Transcript RESOUND LIVE TS Train the Trainer Feb 3rd

General tinnitus knowledge
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Tinnitus
Any Tinnitus treatment must be used in connection with counseling
and possible other treatment
If you are not comfortable with treating tinnitus you should refer the
patient
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General notes on Tinnitus
1- Any Tinnitus treatment must be used in connection with
counseling and possible other treatment.
2- Tinnitus is a perception of involuntary sound. It must be audible
to the person, it originates in the head (McFadden 1982).
3- It is most commonly referred to as ‘ringing in the ears.’
4- Produced centrally, with peripheral influences (e.g. Cochlear
damage). Exact mechanism(s), or epidemiology is unknown.
5- Noise type can vary from pure tones over modulated noise to
crackling sounds that varies significantly with time & Large
intensity variations.
6- Not a ‘phantom’ perception for the patient, it is real
7- Frequency of perception :- Needs to be ‘often’, and perceived as
a problem to be a problem
8- Tinnitus can be described in many different forms, for example:
Ringing
,Chirping ( ‫)نقيق‬, Clicking, Pulsating, Continuous, Sudden
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9- It is important to note that there is no one proven
cause of tinnitus, but there are tinnitus models that
have been studied more extensively than others.
10- Points to remember:
 The origin of subjective tinnitus is produced centrally
(Where? We do not know exactly)
 Peripheral changes (cochlear damage) can influence
the tinnitus perception
 Other modalities and systems play a part in tinnitus
perception, it is not limited to the auditory system
 It is important to note that psychological influences
play a strong role in tinnitus perception
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10- Prevalence:
 Statistics slightly vary depending on the literature, but
generally speaking…
 Approximately 10-15% of the population reports
experiencing tinnitus with regularity.
 Approximately 3-5% of the population has clinically
treatable tinnitus
 1% reporting having it to a severe degree where it
affects their daily Lives (All data from McFadden,
1982; Vesterager, 1997).
 Approx 80-85% of people with tinnitus have hearing
loss
 Increasing trend with age; higher in males than
females (Hoffman, Reed 2004)
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• 11- Tinnitus can be a symptom of a condition that is related
to many forms of hearing loss, or it may exist without
hearing loss.
• Tinnitus is not a disease. Tinnitus is a symptom that may
result from a number of medical conditions.
• Tinnitus may result from age-related hearing loss
(presbycusis typically begins after the age of 55), ear
injury, or a physiological condition.
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12- Neurophysiological Model There are many theories regarding
the causation of tinnitus. While none have been proven, the
most widely accepted theory, when tinnitus occurs with
hearing loss due damage to the hair cells within the cochlea.
Many researchers believe that when the structure of the
hair cell collapses, random stimulation of the auditory
pathways occurs.
OHC & IHC:
 OHC -‘gain adjusters’ of low-level auditory input; also
providers of inhibitory properties to the inner hair cells
(IHC).
 IHC - primarily responsible for sending auditory input
through the auditory brainstem to the brain to be
processed in the auditory cortex.
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13-What causes tinnitus?
 It is thought that when the structure of the OHC collapses, it
can no longer inhibit the neuronal activity of the IHCs.
 The damaged hair cells move randomly in a constant state of
irritation. They are unable to hold their charge and leak
random electrical impulses which travel to the auditory
cortex where they are interpreted as noise.
 This causes atypical behavior, and this spontaneous activity
(firing of neurons), with no auditory input is amplified (over
excitation) in the auditory system and perceived as a sound,
tinnitus.
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(image from hearingcentral.com)
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OHCs and Tinnitus
Increased spontaneous neural activity in the auditory system in the absence of auditory/external stimulation.
Normal excitation
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Abnormal excitation
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13- what causes tinnitus? Additional thoughts
 Evidence of central involvement
 Reports of cutting 8th cranial nerve and tinnitus remaining in
majority of patients
 Mask ipsilateral tinnitus ear, tinnitus appears in contra lateral
ear
 Not limited to OHC damage alone
 IHC damage can also play a role in the generation of tinnitus.
