Sound Stimulation as Tinnitus Treatment

Tinnitus treatment with sound therapy and stimulation.


  1. There is considerable evidence that many forms of tinnitus are caused by central changes that may occur after peripheral lesions.
  2. Auditory stimulation is one of the most employed therapeutic methods for tinnitus, and one of the most beneficial.
  3. Sound generators that emulate environmental sounds are small devices that allow a person to select the favorite kind of sound at the most comfortable volume.
  4. Custom sound generators, for normal hearing persons, are similar to hearing aids, very light, and to be worn behind the ear. They generate a wide-band sound that can be adjusted to the user’s needs.
  5. Hearing aids designed for people with tinnitus and hearing loss provide amplification that facilitates auditory stimulation to ameliorate tinnitus.
  6. Implantable hearing aids are now used by many people, which made it possible to assess their efficacy in tinnitus treatment.
  7. Other devices can be used for tinnitus management for immediate relief before a more complete sound therapy can be initiated.
  8. Prosthesis and “open-ear” hearing aids are preferred for treatment of tinnitus. These devices provide amplification in narrow frequency bands which can be adjusted to coincide with the frequencies of the patient’s hearing loss.
  9. Sound stimulation has its beneficial effect on most forms of tinnitus by activating neural plasticity, which requires time to develop. The time it takes for sound stimulation to reduce an individual’s tinnitus varies and may require a 6- to 8-month time frame.
  10. The selection of hearing aids must be tailored to individual patients, based on the patient’s clinical picture.
  11. The specific guidelines on hearing aid device adaptation are crucial for an effective auditory stimulation of tinnitus-affected patients. 


Effective treatment of tinnitus depends on understanding the cause of tinnitus. Especially regarding treatment with sound, it is important to know if tinnitus is caused by pathology of the ear or the auditory nervous system.

The past years have witnessed a change in the understanding of the cause of tinnitus. Previously, tinnitus was believed to originate from the peripheral auditory system [1, 2]. There is now considerable evidence that most forms of tinnitus are caused by changes in the central nervous system after peripheral lesions [3, 4]. For treatment of tinnitus, it is important to distinguish between these two models, as they imply different therapeutic strategies. In fact, the peripheral model suggests that the aberrant neural activity is responsible for tinnitus perception. This hypothesis has been inspired by the results of an animal study [5], by showing an increase in the spontaneous activity (SA) in the cochlear nerve after the administration of a high dose of salicylate (400 mg/kg in cats) assumed to cause tinnitus. A recent study [6] has shown that salicylate-induced tinnitus may be caused by activation of NMDA receptors expressed in the synapses of cochlear hair cells and dendrites of spiral ganglion neurons. If tinnitus was normally caused by increased activation of NMDA receptors, a possible therapeutic approach that could suppress such “peripheral tinnitus” would be inactivating NMDA receptors [6, 7]. However, NMDA receptor blockage has not been shown as effective treatment of tinnitus.

High doses of salicylate are also known to cause nonspecific (toxic) effects, especially in cats, which lack the enzyme necessary to metabolize salicylate (glucuronyltransferase). Such nonspecific effects could account for the increase in SA in the cochlear nerve after the administration of high doses of salicylate (see above). More recent studies have shown that salicylate, at a dose of approximately 200 mg/kg, known to induce tinnitus in animals [8], does not increase SA in the cochlear nerve [9, 10], but increases neural activity in auditory centers [11–13]. These studies then question the peripheral origin of salicylate-induced tinnitus. It is also worth noting that recent studies suggest that salicylate has strong effects on the central auditory nervous system [14–17]. These findings indicate that salicylate may induce tinnitus through central mechanisms.

