Ent and head neck surgery

1. Tinnitus and its management
Dr. Bigyan Raj Gyawali
MS (ORL-HNS) First year
GMSMA of ENT-HNS
Studies
MMC-TUTH, IOM

2. Definition
• ‘Sound perceived for more than 5 minutes at a time, in
the absence of any external acoustical or electrical
stimulation of ear and not occurring immediately after
exposure to loud noise.’
• ‘Phantom auditory perception’
• ‘Head noise’
Scott Brown 7th edition Otorhinolaryngology, Head & Neck Surgery

3. Historical overview
• Latin word “tinnire”(AD 23- 79)
• Previously termed ‘bewitched ear’

4. Historical overview
Historical views
• Caused by excitement of the sense
( Ibi Sina,980-1037 AD )
• Overstimulation of auditory nerve
( Johanes Miller,1801-1858)
• Irritation at different levels of auditory system
( Mac Naughton Jones,1891)

5. Historical overview
• Joseph Toynbee (1815-1866), father of otology in
England
• Died experimenting himself with valsalva inflation of
vapours of chloroform and prussic acid

6. Types
• Subjective (True tinnitus)
• Objective

7. Epidemiology
• 15% of adult UK population (Multicentre National
Study Of Hearing)
• 32% of all adults in US (National Centre Of Health
Statistics)
• Prevalence of ‘clinical tinnitus’ in urban population :
7.2 %
• M>F
• 38 % < 40 years, 62 % > 40 years

8. Epidemiology
• Associated with hearing loss in majority of patients
• Left>Right
• Higher socioeconomic group
• Depression
• Melanin content in iris and inner ear
• Otologic and medical conditions
• Pregnancy
Scott Brown 7th edition Otorhinolaryngology, Head & Neck Surgery
Ballengers Otolaryngology Head and Neck Surgery 17th Ed

9. Pathophysiology
Auditory feedback system

10. Pathophysiology
• Afferent pathway facilitates excitatory processes
• Efferent pathway facilitates predominantly inhibitory
processes
• Pathological alteration at one level may have functional
consequences at other level(s) of the auditory system ,
eg. noise induced hearing loss

11. Pathophysiology
Tinnitus and central neuronal network
• Tinnitus is the consequence of aberrant spontaneous
neural activity within the auditory system
• Complex neuronal network
• SPECT, PET and fMRI : perception of tinnitus is
associated with alterations in the cortical areas

12. Pathophysiology
Mechanisms underlying Tinnitus
Abnormal afferent excitation at the cochlear level
• 'mechanical' tinnitus based on spontaneous cochlear (OHC)
oscillations
• glutamate neuroexcitotoxicity
• modulation (enhanced sensitivity) of NMDA and non-NMDA
receptors
• abnormal ion channel conductance – calcium channel dysfunction

13. Pathophysiology
Mechanisms underlying Tinnitus
• Efferent dysfunction/reduction of GABA effect
• Alteration of spontaneous activity and tonotopic
reorganization
• Stress/psychological disorders

15. Pathophysiology
Glutamate neurotoxicity
• Main excitatory neurotransmitter of the CNS and cochlear afferents
• Released on to the inner hair cell (IHC) synaptic region
• Neurotoxic effect
• Excessive noise exposure leads to excessive glutamate release
• Excitotoxic intracellular Ca ++ overload, which could be a basis for
tinnitus
• NMDA antagonist (e.g. caroverine), can abolish tinnitus in a
significant number

16. Pathophysiology
Modulation (enhanced sensitivity) of NMDA and nonNMDA
receptors
• Lateral olivocochlear efferents modulate the sensitivity of the
afferent receptors in the cochlea
• Dopamine, provides permanent gain control at the site of the action
potential initiation
• Piribedil : Protective action against glutamate-induced excitotoxicity
• Endogenous opoid peptides dynorphins, as a part of the response to
stress, enhance sensitivity of the NMDA and non-NMDA receptors

