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TINNITUS
DR KANAV RISHI (PGT)
DEFINITION
Sensation of hearing a sound in absence of an external
stimulus or a sound sensation in the absence of an
external or internal acoustical source or electric
stimulation.
CLASSIFICATION
Subjective - only patient is aware of the sound sensation
Objective - sound can be perceived by others, either unaided, using a stethoscope or
a microphone and amplifier
ACCORDING TO CONSISTENCY
Pulsatile
Non-pulsatile
NON-PULSATILE TINNITUS
The prevalence of tinnitus seems similar in men and women
The prevalence of tinnitus increases with age.
Tinnitus is perceived in both ears or in middle of head by
approximately half of sufferers.
The remainder have unilateral tinnitus, with left-sided tinnitus
slightly more common.
RISK FACTORS
socioeconomic class
smoking, alcohol consumption
previous head injuries
cardiovascular disease
Hypertension
Specific otological conditions - Ménière’s disease, otosclerosis and vestibular schwannoma
Drugs- salicylates, quinine, aminoglycoside antibiotics, and some antineoplastic agents, particularly the platinum
based drugs.
PATHOPHYSIOLOGY
PERIPHERAL
MECHANISMS
CENTRAL
MECHANISMS
• Discordant damage of cochlear
hair cells
• Calcium channel dysfunction
• Glutamate receptors
• Increased spontaneous firing
• Increased central neural
synchrony
• Reorganization of the cortical
auditory map
Discordant damage
of cochlear hair cells
outer hair cells have
been damaged but
inner hair cells
remain
the tectorial
membrane is no
longer supported by
the outer hair cells
and can sag onto the
inner hair cells
causing them to
depolarize.
Glutamate receptors
Glutamate is the main
excitatory
neurotransmitter in the
auditory system
AMPA receptors are the
main receptors on the
auditory nerve fibres
under the inner hair cells
and are responsible for
the fast transmission of
information from the
cochlea to the brain.
glutamate in large
quantities is toxic to nerve
fibres. This effect, which
can be observed following
significant noise exposure,
is mediated by AMPA
Increased
spontaneous firing
certain degree of
electrical activity in
the auditory system
Damage to the ear
results in reduced
activity in the
auditory nerve
which in turn
downregulates
inhibitory processes
in higher auditory
centre
thereby potentially
generating
increased
spontaneous
activity in the
auditory cortex that
could be perceived
as tinnitus
Increased central neural
synchrony
Spontaneous neural
activity in the auditory
cortex is normally random
when this activity
becomes synchronized,
this is the signal that a
sound is present.
If the peripheral auditory
system is damaged,
spontaneous cortical
activity tends to become
more synchronized and
there is speculation that
this can give rise to
tinnitus.
Reorganization of the cortical
auditory map
When the peripheral auditory
system is damaged,change
seen in the auditory cortex is
that neurons that received
inputs from parts of the
cochlea that have been
damaged tune in to the
nearest adjacent frequency
input that is still active.
This results in
overrepresentation of
frequencies adjacent to areas
of damage and increased
neural activity at those
frequencies.
It has been suggested that this
produces tinnitus
TINNITUS MODULATION
Influenced by stimulus from outside.
Modulate their symptom by:
Touching their face
Clenching their teeth
Changing their gazelinks between the auditory system and other somatosensory pathways
INVESTIGATIONS
AUDIOGRAM:
Might have history of other symptoms such as aural fullness or decreased
hearing.
TINNITUS SPECIFIC AUDIOLOGICAL MEASUREMENTS:
Tests include assessment of loudness discomfort levels, tinnitus pitch matching,
tinnitus loudness matching and minimal masking levels.
IMAGING:
Patients with unilateral tinnitus, an
asymmetrical sensorineural hearing
loss or associated neurological
symptoms or signs require imaging
to exclude retrocochlear pathology
such as a vestibular schwannoma.
TINNITUS QUESTIONNAIRES
Essential tool for research and also have a role in assessment
of patients during routine clinical practice: recommended in
UK by Department of Health’s good practice guide.