The most frequent causes of tinnitus seem to be cochlear damage, as almost all individuals with tinnitus have hearing loss. Importantly, cochlear damages – induced after noise trauma, for instance – cause a dramatic decrease of SA in the cochlear nerve [18, 19]. Damages to the inner hair cells (or their stereocils) have been shown to decrease the spontaneous release of glutamate from the inner hair cells (cochlear nerve synapses), thereby causing the decrease in SA. This strongly argues against a peripheral origin of tinnitus encountered in human subjects (related to peripheral damages). If the neural activity is decreased in the cochlear nerve, there should be a kind of compensatory mechanism, which could generate an aberrant neural activity in the auditory centers.

In this context, it has been shown that cochlear damage decreases the inhibitory neurotransmission in the auditory centers [20–23]. This decrease in central inhibition is supposed to account for the changes in the evoked and SA after cochlear damage. First, hearing loss of a sufficient extent induces a reorganization of the tonotopic map, i.e., neurons with their characteristic frequency corresponding to the hearing loss region change their frequency tuning toward the cut-off frequency of hearing loss [24, 25]. In addition, a strong neural hyperactivity has been observed in the auditory cortex after a noise trauma [26]. This hyperactivity could be a neural correlate of hyperacusis, i.e., overestimation of loudness, sometimes reported by subjects presenting a hearing loss. Finally, changes in the pattern of spontaneous discharge (increase in firing rate and synchrony), consistent with the psychoacoustic properties of tinnitus [4], have been observed after acoustic trauma [3, 27]. These neural changes of the SA could then be neural correlates of tinnitus.

Rationale for Stimulating the Frequency Range of Hearing Loss: Reversing Central Changes Induced by a Decrease in Afferent Inputs

In summary, the decrease in afferent input caused by peripheral lesions could trigger dramatic central changes, such as a release from central inhibition. These central changes could ultimately result in the emergence of an aberrant neural activity that could induce tinnitus. In this context, we have suggested an approach consisting of preventing/compensating the decrease in afferent input related to hearing loss. This could reverse the central changes normally associated to it and, as a consequence, decrease/suppress tinnitus [3, 4, 28, 29]. The aim of this approach is to normalize the SA over frequency (in patients with high-frequency hearing loss, the approach consists of increasing sensory inputs in this frequency band) and/ or increase the overall level of sensory input (in patients with flat and severe hearing loss). Central inhibition could control a kind of central gain [28, 30], increasing central inhibition, by providing the auditory system with augmented input that is supposed to decrease neural hyperactivity induced after hearing loss. In animals, we have shown that an acoustic environment enriched in high frequencies could prevent the central changes normally induced after a noiseinduced hearing loss [24, 31]. Moreover, we could induce a dramatic decrease of hypersensitivity in human subjects reporting hyperacusis, after these subjects were stimulated a few hours a day for several weeks with a customized stimulus (the long-term spectrum of the stimulus corresponded to the hearing loss of each subject [28]).

Auditory Stimulation Delivery

Auditory stimulation is one of the most employed therapeutic methods and one of the most beneficial for patients suffering from tinnitus [32]. Such therapy has no noticeable side effects and may be administered through simple devices [33]. Sounds used may resemble environment sounds, which enrich the atmosphere in the room they are used. In case sound enrichment should be required all day long (and tinnitus is not associated to hearing loss), “custom” ear level sound generators may be suitable. These are small electronic devices fitted to the ear. For individuals with hearing loss, open-ear hearing aids are suitable [34, 35], as well as tinnitus control combination instruments (Combi), which combine a prosthesis and a sound generator. These devices both amplify environmental sounds and generate sound enrichment.

Sound Environment Generators

Sound environment generators are contained in a small case, in which batteries and speakers are also housed. The volume can be regulated by means of a small roller on the side of the device. Different buttons may be pushed to select different sounds such as sea waves, creeks, waterfalls, rain, the woodlands, and white noise. For most users, these sounds are relaxing, as they are monotonous and repetitive without interruption. Once a given sound has been selected and the volume has been regulated, the user can use the environmental sound as background noise. For this reason, such sound generators are particularly useful during night rest (Picture 1).

