20. Contd …. Spontaneous emissions- increased cochlear gain & auditory disinhibition - efferent mediated suppression & SOAE may cause cochlear gain as a result of central disinhibition resulting in tinnitus. Interaction of SOAE & external sounds- SOAE makes cochlea & auditory system inherently unstable & insensitive to external sounds. External sound act as source of energy to set cochlea into a state of mechanical instability & sustained oscillations.

21. contd … SOAE may interact with external sounds creating distortion products leading to diff. auditory perceptions. Glutamate neurotoxicity- gluatamate is main excitatory neurotransmittor of CNS –(cochlear afferents) , being released on to IHC synaptic region. Highly neurotoxic seen in acoustic trauma , excessice noise exposure leads to excessive release of glutamate & release of intracellular Ca++ overload- basis of tinnitus. Treatment- glutamate receptors eg - NMDA- (N- methyl- D- aspartate ) can be selectively blocked by antagonist ( eg - caroverine )abolishes tinnitus.

22. Modulation (enhanced sensitivity) of NMDA & non- NMDA receptors- lat. Olivocochlear efferents play a role in modulating sensitivity of afferent receptors in cochlea. Dopamine neurotransmitter act as permanent gain control at site of action potential initiation,application of dopamine agonist ( piribedil ) protective action against glutamate induced excitotoxicity (NI tinnitus) Endogenous opoid peptides dynorphins released on to IHC synaptic region by lat. Olivocochlear fibres as response to stress.(enhance NMDA & non-NMDA)

23. Abnormal ion channel conductance- calcium channel dysfunction. Intracellular conc. Of calcium is responsible for multiple func . Of OHC & IHC.including fast & slow motility of OHCs & transmitter release in IHCs. Ca ++ channel blockers slow motility of OHC,which reflects on mechanosensory adaptation , essential for sharp frequency tuning & low threshold sensitivity. Alteration in calcium channel conductance affect functioning of nervous system , with decrease in both extracellular & intracellular Ca++ conc. Leads to bursting firing pattern of neural activity

24. Abnormal peripheral & central neural auditory activation. Various lesions along auditory neural pathway lead to tinnitus. Irritative lesions – tumours / vascular loops – tinnitus is treated with anti-epileptics. Motor/sensory tinnitus – evoked by activation of somatosensory , somatomotor & visual motor systems- through activation of extralemniscal polysensory pathway due to neural sprouting/ neosynaptogenesis – Sx of post. Carnial fossa .

25. Efferent dysfunction Efferent system acts as an inhibitory force within auditory system , its malfunction lead to disinhibition After introduction of OAE & olivocohlear suppression test (recording OAE under C/L acoustic stimulation) Reduction of suppressive effect of med. Olivocochlear system is underlying mechanism of tinnitus. GABA downregulation - degerative changes & changes related to noise trauma,ototxicity /ageing ,alter amino acid neurotransmitter in cochlear nucleus.reduced inhibitory effect forms basis of tinnitus.

26. Alteration of spontaneous activity & tonotopic reorganization Peripheral lesions /dysfunction of diff. aetiologies ,with consequent reduction in afferent input & compensatory dysinhibition within proximal auditory pathway , result in alteration of spontaneous activity & plastic transformation of brain . Altered neural activity results from prolonged discontinuity in spatial pattern across fibres in auditory nerve leading to reduction of inhibition in proximal pathways, alter rate & pattern of spontaneous activity in auditory lemniscal & extraleminscal .

27. Cochlear lesions decrease activity in auditory nerve & ventral cochlear nucleus but increase activity of dorsal cochlear nucleus, ing . Colliculus ,med. Geniculate body & cortical neurons.(this hyperactivity causes tinnitus). Neurotransmitters mediate these changes ( Ach,GABA,glutamate & glycine .) baclofen – gaba agonist reverses noise induced hyperactivity in IC. Damage to cochlea leads to expansion of cortical representation of restricted frequency band adjacent to region of cochlear loss.

28. This plastic alteration is attributed to serotonergic system which regulate/modulate complex autoregulatory circuitry of compensatory mechanism Tinnitus & habituation – in most pts tinnitus dimishes due to habituation but intrusive tinnitus occurs from lack of habituation Mechanism of habituation- amplitude reduction during repititive presentation of same stimulus (adaptive cortical mechanism)protects auditory system from overstimulation. Complex neuronal circuit & multiple neurtransmitters are involved but 5-HT serotonin plays a key role , also k/a gain control.

29. TINNITUS IN CHILDREN Aetiology - childhood tinnitus is ass. With – secretory otitis media,deterioration of existing HL,meningitis,psychological , migraine , juvenile meniere’s ds,CSOM , excessive noise & brainstem tumour . Treatment – similar to that of adults with counselling & reassurance.

30. INVESTIGATION OF TINNITUS History- subjective description of tinnitus,annoyance /impact on sleep & daily life, asso . Auditory & vestibular symptoms. Otological & general medical conditions drugs / noise exposure. Current & pre-existing stress conditions & psychological/psychiatric disorders.