Example- Tinnitus Handicap Questionnaire, Tinnitus
Handicap Inventory (THI)(most popular), Mini Tinnitus
Questionnaire, Tinnitus Functional Index
TINNITUS HANDICAP INDEX
OTHER QUESTIONNAIRES:
Comorbidity of psychological conditions such as anxiety and depression with
tinnitus, helpful to use a mental health questionnaire Hospital Anxiety
Depression Scale (HADS).
Sleep disturbance in tinnitus patients- Insomnia Severity Index
TREATMENT
EXPLANATION AND REASSURANCE:
An explanation of the condition and reassurance is a key
initial step in the management of any patient with tinnitus.
Effective when done in a formal setting.
HEARING AIDS:
Hearing amplification would reduce a patient’s
symptoms, by amplifying external sounds and
masking tinnitus.
SOUND THERAPIES:
Use sound to completely or partly suppress, or mask, tinnitus.
Complete masking is counterproductive as it prevents habituation to tinnitus.
Sound should be used at very low levels at a point where added sound is just
below perceived level of tinnitus. It facilitates habituation.
3 methods of sound therapy:
Patients wear hearing aids producing masking by
amplifying ambient sound,
small ear level devices generate wide-band sound
(known as tinnitus maskers, sound generators, white
noise generators or wide-band sound generators)
combination devices having functions of above two
types of device.
• Alternative to using a wearable device is to use an appliance that
produces sound in patient’s immediate environment.
NOVEL SOUND THERAPIES:
Devices deliver forms of
sound therapy to specifically
target tinnitus rather than
simply offering masking or
distraction.
1. Neuromonics:
Uses music modified to compensate for any hearing loss.
The music has a large dynamic range with peaks and troughs with intention that tinnitus is audible in
troughs.
2. Serenade:
In patient with profound HL and tinnitus who had undergone cochlear implantation showed that certain
stimulation patterns effective in ameliorating tinnitus.
Delivered via a device called SerenadeR and sounds have been dubbed S Tones.
3.Noise cancellation: A possible tinnitus therapy.
One device, Phase-Out, matches
a therapeutic tone to patient’s
tinnitus tone and then phase
shifts therapeutic tone by 6
degrees every 30 seconds.
4.Acoustic CR neuromodulation:
Regarding theory of increased neural synchrony in central auditory system.
A specific form of sound stimulation could be used to disrupt pathological
synchrony: 4 tones are delivered via headphones, two above and two below the
dominant frequency of patient’s tinnitus. Called as Acoustic Co-ordinated Reset.
Sound therapy with vagal nerve stimulation
Direct electrical stimulation of nucleus basalis in
forebrain in conjunction with stimulation of sensory
organ could reverse such changes. Invasive technique.
Stimulate vagus nerve both by electrodes implanted
against nerve in left side of neck and by transcutaneous
route also produce same changes.
Ultrasound:
High-frequency sound
applied by a bone-
conduction transducer.
Rationale- ultrasound
stimulate cochlea without
interfering with patient’s
hearing for sounds occurring
in normal auditory spectrum.
COGNITIVE BEHAVIOURAL THERAPY
A Cochrane systematic review has
considered evidence for
administration of CBT and
concluded that CBT resulted in no
significant difference in tinnitus
loudness, caused significant
improvement in both depression
scores and in quality of life scores.
Other psychological techniques:
Mindfulness meditation and Acceptance
and Commitment Therapy (ACT)
ELECTROMAGNETIC STIMULATION:
Direct electrical stimulation of ear has been shown
to suppress tinnitus but delivering this stimulation
is invasive and risks damage to the inner ear.
SYSTEMIC DRUGS:
Psychoactive drugs have
been used in management
of tinnitus, partly due to
psychological distress and
partly because many of
receptors that
psychoactive drugs act are
also found within central
auditory pathways.
Anaesthetics such as
procaine and lidocaine
produce temporary
suppression of tinnitus
when given IV.
Melatonin helps patients who have sleep disorders associated with tinnitus.
Tinnitus, idiopathic sudden SNHL, has been thought to arise from a lack of
oxygen secondary to vascular insufficiency. Hyperbaric O2 has been tried but
no significant evidence of improvement.
Botulinum toxin inhibit release of other neurotransmitters and neuropeptides
involved in autonomic pathway.