Tinnitus treatment picture - Environmental sound generator used in sound therapy

Picture 1 Example of environmental sound generator used in sound therapy

Custom Sound Generators

Custom sound generators look like regular hearing aids; they are light and designed to be worn behind the ear. A thin wire connects the generator to the speaker placed at the entrance of the ear canal.

Unlike the sound generated by environmental sound machines, the sound generated by custom sound generators can only be heard by the person wearing the device. These devices generate a wide band sound that can be adjusted by the audiologist to meet the final user’s needs by means of high-pass or low-pass filters and may even be modulated in width.

The size of the mini speaker placed at the entrance of the auditory canal is such that it does not affect normal hearing. Custom sound generators are beneficial for individuals with normal hearing.

The small size of these sound generators makes them easy to wear during everyday activity. Once they have been worn and the volume regulated, the person may “forget” they are wearing them for the rest of the day. Their maintenance is limited to periodically replacing the battery which can be done by the user. Custom sound generators are both useful for total masking therapy [36] and for partial masking therapy, according to tinnitus retraining therapy (TRT) [37] (Picture 2).

tinnitus treatment picture - Real size of a custom sound generator or a combi hearing aid used in sound therapy

Picture 2 Real size of a custom sound generator or a combi hearing aid used in sound therapy

Hearing Aid Devices

The most suitable hearing aids for sound therapy are the open-ear hearing aids [38, 39], which have a mini speaker placed at the entrance of the ear canal. The size of the small case housing the battery resembles that of a bean. Like the custom sound generators, their ease is such that wearers often do not even feel them.

Hearing aids are designed to compensate for hearing loss and lack of auditory stimulation. Unfortunately, hearing aids currently available are not able to amplify sounds with a frequency above 6–7 kHz, a range of hearing that is often impaired in individuals with tinnitus; for this reason, ordinary hearing aids may be less efficient in compensating for lost auditory stimulation. Besides hearing aids, the new generation Combi (combination hearing aids) now available, combine common prostheses with the ability to generate an enrichment sound, similar to what custom sound generators provide. The Combi devices represent the most innovative and efficient therapeutic tools for tinnitus and hearing loss, because they can combine auditory stimulation in impaired hearing areas with either partial or total tinnitus masking [40, 41].

Implantable Hearing Aids

Traditional acoustic prostheses and Combi hearing aids are not generally recommended for patients with conductive hearing loss caused by external and middle- ear malformations or in patients with chronic middle-ear infection. Such individuals may benefit from the bone-anchored hearing aids, which transmit sound vibrations to the inner ear through a titanium rod implanted into the bone. The increase in use of implantable hearing aids during recent years has made it possible to assess their efficacy for treatment of tinnitus. Implantable middle-ear prostheses provide better sound therapy for some patients with tinnitus than traditional hearing aids [42], probably because they provide amplification in a wider frequency range and because of the “naturalness of the amplification”. The cost, as well as the required surgery, limits the use of these devices. Cochlear implants can provide input to the auditory nervous system that can reduce tinnitus in many individuals, both in those with severe hearing loss and in individuals with good hearing on one ear who have severe tinnitus referred to that side [43].

Other Sound Therapy Devices

Besides sound generators and acoustic prostheses, other devices that are not specifically designed for treatment of tinnitus can be used for tinnitus management. In fact, a simple fan or fish tank can be used as first-aid treatment of tinnitus. Music players, such as MP3 players with headphones, are often employed to reduce tinnitus. Recorded nature sounds played through home stereo systems are used for this purpose as well.

Can such devices replace custom sound generators or acoustic prostheses? Some specialists do not believe they can for the following reasons: MP3 players and headphones can hardly be worn by individuals carrying out nonsedentary activities; they partially occlude the ear; and they may become intrusive and cannot be worn (and forgotten) for 6–8 h a day. Conversely, these devices may be useful for immediate relief before a more complete sound therapy is started.

