Tinnitus: Chracteristics, causes, mechanisms, & treatments

[byungin]

Tinnitus: Characteristics, causes, mechanisms, and treatments

Byung In Han, M.D ^a., Ho Won Lee, M.D.^b, Tae-You Kim, M.D.^c, Jun-Seong Lim, M.D. ^d, Kyoung Sik Shin, M.D. ^e

Do neurology clinic, Daegu D ^a; Deptartment of Neurology, School of Medicine, Brain Science & Engineering Institute, Kyungpook National University^b; Willis hospital, Busan^c; Department of Neurology, Sung Ae Hospital, Seoul ^d, Jeil neurology clinic, Daejeon^e

Acknowledgements

Byung In Han ^a and Ho Won Lee^b equally contributed to this paper. The authors would like to thank Dr. Hui Jong Oh, President of Oh Neurology Clinic, for his valuable contribution. We also gratefully acknowledge important assistance from In Sang Jung, Jong kyoon Lee, Sun Jeong O, Hae Young Woo, Hee Jung Park, and Hoe Jong Jung in the preparation of this paper.

Address for correspondence: Byung In Han, M.D.

Do Neurology Clinic

925-2 Namsan-dong, Jung-gu, Daegu 700-440, South Korea

Tel.: +82-53-252-2225

Fax: +82-53-289-6502

E-mail: han-byungin@hanmail.net

Han BI, Lee HW, Kim TY, Lim JS, Shin KS. Tinnitus: Characteristics, Causes, Mechanisms, and Treatments. J Clin Neurol 2009;5 (1):11~19.

http://thejcn.com/archive/view.php?py=2009&vol=5&no=1&spage=11

Tinnitus: Characteristics, causes, mechanisms, and treatments

Number of character in this title: 56

Word Count for this Paper: 4864
Abstract

Tinnitus, the perception of sound in the absence of an actual external sound, represents a symptom of an underlying condition rather than a single disease. Several theories have been proposed to explain the mechanisms responsible for tinnitus. Tinnitus generators have been theoretically located in the auditory pathway. These generators and various mechanisms occurring in the peripheral auditory system have been explained in terms of spontaneous otoacoustic emissions, edge theory, and discordant theory. Those occurring in the central auditory system have been explained in terms of the dorsal cochlear nucleus, the auditory plasticity theory, the cross-talk theory, the somatosensory system, and the limbic and autonomic nervous systems. Treatments for tinnitus include pharmacotherapy, cognitive and behavioral therapy, sound therapy, music therapy, tinnitus retraining therapy, massage and stretching, and electrical suppression. This paper reviews the characteristics, causes, mechanisms, and treatments of tinnitus.

Key words: Tinnitus, Discordant theory, Tinnitus retraining therapy

I. Introduction

Tinnitus is defined as a phantom auditory perception; that is, it is a perception of sound without corresponding acoustic or mechanical correlates in the cochlea.¹ Tinnitus represents one of the most common and distressing otological problems, causes a variety of somatic and psychological disorders, and interferes with the quality of life  of sufferers.² A population-based study of hearing loss in adults aged 48 to 92 years showed that the preval‎ence of tinnitus was 8.2% at baseline and the 5-year incidence of tinnitus was 5.7 percent.³ The preval‎ence of tinnitus increases with age. People 65 to 75 years of age are more likely than those in younger age groups to suffer from tinnitus.⁴ Tinnitus also represents a common symptom among children with hearing loss.⁵ Because tinnitus is a subjective phenomenon that is difficult to eval‎uate objectively, it can be measured, quantified, and described only by the responses of patients. Although tinnitus can have many different causes, it most commonly results from otologic disorders, and the most common cause is believed to be noise-induced hearing loss.⁶ Thus far, a variety of therapeutic approaches to tinnitus have produced mixed results. Therefore, it is generally assumed that tinnitus can emerge from multiple physiological causes.⁷