17. Pathophysiology
Abnormal ion channel conductance - calcium channel dysfunction
• Intracellular concentration of calcium is responsible for functions of the OHC
and IHC cells
Observations
• Salicylate, affect intracellular calcium concentration in the hair cells and
neurons
• Noise also increases intracellular calcium concentration, altering stiffness of
the OHCs, compliance of the basilar membrane and leading to increased
activity in the cochlear nerve

18. Pathophysiology
Abnormal peripheral and central neural auditory activation
• Lesions along the auditory neural pathway may e.g. tumours or vascular
loops
• Motor/sensory tinnitus:
- Activation of somatosensory, somatomotor and visual-motor systems
- Activation of extralemniscal polysensory pathways
- Sprouting/neosynaptogenesis following surgery of posterior cranial fossa
tumours
- Gaze-evoked tinnitus, tinnitus provoked by jaw clinching, or tinnitus evoked
by electrical stimulation of the median nerve

19. Pathophysiology
Efferent dysfunction / Reduction of GABA effect
• Efferent system acts as an inhibitory force within the auditory system
• Malfunction may lead to disinhibition
• Studies have suggested dysfunction of the medial olivo cochlear system
• Degenerative changes of the auditory system (noise trauma, ototoxicity or
ageing)
• Altered inhibitory amino acid neurotransmitter receptors in the central
auditory pathways
• Reduce inhibitory function of the efferent system

20. Aetiology
Conductive hearing loss
• Otitis media, cerumen impaction
• Ossicular stiffness/discontinuity
• Otosclerosis
Sensorineural hearing loss
• Meniere’s disease
• Presbyacusis
• Cochlear otosclerosis
• Vestibular schwannoma
• Sudden hearing loss

21. Aetiology
Hormonal changes
• Pregnancy, menopause
• Thyroid dysfunction

22. Aetiology
Some medications or withdrawal from them
Aspirin and aspirin containing compounds
• Percodan, Darvon, Bufferin, Ecotrin
Aminoglycoside antibiotics
Nonsteroidal antiinflammatory drugs
• Fenoprofen, Ibuprofen, Indomethacin ,Ketoprofen, Naproxen,
Phenylbutazone, Sulindac, Tolmetin
Heterocycline antidepressants
• Amitriptyline , Amoxapine , Desipramine , Doxepin , Imipramine,
Maprotiline , Nortriptyline , Protriptyline , Trazodone, Trimipramine

23. Aetiology
Somatosounds
Pulsatile
• Neoplasm
Arterial
Venous
• Beginning of intracranial hypertension
• Great vessel bruits

24. Aetiology
Somatosounds
Nonpulsatile
• Tensor tympani myoclonus
• Tensor veli palatini myoclonus
• Patulous eustachian tube

25. Aetiology
Produced by structures in the ear
• Spontaneous otoacoustic emissions
• Produced by joint abnormalities
• Temporomandibular joint disorders

26. • Meniere’s disease : 100%
• Acute noise induced trauma : 100%
• Chronic noise induced trauma : 50-90%
• Vestibular Schwannoma : 70 %
• Presbyacusis : 70%
• Intoxications : 30-90%
• SSNHL : 50%
• Normal hearing : 15-35 %

27. Diagnosis
• Essential
• Underlying pathology can be life threatening and often
treatable

28. Diagnosis
• No universal rule
History
• Subjective description of tinnitus
• Annoyance and the impact on sleep and daily life
• Associated auditory and vestibular symptoms
• Otological and general medical conditions, drugs, noise exposure
• Current and pre-existing stress conditions and
• Psychological/psychiatric disorders

29. Diagnosis
Neurootological evaluation
Auditory assesment
• Otoscopy
• Pure tone audiometry
• Tympanometry and stapedial reflexes
• Otoacoustic emissions (spontaneous, evoked and olivocochlear
suppression test)
• Auditory brainstem evoked responses