Auditory Stimulation from Theory to Practice

Clinical studies [29, 34, 35] have shown that not only do hearing aids improve hearing ability, but they can also reduce or suppress tinnitus.

For instance, in a study carried out in 1999 [44], 50% of hearing aid wearers experienced relief from tinnitus, with a median improvement of 10% after only 6 weeks from the first application. These results were confirmed by subsequent studies, which extended the investigation to individuals who had tinnitus and mild hearing loss [34, 45].

Prosthesis and open-ear hearing aids are important for proper treatment of tinnitus. Modern hearing aids can provide amplification at the frequencies where hearing loss occurs, without uncomfortable side effects, such as over amplification or rumbling, which were typical in the old generation devices.

Individuals with hearing loss that is limited to mild damage of hair cells not affecting the subjective hearing sensitivity benefit from custom sound generators or sound environment generators [46]. Our experience from daily clinical practice, as well as the experience of others reported in published studies [47], has shown that hearing aids and sound generators can achieve the following goals:

  • Making patients with mild hearing loss less aware of tinnitus or masking it.
  • Favoring the ability to listen to tinnitus according to Jastreboff’s neurophysiologic hypothesis.
  • Improving communication and reducing the discomfort often reported by patients as sounds and voices covered by tinnitus.
  • Stimulating the auditory nervous system in a normal way and not only with tinnitus (phantom sounds).

The Approach to Sound Therapy

The role of the therapist should not be limited to the technical aspects of hearing aids and their application, but should aim at developing an empathic and confident relationship with the individual patient. Only a comprehensive evaluation may allow the therapist to have an accurate picture, in order to tailor the most appropriate and effective therapeutic plan. Hearing device application and control for adaptation may require a series of scheduled visits every 3–4 months, although in some cases a stricter follow-up schedule may be necessary. The results of long-term treatment may be assessed through visual analog questionnaires and the use of different kinds of scales [37] to allow tracking treatment progress. Audiometric test results do not usually reflect variations in tinnitus and thus, are not valid measures of relief [48]; tests, therefore, do not need to be periodically repeated. Cerebral plasticity requires some time to develop, and the needed duration of therapy may, therefore, vary from patient to patient [49]. Optimal relief from tinnitus may require a 6- to 8-month therapy using hearing aids and sound generators [50, 51].

Hearing Aid Selection

The selection of the most appropriate hearing aid device should be based on the individual patient’s needs. For example, sound environment generators are mostly indicated during night rest in patients affected by mild tinnitus. However, patients with disturbing tinnitus and without subjective hearing impairments benefit from custom sound generators, which should be worn at least 8 h during the daytime, in combination with an environment generator during night rest. Combi-type devices are suitable for patients with mild hearing loss. These can also provide environmental sound enrichment during night rest.

Hearing Aid Device Adaptation

In order to achieve an optimal auditory stimulation, specific guidelines on hearing aid device adaptation should be followed, for custom sound generators, Combi devices, or prostheses [29, 34]. The parameters are crucial for auditory stimulation achieving maximal benefits on tinnitus.

The best results are achieved when the external auditory canal is left as accessible as possible. In fact, even partial occlusion of the auditory canal may cause unease of use and may even increase tinnitus perception. It may also affect the natural acoustic properties of the external ear, with further negative side effects causing a loss of the natural acoustic resonance, which is important for naturalness of hearing. Occlusion of the ear canal also causes over-emphasis of low frequencies with rumbling sensations resulting together with diminished perception of sound in the most important frequency range of hearing. It is also important not to underestimate the hearing of one’s own voice which often causes difficulties in the understanding of speech, as well as being unpleasant for the individual and may cause a sensation of “closure” that can worsen tinnitus.