31. Neurotological evaluation Auditory assessment – useful in identifying presence & site of lesion & essential for planning rehabilitation stratergies (amplification of HL). Otoscopy PTA- Tympanometry – identify ME pathology & evaluate neural pathway subserving stapedial reflex. OAE- spontaneous , evoked & olivocochlear supression test) Auditory braimstem evoked response

32. Authentication of tinnitus Psychoacoustic test – developed by fowler-it includes pitch , loudness,masking residual inhibition . Pitch – perceptual corelate of frequency – tinnitus pitch match is procedure of matching frequency of an acoustic tone or narrow band noise to predominant pitch of tinnitus .high frequency >3kHz IS nihl related tinnitus & loew frequency menieres ds . Loudness – psychological magnitude of sound intensity of tinnitus coded by rate of neural activity & number of fibres .

33. Tinnitus loudness match is procedure adjustment of intensity of pure tone or narrow band noise to that of tinnitus,should be b/w 5-10 dB sound sensation level. Masking – refers to reduction in audibility of sound with another sound, on graphical representation frequency dependent masking has peripheral cause & non- frequency dependent has central cause. Residual inhibition – supression or complete elimination of tinnitus for temporary period following masking. Sponatneous spectrum of neural activity within auditory nerve – recording directly from promontory or auditory nerve during vestibular schwannoma increase in neural activity at 200 Hz disappeared with lidocaine .

34. Auditory event related potential Auditory event related potential N100, P200 (>150 ms) & long latency ,P 300 (>300ms) Auditory evoked cortical magnetic fields- in particular M200 ( corresponds to P200) & M100 corresponds to N100

35. TREATMENT Tinnitus is a symptom of diff. pathologies hence no single rule( multidiscipilinary approach) of treatment can be followed , underlying cause is to be treated. Various underlying causes iclude - cardiovascular ,renal , metabolic,autoimmune & medications) Surgical treament of tinnitus- intervention such as nerve section & cochlear destruction have provided very little effectiveness & may even make tinnitus worse.

36. Cont… Tinnitus retraining therapy- based on neurophysiological model of tinnitus , acc to which tinnitus results as a abnormal processing of novel signal generated within auditory system . This signal is subjected to amplification in limbic and autonomic nervous systems ,tinnitus becomes problematic through process of subconscious conditioning , perception of tinnitus is associated with negative perception. Trt includes habituation-based protocol ie sound therapy & cognitive behavioural therapy

37. Trt cont… Directive counselling - aimed at providing clear information of possible mechanism of tinnitus Person centred counselling - stress & possible ways of dealing with problems Cognitive counselling - identifying false beliefs of pt and dispelling them

38. Instrumentation Hearing aid – hypothetical mechanism amplification of external sound hence reducing awareness of tinnitus & improved auditory input is beneficial in enchancing central mechanisms of habituation & promoting central adaptive plasticity. Efficacy – 66 % in hearing aids & 93 % cochlear implants Noise generators – tinnitus maskers are behind ear or in ear devices ,used for presentation of sound in a controlled manner in order to reduce or eliminate perception of tinnitus.

39. Contd.. Low-level sound generators are adjusted to provide constant low-level (at least 6-8 hours a day )neutral auditory signals which compete with but do not mask tinnitus.positive effects take long duration to be effective usually 12-18 months Tinnitus instruments contain both hearing aid & noise generators,they have been developed to enhance frequency bands which could not be sufficiently amplified by hearing aid.

40. Psychotherapy Tinnitus is associated with distress in 25-45 % cases ,they require psychotherapy which includes cognitive behavioural techniques , relaxation , hypnosis , biofeed back & stress management. It does not abolish tinnitus but reduces associative distress & improve QOL. Biofeedback –technique of gaining control of certain physiological functions of body with help of device such as associated muscular tension can be monitored by electromyographic BF device.

41. Pharmacological treatment Anti depressants- TCA , nortrptyline & amitryptyline are effective they act on both peripheral & central auditory system through anti-Ach & anti-histaminic effect. Selective serotonin reuptake inhibitor as modulators of tonic inhibition of auditory pathways. GABAa ( benzodizepines ) & GABAb ( baclofen )- they act as anxiolytic,sedative,hypnotic,anticonvulsant & skeletal muscle relaxant .

42. Cont…. Calcium channel antagonists- abnormal calcium conductance may be responsible for tinnitus , nimodipine is lipophylic Ca2++ channel blocker , preferential activity on cerebral vessels , particularly poorly profused areas. Flunarizine is used to abolish tinnitus in a subset of pts with tinnitus & dizziness. Anti-epileptics- cause depression of neuronal response to excitatory stimuli & hyperpolarization of neuronal membranes, eg – carbamazepine,lamotrigine

43. Contd … Selective glutamate receptor antagonist- neuroexcitotoxicity is one of various mechanisms of tinnitus hence use of antagonist for blocking glutamate receptor / attentuating influx of calcium. Coverine - smooth muscle relaxant & neuroprotective drug blocks post-synaptic glutamate receptors when given intravenously was found effective. Prostaglandin analogue- control microcirculation of cochlea & act as neuromodulators of afferent pathway within cohclea

44. Cont… Lidocaine - most effective ,local injection is given into nasal turbinate/ transtympanic , 83% efficacy , sodium channel blocker operates mst efficiently in nerves with high discharge rate ,reduces max. firing rate of nerve Other treatments – electrical/magnetic stimulation , gingko biloba ,acupuncture or zinc High pulse train electrical stimuli to cochlear round window helps reestablishing code of silence

45. REFERANCES Scott brown – otorhinolaryngology volume 3 edition 7 th

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