II. Clinical manifestations

1. Characteristics of tinnitus

The sound perceived by those with tinnitus may range from a quiet background noise to a noise that is audible over loud external sounds. Tinnitus is generally divided into two categories: objective and subjective tinnitus. Objective tinnitus is defined as tinnitus that is audible to other person. Subjective tinnitus is defined as tinnitus that is audible only to the patient and is usually considered to be devoid of an acoustic etiology and associated movements in cochlear fluids or partitions. Many physicians use the term tinnitus to designate subjective tinnitus and the term somatosound to designate objective tinnitus.⁶

The sounds associated with most cases of tinnitus have been described in terms of cicadas, crickets, winds, falling tap water, grinding steel, escaping steam, fluorescent lights, running engines, and so on. It is believed that this kind of perception results from abnormal neuronal activity at a subcortical level of the auditory pathway.^6,8

The pattern characterizing tinnitus is related to the library of patterns stored in auditory memory and also, via the limbic system, associated with emotional states.⁹ The quality of tinnitus is generally unrelated to the type or severity of any associated hearing impairment, and thus the latter offers little diagnostic value.⁶ The majority of tinnitus patients match tinnitus to a pitch above 3000 Hz.¹⁰ The tinnitus characterizing Meniere’s disease, described as roaring, matches a low frequency tone, usually in the range of 125 to 250 Hz.¹¹ However, in the burned-out condition of Meniere’s disease, tinnitus is often higher in pitch and tonal in quality.¹²

Most patients with both tinnitus and hearing loss report that the frequency of the tinnitus correlates with hearing loss severity and configuration, and the intensity of the tinnitus is usually less than 10 dB above the patient's hearing threshold at that frequency.⁶ Among patients who have central auditory processing disorders, some patients who have difficulties understanding speech in noise report tinnitus although their pure tone audiometric thresholds are normal.^8,13 Less preval‎ent forms of tinnitus, such as those involving well-known musical tunes or voices without any understandable speech, occur among older people with hearing loss and are believed to represent a central type of tinnitus involving reverberatory activity within neural loops at a high level of processing in the auditory cortex.^8,14

Somatic tinnitus is a type of subjective tinnitus in which the frequency or intensity is altered with body movements such as clenching the jaw, turning the eyes, or applying pressure to the head and neck.¹⁵

Reports that tinnitus is louder upon awakening raise the possibility that somatic factors, such as bruxism. Reports that tinnitus vanishes during sleep but returns in a few hours raise the possibility that psychosomatic factors, such as neck muscle contractions occurring in an upright position or jaw clenching, may play etiological roles.¹⁶

Tinnitus that is audible to other person is objective tinnitus. Because objective tinnitus represents the semantic opposite of subjective tinnitus, a better nosological approach might involve using the term somatosound instead of objective tinnitus, whether or not the sounds are audible to others, and reserving the term tinnitus for the experience of sound in the absence of any acoustic source. Thus, tinnitus would be used to describe cases previously diagnosed as subjective tinnitus.⁶ Objective tinnitus may be vascular or mechanical in origin. Objective tinnitus of vascular origin may be a referred bruit from stenosis in the carotid or vertebrobasilar system. Objective mechanical tinnitus is due to abnormal muscular contraction of the nasopharynx or middle ear, as may occur in palatal myoclonus.¹⁷ Pulsatile tinnitus can also arise as a subjective phenomenon from an increased awareness of blood flow in the ear. Indeed, the cause of somatosensory pulsatile tinnitus syndrome is not vascular, and the syndrome derives from cardiac-synchronous somatosensory activation of the central auditory pathway or failure of the somatosensory-auditory central nervous system interactions to suppress cardiac somatosounds.¹⁸ Pulsatile tinnitus superimposed on other steady tinnitus may result from the pulsation of the spiral capillary of the basilar membrane.¹⁹

2. Associated symptoms

The most common associated symptoms or subjective discomforts, involve concentration difficulties, insomnia, and decreased speech discrimination.²⁰ The annoyance of tinnitus does not correlate with the acoustic characteristics, but there is a significant correlation with psychological symptoms.²¹ The difference between someone's simply experiencing tinnitus and someone's being annoyed or distressed by it depends exclusively on the activation of the limbic and autonomic nervous systems.⁸ Most patients with significant tinnitus have difficulty falling asleep due to accompanying anxiety. They also experience difficulties in returning to sleep during periods of wakefulness during the night.⁸