INTRATYMPANIC DRUGS:
Transtympanic administration allows direct
labyrinthine drug absorption which improves
labyrinthine metabolism and reduction of tinnitus in
patients having tinnitus in association with cochlear
pathology.
Various agents- steroids, local anaesthetic
agents,anticholinergic drugs, glutamate antagonists,
antioxidant delivered into ME by transtympanic
injections.
DIETARY SUPPLEMENTATION:
Some evidence that some compounds, particularly the B vitamins, can help to defend the
cochlea against noise trauma.
Some studies demonstrated a significant decrease in zinc levels in some patients suffering
from tinnitus and rectifying this deficiency has shown to decrease tinnitus significantly.
Paaske et al. however, demonstrated little correlation between hypozincaemia and
tinnitus.
LASERS:
Low-power lasers have been
used in treatment of tinnitus,
applied either trans-meatally
or mastoid process.
SURGERY
Surgery has a definite role in management of tinnitus associated with certain conditions such as
otosclerosis, when stapedectomy is reported as improving or eradicating tinnitus in 80–88.3% of cases.
Tinnitus associated with profound HL, tinnitus suppression has been found as a secondary benefit of
cochlear implantation.
Improvement of tinnitus occurs in up to 86% of implanted patients.
In 67% patients, the benefit applies to both the ears.
Destructive surgical procedures including
VIIIth nerve neurectomy or selective
cochlear neurectomy have been tried but
there is no trial using good scientific
methodologies such as validated outcome
measures.
PULSATILE TINNITUS
Perceived sound takes on form
of a pulsation, clicking or
fluttering.
Classified as either
synchronous or non-
synchronous, depending on
whether tinnitus takes on
characteristics of a pulsation in
synchrony with patient’s heart.
SYNCHRONUS PULSATILE
TINNITUS:
Synchronous pulsatile
tinnitus is direct result of
abnormal vascular
anatomy in vicinity of
peripheral auditory
system.
Systemic aberrations of
circulation, such as
hyperdynamic
circulation, also leads to
this type.
Conditions-
pseudotumor cerebri,
Superior semicircular
canal dehiscence.
INVESTIGATIONS:
After excluding anaemia and thyrotoxicosis or any obvious cause, synchronous
pulsatile tinnitus requires imaging.
In case of any Retrotympanic mass, a CECT of temporal bone, brain and scalp is
indicated.
For Atherosclerotic carotid artery disease- duplex carotid ultrasonography is
done.
Gold standard
mode of
imaging
vascular
system of
temporal bone
is angiography.
TREATMENT
SUPPORTIVE:
When no obvious
cause is identified,
reassurance is an
important aspect
of treatment- CBT
or TRT.
SURGERY:
MRI- vascular loops are
commonly in close proximity
to cochlear nerves of
patients with tinnitus.
Laterally placed loops-
pulsatile tinnitus whereas
vessels adjacent to medial
half of nerve generate non-
pulsatile tinnitus.
Microvascular
decompression of
vascular loops in
tinnitus patients has
been used with very
variable results,
ranging from 40%
improvement to
77%.
NON-SYNCHRONUS
PULSATILE TINNITUS
Manifest itself as a train
of rhythmical clicks or a
buzzing or fluttering
noise or sensation that is
not synchronous with
the pulse.
Sounds are often related
to myoclonic activity
resulting in repetitive
contractions of the
middle ear muscles.
Contraction of tensor
tympani- clicking noise
and stapedius muscle-
buzzing noise.
INVESTIGATION:
Middle ear myoclonus can be diagnosed based on history and impedance changes on tympanometry.
TREATMENT:
Use of benzodiazepines, orphenadrine, carbamazepine, piracetam and botulinum toxin.
Supportive treatment- relaxation therapy, psychotherapy, tinnitus masking.
Surgical- division of the middle ear tendons.
PREVENTION
Cochlear damage caused by exposure to agents including noise, ototoxic
agents and cytotoxic drugs acts as a trigger for tinnitus. Avoid exposure.
Damage is generally mediated by a process of apoptosis and this cascade.