 Suggests there are additional mechanisms that are also
responsible in tinnitus generation beyond OHC damage
(Jastreboff PJ & Hazell, JWP, 1993).
 Similar best frequency
 Following hearing loss, adjacent frequency regions can create
over representation
 E.g. 3kHz will ‘take over’ damaged 4kHz region, but 3kHz is
already represented, therefore a 3kHz tinnitus is perceived
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What causes tinnitus?
•
Other causes of tinnitus:
 Otosclerosis
 TM perforations
 Cerumen build-up (wax)
 TMJ (tempro-mandibular joint dysfunction)
 Palatal myoclonus – clicking of palate
 Muscular problems – clicking or popping-like tinnitus
 Vascular/glomus tumors – occlusion of jugular veins, can result in
pulsatile tinnitus
 Superior canal dissonance (‫ – )التنافر‬3rd window, can hear
footsteps and eyeball movement
 Medications
 Aspirin (reversible with decreased dosage)
 Cis-platinum – chemotherapy
 Vicodin
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13- What causes tinnitus? Psychological components
 As person experiences tinnitus, they may or may not
give it much attention, or priority.
 When ‘ignored’ it is blended into the surrounding
listening environment, and often goes undetected, or
is transient tinnitus.
 When given high priority (Prioritization) it can become
a focal point. If attention is continually paid to it and it
is put as high priority, the brain will more easily detect
it with time, even in the presence of other background
sounds (brain can remember consistent neural
patterns).
 When tinnitus stands out and is given high priority, it
can lead to negative emotions, such as anxiety and
stress, which can result in other issues such as
insomnia or withdrawal.
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Sound Therapy
• Goal: decrease overall perceived signal strength of
tinnitus
• Based on contrast of stimulus and background (i.e.
tinnitus and TSG noise)
The perceived candle strength is decreased at a busy dinner table,
as opposed to being isolated in the dark
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What causes tinnitus?
• Neurophysiological Model cont. – Perception & Reaction - TRT
 Once this connection is established a cycle can begin that includes
the limbic system (emotion/associations) and autonomic nervous
system (physical/bodily reactions).
 The cycle is called the ‘Vicious Cycle/Circle’
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How is tinnitus diagnosed?
•
Questionnaires (TRI,TRQ, THQ, etc.)
 Help to better understand the severity of a person’s tinnitus
 Can be used as pre and post-training measures to identify changes in
tinnitus perception
 Not all questionnaires are created equally; sensitivity, scoring and scaling
differences amongst them
•
Consultations
 Often spend more time than a hearing-aid consultation, many up to 2 hrs
on a first consultation.
 Helps with collecting a history and possible roots of tinnitus, helps to
better understand the severity of a person’s tinnitus and helps to
understand how the tinnitus is truly affecting a person’s life.
Keep in mind, an Audiologist may not always be
the first point of contact, and other disciplines
may have other diagnosing methods.
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• Diagnostics
 Audiogram – could it be a product of hearing loss (ultra highfrequency testing, >8kHz), or middle/ retrocochlear
pathology
 OAEs – measure function/integrity of the hair cells (OHC)
 Pitch Matching – match tinnitus to a specific frequency; can
help characterize and monitor changes to tinnitus; can help
with TSG settings to find preferred setting of frequency
shaping (if broadband is not preferred).
 Loudness Matching – match the tinnitus to a specific
intensity (can use 1kHz); can help characterize and monitor
changes to tinnitus; can help with TSG settings (will probably
fall somewhere in between the TSG threshold and mixing
point).
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– MMLs – how much noise is need to just mask the
tinnitus; important for TSG (tinnitus signal generator)
instrument settings; monitor changes (reduction over
time can imply improvement to tinnitus perception)
– LDLs/UCLs – how loud can the person tolerate; important
for TSG instrument setting limits, especially for those with
hyperacusis, misophonia and general tolerance issues.
– Residual inhibition – fragility of tinnitus neural network.
Tinnitus is altered for a period of time after some sound
exposure. Can imply tinnitus perception can be changed
due to sound therapy.
– Mixing/Blending Point – where the tinnitus and noise
generated are perceived to mix or blend together;
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important for TSG settings