Neuronal activity in the auditory pathways is pronounced during sleep, because the auditory system continuously monitors the sound environment even during sleep.⁸ Common detrimental activities and/or conditions include noise exposure, location in a quiet place, emotional stress, loss of sleep, and physical exhaustion.²² Patients with Meniere’s disease experience more annoyance, depression, and interference with sleep and also report louder tinnitus than patients with tinnitus deriving from other etiologies.²² Furthermore, following the successful control of vertigo, some patients with Meniere’s disease focus more on their tinnitus and are therefore more distressed by this condition.²³ The strength of the reaction to tinnitus is determined by its significance and by past experience; sound intensity is secondary.²⁴

3. Natural course

Noise-induced tinnitus can be acute or chronic. Acute tinnitus can last from a few minutes to a few weeks after noise exposure.²⁵  In some cases, tinnitus has a gradual onset and several years may pass before an intermittent, low-intensity tinnitus becomes bothersome.²⁶ Spontaneous remission by natural habituation is experienced by more than three-quarters of sufferers. Habituation occurs within the central nervous system, whereas adaptation involves a peripheral sensory organ.⁸ For those who get worse, tinnitus loudness and severity increase over time, but tinnitus pitch tends to remain stable.²⁷ If tinnitus persists for more than two years, it is considered permanent and irreversible.²⁸ However, chronicity has no association with favorable response to treatment.²⁹

III. Causes and pathophysiology

1. Causes

Tinnitus does not represent a disease itself but instead represents a symptom resulting from a range of underlying causes. Otologic causes include noise-induced hearing loss, presbycusis, otosclerosis, otitis, impacted cerumen, sudden deafness, Meniere's disease, and other causes of hearing loss. Neurologic causes include head injury, whiplash, multiple sclerosis, vestibular schwannoma (commonly called an acoustic neuroma), or other cerebellopontine angle tumors. Infectious causes include otitis media and sequelae of Lyme's disease, meningitis, syphilis, and other infectious or inflammatory processes that affect hearing. Tinnitus is also a side effect of some oral medications, such as salicylates, nonsteroidal antiinflammatory drugs, aminoglycoside antibiotics, loop diuretics, and chemotherapy agents (e.g., platins and vincristine). Temporomandibular joint dysfunction and other dental disorders can also cause tinnitus. In many cases, however, no underlying physical cause can be identified.³⁰ For many years, hearing loss has been understood to be the most common cause of tinnitus.³¹ Based on population-based data, excessive noise exposure represents the second most common cause of tinnitus. About 40% of patients cannot identify any cause associated with tinnitus onset.²⁸

Any pathologic lesion in the auditory pathway or any reduction in auditory nerve function has the potential to produce tinnitus.¹⁹ The location of the hearing problem (i.e., in the middle ear or in the inner ear) and the otologic disorder causing the hearing loss do not seem to matter in terms of etiologic potential.⁶ Interestingly, most patients with tinnitus complain about a sensation of fullness or blockage in the middle ear, suggesting some problem with middle ear pressure or increased impedance of the ossicular chain.³²

Unilateral high-frequency hearing loss combined with poor speech discrimination suggests the possibility of a tumor, usually a vestibular schwannoma (commonly called an acoustic neuroma) or a meningioma.³⁰ Bilateral subjective tinnitus requires assessment of hearing and can be associated with presbyacusis, noise-induced hearing loss, endolymphatic hydrops, and vascular labyrinthine lesion.²¹ However, most cases of unilateral tinnitus are not associated with life-threatening otologic disease.⁶

2. Trigger factors

Small temporary changes in the outer hair cells (OHCs) following noise exposure can act as a trigger by increasing the gain of the central auditory system, thereby resulting in the emergence of tinnitus.⁸ In general, tinnitus represents a threshold phenomenon such that any one factor, such as chronic progressive hearing loss, is not sufficient to elicit its emergence. Two or more trigger factors (i.e., psychosocial stress, noise-exposure, and somatic factors) may act synergistically, leading to the tinnitus becoming symptomatic.¹⁵ About 75% of new cases are related to emotional or stress as the trigger factors rather than to precipitants involving cochlear lesions.⁸