Several studies are researching the use of antioxidants including D-methionine
(D-met), Ebselen or a combination of beta carotene, vitamin C, E and
magnesium. Stem-cell and gene therapies are also being investigated.
THANK YOU

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TINNITUS.pptx

  • 2. DEFINITION Sensation of hearing a sound in absence of an external stimulus or a sound sensation in the absence of an external or internal acoustical source or electric stimulation.
  • 3. CLASSIFICATION Subjective - only patient is aware of the sound sensation Objective - sound can be perceived by others, either unaided, using a stethoscope or a microphone and amplifier ACCORDING TO CONSISTENCY Pulsatile Non-pulsatile
  • 4.
  • 5.
  • 6. NON-PULSATILE TINNITUS The prevalence of tinnitus seems similar in men and women The prevalence of tinnitus increases with age. Tinnitus is perceived in both ears or in middle of head by approximately half of sufferers. The remainder have unilateral tinnitus, with left-sided tinnitus slightly more common.
  • 7. RISK FACTORS socioeconomic class smoking, alcohol consumption previous head injuries cardiovascular disease Hypertension Specific otological conditions - Ménière’s disease, otosclerosis and vestibular schwannoma Drugs- salicylates, quinine, aminoglycoside antibiotics, and some antineoplastic agents, particularly the platinum based drugs.
  • 8. PATHOPHYSIOLOGY PERIPHERAL MECHANISMS CENTRAL MECHANISMS • Discordant damage of cochlear hair cells • Calcium channel dysfunction • Glutamate receptors • Increased spontaneous firing • Increased central neural synchrony • Reorganization of the cortical auditory map
  • 9. Discordant damage of cochlear hair cells outer hair cells have been damaged but inner hair cells remain the tectorial membrane is no longer supported by the outer hair cells and can sag onto the inner hair cells causing them to depolarize.
  • 10.
  • 11. Glutamate receptors Glutamate is the main excitatory neurotransmitter in the auditory system AMPA receptors are the main receptors on the auditory nerve fibres under the inner hair cells and are responsible for the fast transmission of information from the cochlea to the brain. glutamate in large quantities is toxic to nerve fibres. This effect, which can be observed following significant noise exposure, is mediated by AMPA
  • 12. Increased spontaneous firing certain degree of electrical activity in the auditory system Damage to the ear results in reduced activity in the auditory nerve which in turn downregulates inhibitory processes in higher auditory centre thereby potentially generating increased spontaneous activity in the auditory cortex that could be perceived as tinnitus
  • 13. Increased central neural synchrony Spontaneous neural activity in the auditory cortex is normally random when this activity becomes synchronized, this is the signal that a sound is present. If the peripheral auditory system is damaged, spontaneous cortical activity tends to become more synchronized and there is speculation that this can give rise to tinnitus.
  • 14. Reorganization of the cortical auditory map When the peripheral auditory system is damaged,change seen in the auditory cortex is that neurons that received inputs from parts of the cochlea that have been damaged tune in to the nearest adjacent frequency input that is still active. This results in overrepresentation of frequencies adjacent to areas of damage and increased neural activity at those frequencies. It has been suggested that this produces tinnitus
  • 15. TINNITUS MODULATION Influenced by stimulus from outside. Modulate their symptom by: Touching their face Clenching their teeth Changing their gazelinks between the auditory system and other somatosensory pathways
  • 16. INVESTIGATIONS AUDIOGRAM: Might have history of other symptoms such as aural fullness or decreased hearing. TINNITUS SPECIFIC AUDIOLOGICAL MEASUREMENTS: Tests include assessment of loudness discomfort levels, tinnitus pitch matching, tinnitus loudness matching and minimal masking levels.
  • 17. IMAGING: Patients with unilateral tinnitus, an asymmetrical sensorineural hearing loss or associated neurological symptoms or signs require imaging to exclude retrocochlear pathology such as a vestibular schwannoma.
  • 18. TINNITUS QUESTIONNAIRES Essential tool for research and also have a role in assessment of patients during routine clinical practice: recommended in UK by Department of Health’s good practice guide. Example- Tinnitus Handicap Questionnaire, Tinnitus Handicap Inventory (THI)(most popular), Mini Tinnitus Questionnaire, Tinnitus Functional Index
  • 19.