The introduction of the so-called open-ear hearing aids helped overcome some of these problems, allowing application of hearing aids to individuals with mild hearing loss, such as many individuals with tinnitus have. Open-ear hearing aids also provide a stimulation mainly in the frequency region of the tinnitus pitch. The open-ear hearing aids, thus, provide important advantages, such as sound enrichment, that reduce tinnitus by activating the neural plasticity. Open-ear prostheses can also be employed in patients with severe hearing loss; acoustic feedback is reduced (or eliminated) by computer programs in modern digital hearing aids. Hearing naturalness and ease of use are important factors or advantages of digital hearing aids. In the selection of hearing aids, all elements that can cause a patient’s discomfort and increase the perception of tinnitus must be taken into account, including cosmetic aspects. Hearing aids and sound generators should ideally be forgotten after they have been applied. In other words, people should become unaware of wearing a hearing aid device.

Hearing aid devices should simultaneously be worn in both ears, in order to favor a complete and simultaneous stimulation of the entire auditory nervous system. This is also important for unilateral tinnitus. Moreover, the frequency band of hearing aids should be adjusted to mostly amplifying the frequency range that is most important for hearing. Sound generators should be adjusted to the frequency of the tinnitus in order to activate the auditory nerve close to tinnitus frequency.

Specialist clinical experience supports the use of prescription formulas of gain/output suggested by device manufacturers, although major modifications are very often necessary. In fact, many tinnitus patients are sensitive to amplification, which sometimes requires less gain and maximum output than in patients who do not have tinnitus. Patients with moderate to severe hearing loss often benefit from amplifications that are 50–70% lower than traditional prescription formulas. The large variability of the requirements for tinnitus patients regarding amplification has prevented adaptation of an uniform formula that is suitable for all tinnitus patients. Individuals with tinnitus often benefit from having the option of noise reduction switched off or turned down.

Patients must be properly instructed in how to adjust the volume on their devices. Patients are generally able to fully understand the volume regulation procedure and to safely carry it out, but often more than one round of counseling is necessary and analog scales should be used to track the intensity of both tinnitus and therapeutic sound. During TRT therapy, the correct balance between sound stimulation and amplification can be determined with in situ instruments after some weeks of use [52]. The intensity of auditory stimulation should be 5–6 dB higher than the threshold level in order to prevent stochastic resonance phenomena [37].

Optimal results in management of tinnitus are not only obtained with the application of technologically advanced hearing aid devices but, most of all, with their adjustment to the individual person’s needs and through patient counseling. Each single patient must be listened to, counseled, and informed throughout therapy planning and during follow-up. This enables therapists to fully understand their patient’s problems and to solve them to the greatest extent through a proper selection of prosthetic devices and finding the optimal settings.


1. Tonndorf J (1987) The analogy between tinnitus and pain: a suggestion for a physiological basis of chronic tinnitus. Hear Res 28:271–5.

2. Jastreboff PJ (1990) Phantom auditory perception (tinnitus): mechanisms of generation and perception. Neurosci Res 8:221–54.

3. Norena AJ and JJ Eggermont (2003) Changes in spontaneous neural activity immediately after an acoustic trauma: implications for neural correlates of tinnitus. Hear Res 183:137–53.

4. Norena A, C Micheyl, S Chery-Croze et al (2002) Psychoacoustic characterization of the tinnitus spectrum: implications for the underlying mechanisms of tinnitus. Audiol Neurootol 7:358–69.

5. Evans EF and TA Borerwe (1982) Ototoxic effects of salicylates on the responses of single cochlear nerve fibres and on cochlear potentials. Br J Audiol 16:101–8.

6. Puel JL, J Ruel, M Guitton et al (2002) The inner hair cell synaptic complex: physiology, pharmacology and new therapeutic strategies. Audiol Neurootol 7:49–54.

7. Puel JL (2007) Cochlear NMDA receptor blockade prevents salicylate-induced tinnitus. B-Ent 3 Suppl 7:19–22.

8. Jastreboff PJ and CT Sasaki (1994) An animal model of tinnitus: a decade of development. Am J Otol 15:19–27.

9. Stypulkowski PH (1990) Mechanisms of salicylate ototoxicity. Hear Res 46:113–45.

10. Muller M, R Klinke, W Arnold et al (2003) Auditory nerve fibre responses to salicylate revisited. Hear Res 183:37–43.