3. Pathophysiology

Tinnitus represents a symptom of many pathologies. It is proposed that all levels of the nervous system are, to varying degrees, involved in tinnitus manifestation.^{1, 33}

[1] Peripheral auditory system

(1) Spontaneous otoacoustic emissions

SOAEs, first discovered by Kemp,³⁴ are small acoustic signals presumed to be generated by the electromotile activity of the OHCs of the cochlea and propagated into the external auditory canal.³⁵ SOAEs produced by the cochlea can be perceived as tinnitus.³⁶ In general, SOAEs are inaudible but, when unstable, SOAEs might be audible.³⁷ These atypical SOAEs are much more preval‎ent in the higher frequency range and are audible at up to 55 dB sound pressure level.³⁸ Tinnitus due to SOAEs is mild and is likely found in people with normal hearing and in those with only middle ear disorders.³⁹ As hearing loss progresses, SOAEs decrease; therefore otoacoustic emissions are not likely to cause tinnitus when the degree of hearing loss is up to 35 or 40 dB.⁴⁰ SOAEs cannot fully explain the mechanism of tinnitus, because aspirin largely abolishes SOAEs without improving tinnitus.⁴¹

(2) Edge theory 

Edge theory, also known as contrast theory, proposes that increased spontaneous activity in the edge area induces tinnitus.⁴² The edge represents a transition from the relatively normal morphology and function of hair cells in the organ of Corti on the apical (or low frequency) side of the lesion to missing or pathologic-appearing, poorly functioning hair cells toward the basal side.¹⁹ Edge theory can be explained by discordant theory.⁹

(3) Discordant theory

According to discordant theory, tinnitus is induced by the discordant dysfunction of damaged OHCs and intact inner hair cells (IHCs) of the organ of Corti. Intense noise and ototoxic agents initially damage the basal turn of the cochlea and OHCs, and only later, if continued or repeated, affect IHCs; IHCs are more resistant to such damage.⁹ IHCs represent the true receptor cells for sound transduction, and most fibers in the auditory nerve (95%) connect with IHCs.⁸ OHCs work as mechanical amplifiers, enhancing weak sounds by providing up to 50 dB of amplification, which can be eval‎uated by measurement of otoacoustic emissions.⁸ Except in a very few situations, OHCs are damaged more than IHCs; this, in turn, results in the disinhibition of neurons in the dorsal cochlear nuclei.⁸ When neurons in the dorsal cochlear nucleus receive excitation from IHCs but not from the damaged OHCs, increased spontaneous activity is produced. This is perceived as tinnitus.⁸ In the area in which OHCs are affected but IHCs are intact, the coupling between the tectorial membrane and the basilar membrane is affected to the extent that the tectorial membrane might directly impinge upon the cilia of the IHCs, thus causing the IHCs to depolarize.⁴³ Recovery of OHCs occurs over a few days but can be delayed for up to a few months.^44,45 Therefore, it is  hypothesize that tinnitus represents a consequence of a central gain adaptation mechanism when the auditory system is confronted with hearing loss.⁴⁶ Discordant theory explains why many individuals with tinnitus have normal hearing if damage to outer hair cells is partial. Up to 30% of OHCs may be damaged without inducing hearing loss.⁴⁷ OHCs die at approximately 0.5 % per year beginning during the first years of life, and the appearance of a hearing loss is not usually expected before the end of the fifth decade.⁸ In totally deaf individuals, when damage to outer and inner hair cells is complete, there is no discordance, and tinnitus is not induced. If there is increased gain within the central nervous system, tinnitus is present even in deaf people.²⁴ Noise-induced tinnitus is caused by discordant damage between outer and inner hair cells.⁴³ Two types of noise-induced tinnitus have been identified: tonal tinnitus and complex tinnitus. Tonal tinnitus results from a single area's manifesting the discordant dysfunction of outer and inner hair cells, whereas complex tinnitus results from many areas of discordance.⁴⁸ When patients clearly have the central type of tinnitus, such as after transection of the auditory nerve, the OHC concept is not applicable and alternative mechanisms should be discussed.²⁴