30. Diagnosis
Neurootological evaluation
Vestibular assesment
• In view of pathology at the labyrinthine and vestibulocochlear nerve
levels
Nervous system assesment
• Gross examination of the nervous system and cranial nerve

31. Psychoacoustical measurements of tinnitus
• ‘Authentication' of the presence of tinnitus
• General characterization of tinnitus
• No influence on treatment
• Quantification of tinnitus, may be useful in the evaluation
of treatment
• Clinical trials and other forms of research

32. Psychoacoustical measurements of tinnitus
• Assessment of the pitch
• Bandwidth
• Loudness
• Maskability of tinnitus
• Residual inhibition

33. Psychoacoustical measurements of tinnitus
Pitch
• Tinnitus pitch match
• Hhigh frequency (> 3 kHz) for NIHL-related tinnitus, and
low-frequency loss for Meniere's disease

34. Psychoacoustical measurements of tinnitus
Loudness
• Psychological magnitude of sound intensity of tinnitus
• Rate of neural activity and by the number of nerve fibres
involved

35. Psychoacoustical measurements of tinnitus
Masking
• Reduction of the audibility of a sound by another sound
• Frequency dependent masking is more consistent with a
'peripheral’ locus of tinnitus
• Broadband, frequency nonspecific masking occurs in
tinnitus of 'central' origin

36. Psychoacoustical measurements of tinnitus
Residual inhibition
• Suppression or complete elimination of tinnitus for a
temporary period following masking
• Forward (central) masking

37. Recording of tinnitus related neuronal activity
• Spontaneous spectrum of neural activity within the
auditory nerve
• Auditory event-related potentials
• Auditory-evoked cortical magnetic fields
• Functional imaging

38. Diagnosis
Psychological profiling
• Important part of the investigation
• Formal ’psychological' assessment is necessary in
patients with significant psychological/ psychiatric
conditions

39. Diagnosis
Medical evaluation
• Treatable cause
• Anaemia, cardiovascular, renal, metabolic and
autoimmune disease
• Medications or drugs
• Standard haematological and biochemical investigations,
syphilis serology and an autoimmune screen

40. Diagnosis
Imaging
• Suspicion of a retrocochlear abnormality
• Gadolinium contrast enhanced MRI
• HRCT

41. Diagnosis
Approach to pulsatile tinnitus
Detailed history
• Synchrony of tinnitus with the pulse
• Effects of neck movements or compression
• Effect of respiration

42. Diagnosis
Approach to pulsatile tinnitus
Physical examination
• Palpation and light compression of the jugular vein
• Valsalva manoeuvre
• Auscultation of the neck and cranium
Otoscopy/Otomicroscopy
• Glomus tumours or tympanal haemangioma
Oropharyngeal examination
• Contraction of the soft palate in palatal myoclonus

43. Diagnosis
Approach to pulsatile tinnitus
Tympanometry
Myoclonic activity and patulous Eustachian tube
Pure tone audiometry
Conductive hearing loss secondary to vascular lesions

44. Diagnosis
Imaging
• Gadolinium-enhanced computed tomography (CT) and
magnetic resonance imaging (MRI)
• Magnetic resonance angiography (MRA) and ultrasound

45. Neurophysiologic model
Habituation
“The extinction of a conditioned reflex by repetition of the conditioned
stimulus, the method by which the nervous system reduces or inhibits
responsiveness during repeated stimulation.”
Types
Habituation of reaction
Habituation of perception

46. Neurophysiologic model
Specific stimulus
Passed to higher
cortical centre for
evaluation
Compared with patterns
stored in memory
sympathetic autonomic
nervous system is activated
Classified as unimportant
Blocked at subconscious
level
Doesn’t reach the level
of awareness

47. Neurophysiologic model
Specific stimulus classified as important attracts attention
sympathetic autonomic
nervous system is activated
reinforces memory
patterns
faster identification of next
appearence
Prevention of
habituation