  • 21. OTHER QUESTIONNAIRES: Comorbidity of psychological conditions such as anxiety and depression with tinnitus, helpful to use a mental health questionnaire Hospital Anxiety Depression Scale (HADS). Sleep disturbance in tinnitus patients- Insomnia Severity Index
  • 22. TREATMENT EXPLANATION AND REASSURANCE: An explanation of the condition and reassurance is a key initial step in the management of any patient with tinnitus. Effective when done in a formal setting.
  • 23. HEARING AIDS: Hearing amplification would reduce a patient’s symptoms, by amplifying external sounds and masking tinnitus.
  • 24. SOUND THERAPIES: Use sound to completely or partly suppress, or mask, tinnitus. Complete masking is counterproductive as it prevents habituation to tinnitus. Sound should be used at very low levels at a point where added sound is just below perceived level of tinnitus. It facilitates habituation.
  • 25. 3 methods of sound therapy: Patients wear hearing aids producing masking by amplifying ambient sound, small ear level devices generate wide-band sound (known as tinnitus maskers, sound generators, white noise generators or wide-band sound generators) combination devices having functions of above two types of device.
  • 26. • Alternative to using a wearable device is to use an appliance that produces sound in patient’s immediate environment.
  • 27. NOVEL SOUND THERAPIES: Devices deliver forms of sound therapy to specifically target tinnitus rather than simply offering masking or distraction.
  • 28. 1. Neuromonics: Uses music modified to compensate for any hearing loss. The music has a large dynamic range with peaks and troughs with intention that tinnitus is audible in troughs. 2. Serenade: In patient with profound HL and tinnitus who had undergone cochlear implantation showed that certain stimulation patterns effective in ameliorating tinnitus. Delivered via a device called SerenadeR and sounds have been dubbed S Tones.
  • 29. 3.Noise cancellation: A possible tinnitus therapy. One device, Phase-Out, matches a therapeutic tone to patient’s tinnitus tone and then phase shifts therapeutic tone by 6 degrees every 30 seconds.
  • 30. 4.Acoustic CR neuromodulation: Regarding theory of increased neural synchrony in central auditory system. A specific form of sound stimulation could be used to disrupt pathological synchrony: 4 tones are delivered via headphones, two above and two below the dominant frequency of patient’s tinnitus. Called as Acoustic Co-ordinated Reset.
  • 31. Sound therapy with vagal nerve stimulation Direct electrical stimulation of nucleus basalis in forebrain in conjunction with stimulation of sensory organ could reverse such changes. Invasive technique. Stimulate vagus nerve both by electrodes implanted against nerve in left side of neck and by transcutaneous route also produce same changes.
  • 32. Ultrasound: High-frequency sound applied by a bone- conduction transducer. Rationale- ultrasound stimulate cochlea without interfering with patient’s hearing for sounds occurring in normal auditory spectrum.
  • 33. COGNITIVE BEHAVIOURAL THERAPY A Cochrane systematic review has considered evidence for administration of CBT and concluded that CBT resulted in no significant difference in tinnitus loudness, caused significant improvement in both depression scores and in quality of life scores.
  • 34. Other psychological techniques: Mindfulness meditation and Acceptance and Commitment Therapy (ACT)
  • 35. ELECTROMAGNETIC STIMULATION: Direct electrical stimulation of ear has been shown to suppress tinnitus but delivering this stimulation is invasive and risks damage to the inner ear.
  • 36. SYSTEMIC DRUGS: Psychoactive drugs have been used in management of tinnitus, partly due to psychological distress and partly because many of receptors that psychoactive drugs act are also found within central auditory pathways. Anaesthetics such as procaine and lidocaine produce temporary suppression of tinnitus when given IV.
  • 37. Melatonin helps patients who have sleep disorders associated with tinnitus. Tinnitus, idiopathic sudden SNHL, has been thought to arise from a lack of oxygen secondary to vascular insufficiency. Hyperbaric O2 has been tried but no significant evidence of improvement. Botulinum toxin inhibit release of other neurotransmitters and neuropeptides involved in autonomic pathway.