[2] Central auditory system

(1) The dorsal cochlear nucleus (DCN)

The DCN has been implicated as a possible site for the generation of tinnitus-producing signals owing to its tendency to become hyperactive following exposure to tinnitus-inducing agents such as intense sound and cisplatin.⁴⁹ Outer hair cell damage triggers plastic readjustments in the DCN, resulting in hyperactivity in the DCN.⁵⁰ It is hypothesized that a reduction in auditory-nerve input leads to disinhibition of the DCN and an increase in spontaneous activity in the central auditory system, which is experienced as tinnitus.⁵¹ This mechanism could explain the temporary ringing sensation that may follow exposure to noise.⁵² The plastic readjustments in the DCN are slow and lead to tinnitus with a delayed onset. Inner hair cell damage prevents hyperactivity in the DCN.⁵³

( 2) Auditory plasticity theory

According to auditory plasticity theory, when the cochlea is damaged, neural activity in the central auditory pathway is enhanced.⁵⁴ Auditory plasticity emerges a consequence of the aberrant new pathways, and tinnitus might be considered to be the auditory system analog to phantom limb sensations in amputees.⁵⁵ The temporal lobe in the auditory association cortex⁵⁶ and inferior colliculus may represent the sites of tinnitus generation.⁵⁷ The ability of some individuals to modulate tinnitus by performing voluntary somatosensory or motor acts is likely the result of plastic changes involving the development of aberrant connections between the auditory and sensory-motor systems in the brains of these patients.⁵⁸

(3) Crosstalk theory

According to crosstalk theory, when auditory nerve fibers are intact and some other cranial nerves are damaged, artificial synapses (crosstalk) can develop between individual auditory nerve fibers, resulting in the phase-locking of the spontaneous activity of groups of auditory neurons. In the absence of external sounds, this creates a neural pattern that resembles patterns evoked by actual sounds.⁵⁹ These cranial nerves are sensitive to compression at the root entry zone, where they are covered by myelin. Compression of the nerve causes crosstalk between nerve fibers, and the breakdown of the myelin insulation of the nerve fibers establishes ephaptic coupling between them. This notion is applied to the cochlear-vestibular nerve, which is covered by central myelin for the majority of its length and hence is vulnerable to compression from blood vessels or tumors impinging upon the nerve (e.g., vestibular schwannoma). Such compression and consequent ephaptic coupling might lead to tinnitus if synchronization of the stochastic firing in the human cochlear nerve is perceived as sound⁵⁹.

[3] Somatosensory system

The activity of the DCN is also influenced by stimulation of non-auditory structures.⁴⁹ Of all the non-auditory sensory systems, only the somatosensory system seems to be related to tinnitus (e.g., in temporomandibular joint syndrome and whiplash).⁵¹ Somatic tinnitus can develop from activation of latent oto-somatic interaction.¹⁶ Somatic (craniocervical) tinnitus, like otic tinnitus, is caused by disinhibition of the ipsilateral DCN. Nerve fibers whose cell bodies lie in the ipsilateral medullary somatosensory nuclei mediate this effect. These neurons receive inputs from the nearby spinal trigeminal tract; the fasciculus cuneatus; and the facial, vagal, and glossopharyngeal nerve fibers innervating the middle and external ear.⁵¹

Pain sensation from the cochlea, carried by the cochlear c fibers, might also be interpreted by the central nervous system as tinnitus.⁶⁰ It is further hypothesized that somatic tinnitus might be due to central crosstalk within the brain, because certain head and neck nerves enter the brain near regions known to be involved in hearing.⁵⁹

[4] Limbic and autonomic nervous system

The aforementioned theories cannot explain why some people suffer from tinnitus while others do not. More than 80% of those experiencing tinnitus for the first time do not associate the sound with any negative meaning and experience spontaneous habituation. If, however, the first experience of tinnitus induces high levels of annoyance or anxiety by association with unpleasant stimuli or with periods of stress and anxiety, such high levels of annoyance or anxiety will subsequently be experienced in response to tinnitus. At the unconscious level, tinnitus can be progressively enhanced outside the awareness of the patient, resulting in enhanced activity in the autonomic nervous system and limbic system. In such situations, tinnitus emerges as a clinically significant problem.⁸

