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General tinnitus knowledge. 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. General notes on Tinnitus.

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General tinnitus knowledge


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    1. General tinnitus knowledge

    2. 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

    3. 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

    4. 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

    5. 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)

    6. 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.

    7. 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.

    8. 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. (image from hearingcentral.com)

    9. OHCs and Tinnitus • Increased spontaneous neural activity in the auditory system in the absence of auditory/external stimulation. Normal excitation Abnormal excitation

    10. 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

    11. 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(التنافر) – 3rd window, can hear footsteps and eyeball movement • Medications • Aspirin (reversible with decreased dosage) • Cis-platinum – chemotherapy • Vicodin

    12. 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.

    13. 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

    14. 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’

    15. 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.

    16. Diagnostics • Audiogram – could it be a product of hearing loss (ultra high-frequency 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).

    17. 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; important for TSG settings