  • 38. INTRATYMPANIC DRUGS: Transtympanic administration allows direct labyrinthine drug absorption which improves labyrinthine metabolism and reduction of tinnitus in patients having tinnitus in association with cochlear pathology. Various agents- steroids, local anaesthetic agents,anticholinergic drugs, glutamate antagonists, antioxidant delivered into ME by transtympanic injections.
  • 39. DIETARY SUPPLEMENTATION: Some evidence that some compounds, particularly the B vitamins, can help to defend the cochlea against noise trauma. Some studies demonstrated a significant decrease in zinc levels in some patients suffering from tinnitus and rectifying this deficiency has shown to decrease tinnitus significantly. Paaske et al. however, demonstrated little correlation between hypozincaemia and tinnitus.
  • 40. LASERS: Low-power lasers have been used in treatment of tinnitus, applied either trans-meatally or mastoid process.
  • 41. SURGERY Surgery has a definite role in management of tinnitus associated with certain conditions such as otosclerosis, when stapedectomy is reported as improving or eradicating tinnitus in 80–88.3% of cases. Tinnitus associated with profound HL, tinnitus suppression has been found as a secondary benefit of cochlear implantation. Improvement of tinnitus occurs in up to 86% of implanted patients. In 67% patients, the benefit applies to both the ears.
  • 42. Destructive surgical procedures including VIIIth nerve neurectomy or selective cochlear neurectomy have been tried but there is no trial using good scientific methodologies such as validated outcome measures.
  • 43. PULSATILE TINNITUS Perceived sound takes on form of a pulsation, clicking or fluttering. Classified as either synchronous or non- synchronous, depending on whether tinnitus takes on characteristics of a pulsation in synchrony with patient’s heart.
  • 44. SYNCHRONUS PULSATILE TINNITUS: Synchronous pulsatile tinnitus is direct result of abnormal vascular anatomy in vicinity of peripheral auditory system. Systemic aberrations of circulation, such as hyperdynamic circulation, also leads to this type. Conditions- pseudotumor cerebri, Superior semicircular canal dehiscence.
  • 45. INVESTIGATIONS: After excluding anaemia and thyrotoxicosis or any obvious cause, synchronous pulsatile tinnitus requires imaging. In case of any Retrotympanic mass, a CECT of temporal bone, brain and scalp is indicated. For Atherosclerotic carotid artery disease- duplex carotid ultrasonography is done.
  • 46. Gold standard mode of imaging vascular system of temporal bone is angiography.
  • 47. TREATMENT SUPPORTIVE: When no obvious cause is identified, reassurance is an important aspect of treatment- CBT or TRT. SURGERY: MRI- vascular loops are commonly in close proximity to cochlear nerves of patients with tinnitus. Laterally placed loops- pulsatile tinnitus whereas vessels adjacent to medial half of nerve generate non- pulsatile tinnitus.
  • 48. Microvascular decompression of vascular loops in tinnitus patients has been used with very variable results, ranging from 40% improvement to 77%.
  • 49. NON-SYNCHRONUS PULSATILE TINNITUS Manifest itself as a train of rhythmical clicks or a buzzing or fluttering noise or sensation that is not synchronous with the pulse. Sounds are often related to myoclonic activity resulting in repetitive contractions of the middle ear muscles. Contraction of tensor tympani- clicking noise and stapedius muscle- buzzing noise.
  • 50. INVESTIGATION: Middle ear myoclonus can be diagnosed based on history and impedance changes on tympanometry. TREATMENT: Use of benzodiazepines, orphenadrine, carbamazepine, piracetam and botulinum toxin. Supportive treatment- relaxation therapy, psychotherapy, tinnitus masking. Surgical- division of the middle ear tendons.
  • 51. PREVENTION Cochlear damage caused by exposure to agents including noise, ototoxic agents and cytotoxic drugs acts as a trigger for tinnitus. Avoid exposure. Damage is generally mediated by a process of apoptosis and this cascade. Several studies are researching the use of antioxidants including D-methionine (D-met), Ebselen or a combination of beta carotene, vitamin C, E and magnesium. Stem-cell and gene therapies are also being investigated.