IV. Treatments

Tinnitus treatments can be organized into two categories: those aimed at directly reducing the intensity of tinnitus and those aimed at relieving the annoyance associated with tinnitus. The former include pharmacotherapy and electrical suppression,⁶¹ and the latter include pharmacotherapy, cognitive and behavioral therapy, sound therapy, habituation therapy⁶², massage and stretching, and hearing aids.

1. Pharmacotherapy

Extensive reviews of randomized clinical trials have revealed that only nortriptyline, amitriptyline, alprazolam, clonazepam, and oxazepam are associated with some benefit than placebo.^61,63  Dobie et al. reported that nortriptyline were stastically superior to placebo,  although placebo were also effective.⁶⁴ Podoshin et al. reported that amitriptyline was superior to placebo with respect to sleep disturbance and interference with activities.⁶⁵ Johnson et al. reported that alprazolam was effective than placebo in reducing tinnitus loudness.⁶⁶ Lechtenberg and Shulman noted that clonazepam and oxazepam were effective with success rate of greater than 50 %.⁶⁷ However when patients stopped taking either of these drugs, tinnitus recurred to its prior level or worse. ⁶⁷ The only medication providing a reliable reduction of tinnitus is intravenous lidocaine, and there is a close association between lidocaine and oral carbamazepine effects.⁶⁸ Intravenous lidocaine produces a change in the neural activity in the right temporal lobe in the auditory association cortex.⁵⁶ Unfortunately, lidocaine cannot be used clinically because it must be injected, its effects are of short duration, and it frequently produces annoying side effects.⁶³ Tocainide, an oral antiarrhythmic drug closely related to lidocaine, failed to show benefits. ⁶⁹ Tinnitus due to spontaneous otoacoustic emissions can be diminished by aspirin.⁷⁰ A recent three-month randomized clinical trial among 50 patients found that acamprosate, a drug used in the treatment of alcoholism, showed benefit over placebo.⁷¹  Flecainide, mexiletine, betahistine, carbamazepine, ginko extract, amylobarbiturate, baclofen, lamotrigine, misoprostol, zinc, cinnarizine, flunarizine, caroverine, eperisone, and melatonin showed no advantage over placebo.⁶¹ Diazepam and flunazepam caused no significant change in tinnitus intensity and severity.⁶³

2. Cognitive and behavioral therapy

Cognitive therapy focuses on how one thinks about tinnitus and on the avoidance of negative ideation, whereas behavioral therapy uses the systematic desensitization approach that is applied to many phobias.⁷² Cognitive therapy involves teaching patients to cope with their tinnitus by replacing catastrophic thinking with more positive thinking. Cognitive therapy includes counseling and cognitive restructuring. Counseling should include: (a) informing patients that it is unlikely that their annoyance with tinnitus will change dramatically, (b) informing patients about the usefulness of tinnitus self-help groups, (c) helping patients to minimize the time devoted to activities and/or conditions in which the severity of tinnitus is increased and to maximize the time devoted to activities and/or conditions in which the severity of tinnitus is decreased, and (d) stressing the avoidance of noise exposure due to the relationship between noise-induced hearing loss and tinnitus.⁷³ Cognitive restructuring involves changing thoughts associated with tinnitus. In this context, patients are encouraged to accept the idea that tinnitus does not deserve all the attention it gets.⁷⁴  Behavioral therapy focuses on positive imagery, attention control, and relaxation training.⁷² Positive imagery involves focusing thoughts on something pleasant, thereby diverting thoughts from tinnitus. Patients begin with pleasant visual (e.g., lying on a beach) and auditory (e.g., the sound of waves or wind through the leaves) images.⁷² Attention control is to switch attention away from the tinnitus when the tinnitus is bothersome. This process might begin by placing two pictures next to one another and then presenting two acoustic stimuli (e.g., a fan noise and conversational speech) emanating from an adjacent room. Next, a picture and the tinnitus are paired, followed by the pairing of a thought and the tinnitus.⁷² Relaxation training uses a guided protocol to teach participants to apply progressive muscle relaxation, involving tensing and relaxing arms, face, neck, shoulders, abdomen, legs, and feet.⁷²