48. Neurophysiologic model
• Observations strongly argue that the auditory system plays a secondary role
• Other systems in the brain are dominant in clinically relevant tinnitus
• 20% of tinnitus produce significant symptoms
• Limbic and autonomic nervous systems are crucial in individuals with
clinically relevant tinnitus

49. Neurophysiologic model
Processing of tinnitus related neuronal activity
2 feedback loops
• Loops involving the conscious perception of tinnitus
• Loops that act at a subconscious level
Activation of the limbic and autonomic nervous systems by
tinnitus related neuronal activity follows the principles of conditioned
reflexes

50. Neurophysiologic model
Medial geniculate
body
Higher cortical areas
Autonomic and
limbic system
Lower level
auditory
centre
Amygdala
High road
Low road/Subconscious
level

53. Neurophysiologic model
• At the early stage of tinnitus, the high loop is dominant
• Once negative associations initiated, the low loop
becomes dominant
• Low loop controlled by principles governing conditioned
reflexes
• Fast and cannot be modified by conscious thinking

54. Neurophysiologic model
• Continuous presence of tinnitus, combined with attention
given to it, results in plastic modifications of synaptic
connections
• Subsequent enhancement

55. Neurophysiologic model
• Initial signal provided by the auditory system
• However, extent of activation of the limbic and autonomic
nervous systems depends on the strength of negative
associations linked to tinnitus

56. Treatment
• No treatment can yet be considered well established
• No specific therapy is found to be satisfactory
• Even in the absence of a specific treatment, tinnitus
tends to improve, underlying the importance of the
psychological factor

57. Treatment
How to approach a patient ?
• Listen attentively to their story
• Examine them carefully, not only as an otologist, but also as a
physician
• Investigate auditory function
• Tell them the results of investigations in a clear, confident and
reassuring manner
• Explain in simple terms the suspected mechanism of
their tinnitus
• Explain treatment options

58. Treatment
• May range from a very simple to a complex strategy
• May require a multidisciplinary approach management

59. Treatment
Management options
• Treatment of underlying disorders
• Pharmacological
• Psychotherapy
• TRT
• Instrumentation/Masker
• Surgical
• Electrical/Magnetic stimulation

60. Pharmacological Treatment
Antidepressants
1. Tricyclic antidepressants
• Nortriptyline
• Amitriptyline
2. SSRI

61. Pharmacological Treatment
GABA analouges
1. Benzodiazepines
• Alprazolam
• Clonazepam
2. Gabapentin
3. Baclofen
Glutamate receptor antagonists
• Caroverine

62. Pharmacological Treatment
Ca ++ antagonists
• Nimodipine
• Flunarizine
Antiepileptics
• Carbamzepine
• Lamotrigine
• Sodium Valporate
Prostaglandin analouge
Misoprostol
Lidocaine

63. Pharmacological Treatment
Antidepressants
• Found to be effective in a significant number
• Mechanism is unclear
• May act at both the peripheral and central auditory system through
anticholinergic and antihistaminic effect
Selective serotonin reuptake inhibitors (SSRI)
• Modulators of tonic inhibition of auditory pathways
• Found to be effective in some patients with tinnitus
• Those with associated depression and mood
• In the elderly

64. Pharmacological Treatment
GABA analogues
• Rationale for the use: Hypothetical dysfunction of the efferent
auditory pathways and GABA downregulation
• Alprazolam has been reported to be beneficial
• Clonazepam facilitates central“ serotonin synthesis and has
anxiolytic, sedative and serotonergic properties
• Risk : Dependency
Post-withdrawal enhancement of tinnitus consideration

65. Pharmacological Treatment
Ca ++-channel antagonists
• Rational for use : abnormal calcium conductance
• Nimodipine found beneficial in some patients with tinnitus
• Flunarazine demonstrated to reduce/abolish tinnitus in a subset of
patients with dizziness