11. Chen GD and PJ Jastreboff (1995) Salicylate-induced abnormal activity in the inferior colliculus of rats. Hear Res 82:158–78.

12. Ochi K and JJ Eggermont (1996) Effects of salicylate on neural activity in cat primary auditory cortex. Hear Res 95:63–76.

13. Jastreboff PJ and CT Sasaki (1986) Salicylate-induced changes in spontaneous activity of single units in the inferior colliculus of the guinea pig. J Acoust Soc Am 80:1384–91.

14. Bauer CA, TJ Brozoski, TM Holder et al (2000) Effects of chronic salicylate on GABAergic activity in rat inferior colliculus. Hear Res 147:175–82.

15. Wang HT, B Luo, KQ Zhou et al (2006) Sodium salicylate reduces inhibitory postsynaptic currents in neurons of rat auditory cortex. Hear Res 215:77–83.

16. Sun W, J Lu, D Stolzberg et al (2009) Salicylate increases the gain of the central auditory system. Neuroscience 159:325–34.

17. Su YY, B Luo, HT Wang et al (2009) Differential effects of sodium salicylate on current-evoked firing of pyramidal neurons and fast-spiking interneurons in slices of rat auditory cortex. Hear Res 253:60–6.

18. Liberman MC and LW Dodds (1984) Single-neuron labeling and chronic cochlear pathology. III. Stereocilia damage and alterations of threshold tuning curves. Hear Res 16:55-74.

19. Liberman MC and LW Dodds (1984) Single-neuron labeling and chronic cochlear pathology. II. Stereocilia damage and alterations of spontaneous discharge rates. Hear Res 16:43–53.

20. Milbrandt JC, TM Holder, MC Wilson et al (2000) GAD levels and muscimol binding in rat inferior colliculus following acoustic trauma. Hear Res 147:251–60.

21. Argence M, I Saez, R Sassu et al (2006) Modulation of inhibitory and excitatory synaptic transmission in rat inferior colliculus after unilateral cochleectomy: an in situ and immunofluorescence study. Neuroscience 141:1193–207.

22. Kotak VC, S Fujisawa, FA Lee et al (2005) Hearing loss raises excitability in the auditory cortex. J Neurosci 25: 3908–18.

23. Dong S, WH Mulders, J Rodger et al (2009) Changes in neuronal activity and gene expression in guinea-pig auditory brainstem after unilateral partial hearing loss. Neuroscience 159:1164–74.

24. Norena AJ and JJ Eggermont (2005) Enriched acoustic environment after noise trauma reduces hearing loss and prevents cortical map reorganization. J Neurosci 25:699–705.

25. Robertson D and DR Irvine (1989) Plasticity of frequency organization in auditory cortex of guinea pigs with partial unilateral deafness. J Comp Neurol 282:456–71.

26. Norena AJ, M Tomita and JJ Eggermont (2003) Neural changes in cat auditory cortex after a transient pure-tone trauma. J Neurophysiol 90:2387–401.

27. Mulders WH and D Robertson (2009) Hyperactivity in the auditory midbrain after acoustic trauma: dependence on cochlear activity. Neuroscience 164:733–46.

28. Norena AJ and S Chery-Croze (2007) Enriched acoustic environment rescales auditory sensitivity. Neuroreport 18:1251–5.

29. Moffat G, K Adjout, S Gallego et al (2009) Effects of hearing aid fitting on the perceptual characteristics of tinnitus. Hear Res 254:82–91.

30. Formby C, LP Sherlock and SL Gold, (2003) Adaptive recalibration of chronic auditory gain : interim findings, in Proceedings of the Seventh International Tinnitus Seminar, Perth, Australia : March 5th-9th, 2002, RB Patuzzi, Editor. 2003, Physiology Dept., University of Western Australia: Perth, Australia. 165–9.