3. Sound therapy

Sound therapy uses sounds found in natural settings, including those associated with streams, rain, waterfalls, and wind, to decrease the strength of the tinnitus-related neuronal activity within the auditory system.⁷⁵ Toward this end, the background neuronal activity in the auditory system is increased by exposing the patient to low-level, continuous, neutral sound²⁴ that is non-intrusive, not annoying, and easy to ignore. Such sound should not be meaningful, pleasant, or arousing in a way that attracts attention. Thus, listening to television or radio would not meet the criteria because these attract attention. Likewise, music would not be recommended as continuous background sound, because it tends to induce emotion and attract attention.⁸ Neutral sounds should be stable and not overwhelming; therefore, the sounds of waves or waterfalls are not recommended.²⁴ Some patients are distracted by the sounds of bird calls, crickets, or thunderstorms, and these sounds should be used carefully.⁷⁵ Sound therapy can include a variety of sound sources, including using table-top sound machines and compact disc players. The strength of the sound used should be adjusted to be at or below the level at which the patient can perceive the tinnitus and the external sound separately.²⁴ Instrument fittings must be bilateral to avoid asymmetrical stimulation of the auditory system. Stimulating only one side in unilateral tinnitus frequently results in a shift of the perceived location of the tinnitus to the opposite side due to the strong interaction within the auditory pathways. Occlusion with ear plugs should be minimized by using open-ear molds to allow normal access of environmental sounds to the ear.⁸ Sound therapy performed during the night can be helpful for individuals without sleep problems because the auditory pathways are fully active up to the level of the inferior colliculi during sleep.²⁴ An additional benefit of sound therapy is that the continuous sound exposure can increase blood flow to the inner ear.⁷⁶

4. Hearing aids

Hearing aids represent another form of sound therapy that usually benefits tinnitus patients with significant hearing loss.⁷⁵ Hearing aids are designed to improve the audibility of speech and to amplify ambient noise. Amplification of speech diverts attention away from tinnitus, induces amplification of ambient noise, and serves to partially mask tinnitus. Hearing aids are not appropriate for those with hearing loss confined to above 6 KHz, because most hearing aids have limited ability in high-frequency amplification.⁷⁷ The use of hearing aids can contribute to a permanent reduction in the neural activity responsible for tinnitus generation and perception,⁷⁵ and usually represents the first intervention for patients with hearing impairment.⁷⁷ Many hearing-impaired patients have normal or near-normal hearing at low frequencies. Typical environmental sounds contain a significant amount of energy in the frequency range below 200 Hz, which provides constant sound stimulation and thus helps to prevent difficulties as a function of increased gain in the auditory system. Therefore, it is crucial to fit hearing aids with open molds to avoid blocking these low frequencies.⁸

5. Music therapy

Music therapy is a desensitization method that utilizes music spectrally modified according to the hearing characteristics of each patient to allow the masking of tinnitus and to facilitate relaxation at a comfortable listening level.⁷⁸ Davis PB     Music directly interacts with the limbic system, bypassing the slower linguistically-based processing in the auditory cortex.⁷⁸ Hearing thresholds decline substantially above 3 KHz among a typical sample of tinnitus patients. Therefore, spectral modification should include weaker sound energy in the lower frequency components of the music.⁷⁸

6. Tinnitus retraining therapy

Tinnitus retraining therapy (TRT) is a form of habituation therapy designed to help people who suffer from tinnitus. The main target of TRT is non-auditory systems, particularly the limbic and the autonomic nervous system. TRT is based on the assumption that tinnitus represents a side effect of the normal compensatory mechanisms in the brain. TRT uses naturally-occurring mechanisms of plasticity in the brain to achieve habituation to the physiological reactions to tinnitus and, subsequently, to achieve habituation to the very perception of tinnitus.⁸ Typically, habituation is achieved by repeating the sensory stimulus. However, this method cannot be directly applied to tinnitus because it is impossible to eliminate the reactions of the autonomic nervous system that act as a negative reinforcement. Therefore, TRT involves decreasing both the stimulus and the reinforcement, even though these remain present.⁸