66. Pharmacological Treatment
Antiepileptics
• Cause depression of the neuronal response to excitatory stimuli and
hyperpolarization of neuronal membranes
• Effective in patients with tinnitus, in whom abnormal auditory neural
activation is suspected
• Carbamezepine, Sodium valproate, Lamotrigine

67. Pharmacological Treatment
Selective glutamate receptor antagonist
• Rationale for use : Glutamate neuroexcitotoxicity
• Caroverine blocks post-synaptic glutamate receptors
• Reported to be effective in a group of patients, following a
randomized, single-blind study

68. Pharmacological Treatment
Prostaglandin analogue
• Suspected to control the microcirculation of the cochlea and to act
as neuromodulators of the afferent pathway
• Misoprostol may provide relief for some patients with tinnitus

69. Pharmacological Treatment
Lidocaine
• The most effective one
• Sodium-channel blocker
• Operates most efficiently in nerves with the high discharge rates
• Effect at the central level of the auditory system, as well as at
periphery
• Possibility of side effects and intravenous mode of delivery make
this drug impractical
• Transtympanic application has also been reported as successful

70. Treatment
Tinnitus retraining therapy
• Based on the neurophysiological model of tinnitus
• The TRT implements a habituation-based protocol
• Includes
1. Sound therapy
2. Cognitive-behavioural techniques (CBT)

71. Treatment
Cognitive-behavioural techniques (CBT)
1. Directive counselling
2. Person-centred counselling
3. Cognitive counselling
• Has become one of the main tinnitus treatment
strategies in a number of audiology departments

72. Treatment
Instrumentation
Hearing aids
• First line in management for patients with tinnitus and hearing loss
• Rationale for use :
-May reduce awareness of tinnitus by amplification of external
sounds
-Improved auditory input may be beneficial in enhancing central
mechanisms of habituation and promoting central adaptive plasticity

73. Treatment
• Cochlear implants, can be used in management of
patients with profound hearing loss
• Found useful in abolishing/reducing tinnitus in a
significant number of cases

74. Treatment
Noise generators
• 'greater sound drives out less'
• Rationale for use : Promoting adaptive plasticity and the process of
habituation
• At present, different 'masking' strategies and devices are applied

75. Treatment
• Tinnitus maskers are wearable behind the ear or in the ear
• Presentation of sound in a controlled manner
• Low-level sound generators
 Provide constant low-level (at least six to eight hours a day),
neutral auditory signals
 Compete' with, but do not mask tinnitus
 Recommended as a part of TRT
 Positive effects develop in the long term
 At least 18 months treatment is recommended to prevent relapse

76. Treatment
Other device options
• Combination units
• Pillow speaker
• Tape recorder
• Mistuned FM radio
• Walkmans or MP3 players

77. Treatment
Psychotherapy
• Cognitive-behavioural techniques,
• Relaxation,
• Hypnosis,
• Biofeedback and
• Stress management.
Reduces associated distress and improve the quality of life

78. Treatment
Psychotherapy
• Cognitive-behavioural techniques,
• Relaxation,
• Hypnosis,
• Biofeedback and
• Stress management.
Reduces associated distress and improve the quality of life

79. Treatment
Electrical or magnetic stimulation
• Rationale for use : ReductIon in neural hyperactivation associated
with tinnitus and an attempt to restore normal rate and the pattern of
spontaneous activity
• High-pulse train electrical stimulation to the cochlear round windo
seems promising in reestablishing the 'code of silence'

80. Treatment
Gingko biloba
• Leaves of the Maidenhair plant
• Flavonoids (ginkgo-flavone glycosides) and terpenoid (ginkgolides
A, B, C, J and bilobalide)
• Possible effects on vasoregulation and alteration in neuronal
metabolism
• Different outcomes in several studies

81. References
• Glasscock-Shambaugh Surgery of the Ear 5th Ed
• Scott Brown 7th edition Otorhinolaryngology, Head
& Neck Surgery
• Ballengers Otolaryngology Head and Neck Surgery
17th Ed

82. Thank you for your attention!!!!!!!!!!