31. Norena AJ and JJ Eggermont (2006) Enriched acoustic environment after noise trauma abolishes neural signs of tinnitus. Neuroreport 17:559–63.

32. Han BI, HW Lee, TY Kim et al (2009) Tinnitus: characteristics, causes, mechanisms, and treatments. J Clin Neurol 5:11–9.

33. Jastreboff PJ (2007) Tinnitus retraining therapy. Prog Brain Res 166:415–23.

34. Del Bo L and U Ambrosetti (2007) Hearing aids for the treatment of tinnitus. Prog Brain Res 166:341–5.

35. Trotter MI and I Donaldson (2008) Hearing aids and tinnitus therapy: a 25-year experience. J Laryngol Otol 122:1052–6.

36. Vernon JA and MB Meikle, (2000) Tinnitus masking, in Tinnitus handbook, RS Tyler, Editor. 2000, Singular Pub. Group: San Diego. 313–56.

37. Jastreboff PJ and JWP Hazell (2004) Tinnitus retraining therapy: implementing the neurophysicological model. Cambridge, U.K.: Cambridge University Press. 276.

38. Del Bo L, U Ambrosetti, M Bettinelli et al (2006) Using open-ear hearing aids in tinnitus therapy. Hear Rev 13:30–2.

39. Lantz J, OD Jensen, A Haastrup et al (2007) Real-ear measurement verification for open, non-occluding hearing instruments. Int J Audiol 46:11–6.

40. Carrabba L, G Coad, M Costantini et al. Combination open ear instrument for tinnitus sound treatment. in IXth International Tinnitus Seminars 2009. Sweden.

41. Van de Heyning P, K Vermeire, M Diebl et al (2008) Incapacitating unilateral tinnitus in single-sided deafness treated by cochlear implantation. Ann Otol Rhinol Laryngol 117:645–52.

42. Holgers KM and BE Hakansson (2002) Sound stimulation via bone conduction for tinnitus relief: a pilot study. Int J Audiol 41:293–300.

43. Baguley DM and MD Atlas (2007) Cochlear implants and tinnitus. Prog Brain Res 166:347–55.

44. Surr RK, JA Kolb, MT Cord et al (1999) Tinnitus Handicap Inventory (THI) as a hearing aid outcome measure. J Am Acad Audiol 10:489–95.

45. Folmer RL and JR Carroll (2006) Long-term effectiveness of ear-level devices for tinnitus. Otolaryngol Head Neck Surg 134:132–7.

46. Henry JA, TL Zaugg and MA Schechter (2005) Clinical guide for audiologic tinnitus management II: treatment. Am J Audiol 14:49–70.

47. Molini E, M Faralli, C Calenti et al (2009) Personal experience with tinnitus retraining therapy. Eur Arch Otorhinolaryngol. In press.

48. Forti S, S Costanzo, A Crocetti et al (2009) Are results of tinnitus retraining therapy maintained over time?. 18-month follow-up after completion of therapy. Audiol Neurootol 14:286–9.

49. Hatanaka A, Y Ariizumi and K Kitamura (2008) Pros and cons of tinnitus retraining therapy. Acta Otolaryngol 128: 365–8.

50. Baracca GN, S Forti, A Crocetti et al (2007) Results of TRT after eighteen months: Our experience. Int J Audiol 46: 217–22.

51. Sheldrake JB, JWP Hazell and RL Graham, (1999) Results of tinnitus retraining therapy, in Proceedings of the sixth International Tinnitus Seminar, Cambridge UK September 5th-9th 1999, J Hazell, Editor. 1999, Tinnitus and Hyperacusis Centre: London. 292–6.

52. Ito M, K Soma and R Ando (2009) Association between tinnitus retraining therapy and a tinnitus control instrument. Auris Nasus Larynx 36:536–40.