TRT consists of two components: retraining counseling and sound therapy. Retraining counseling aims at helping patients to think of their tinnitus as a kind of neutral sound.⁸ Neutralizing tinnitus is achieved by providing valid information and showing that tinnitus is not associated with threatening pathology.²⁴ The creation of positive associations with tinnitus represents an additional way of neutralizing tinnitus. Descriptions like screeching, tearing, and steam jets should be replaced by benign, more peaceful descriptions, such as "music of the brain."⁸ Sound therapy aims at facilitating habituation at an unconscious level by decreasing the strength of the signal. By adding sound, the difference between tinnitus and background sound decreases.⁸ However, TRT is time consuming, requiring about 18 months to achieve observable stable effects. In addition, some patients do not achieve satisfactory results even after this long period of treatment. TRT requires patience and discipline from both the patient and a well-educated, experienced professional. ³⁰

7. Massage and stretching

Massage and stretching of the neck and masticatory muscles have been associated with significant improvement in tinnitus.⁶¹ Patients with somatic tinnitus may have symptoms of cervical spine disorders, including head, neck and shoulder pain as well as limitations in side-bending and rotation. Treatment of jaw and neck disorders has a beneficial effect on tinnitus. Injection of lidocaine in jaw muscles, such as the lateral pterygoid, also reduces tinnitus.⁷⁹

8. Electrical suppression

Electrical stimulation of the cochlea with 5000-pps pulse trains shows substantial or complete tinnitus suppression with either no perception or only a transient perception of the stimulus. A high rate of electrical pulses (5000-pps) restores spontaneous-like patterns of spike activity in the auditory nerve, and this may be how it suppresses tinnitus.⁸⁰

Trans-electrical nerve stimulation (TENS) of areas of skin close to the ear increases the activation of the dorsal cochlear nucleus through the somatosensory pathway and may augment the inhibitory role played by this nucleus on the CNS, thereby ameliorating tinnitus.⁸¹

V. Conclusion

Tinnitus is frequently a symptom of an associated disease process. Recent research using modern technology has examined tinnitus-related activity in the ear, auditory nerve, and auditory tracts of the brain. These studies have increasingly focused on exploring brain-related hypotheses. The complexity of the changes in the nervous system associated with tinnitus might explain why this condition has proved so resistant to treatment.³⁰ Although numerous therapeutic modalities have been tried, no consensus regarding effective therapeutic agents has emerged at this point. At times, no treatment represents the better alternative, mandating that clinicians deal with the pressure to do something without using prescriptions to placate patients.³⁰ Although treatment may not relieve tinnitus, accurate diagnosis and treatment are important for reducing the annoyance associated with tinnitus and for preventing additional disability. Furthermore, many randomized clinical trials have found that placebo effects are strong and these have been attributed, in part, to responses to attention.

Nevertheless, counseling represents an essential part of treatment, regardless of the management approach adopted for a particular patient. An informed explanation of tinnitus, together with reassurance, improves the condition of most patients over time. For those with persistent tinnitus, cognitive and behavioral therapy, augmented by pharmacologic intervention, might represent the most promising treatment regimen. Most importantly, a strong doctor–patient relationship underpins successful management and high levels of satisfaction among patients.

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Tinnitus being loud does not preclude habituation but only means that the patient may requirea longer period of adaptation. Tinnitus is rated as more severe when it consists of a complex of different and changing sounds. Dineen R, Doyle J, Bench J.Audiological and psychological characteristics of a group of tinnitus sufferers, prior to tinnitus management training.Br J Audiol. 1997 Feb;31(1):27-38. Hallberg LR, Erlandsson SI.Tinnitus characteristics in tinnitus complainers and noncomplainers.Br J Audiol. 1993 Feb;27(1):19-27.

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