Tinnitus review 원본

[byungin]

Tinnitus review

한병인 (두신경과 원장, 미국이명학회 회원)

Introduction

Tinnitus is the perception of sound in the absence of an external sound. Tinnitus aurium is ringing of the ears and tinnitus cerebri is noises of the head. The term tinnitus is usually used without qualification and refers to tinnitus aurium. Many normal people may experience a high-pitched ringing tinnitus after a slap across the head or close exposure to a sudden very loud noise. This tinnitus usually subsides within a few hours.

There are "patients who have tinnitus" and there are "tinnitus patients". The "patients who have tinnitus" are individuals who are not bothered by tinnitus. "Tinnitus patients" are those who need help due to tinnitus having affected their lives; their sleep, concentration, and quality of life. Tinnitus affects about 15 % of the world population [Martin WH, 1993] and is frequently associated with hearing loss, being present in 70-80 % of patients with ear disorders [Ito J & Sakakihara J, 1994]. The preval‎ence of tinnitus increases with age. People 65 to 75 years old have tinnitus more often than younger age group. Tinnitus is also a common symptom among children with hearing loss.

There are essentially two types of tinnitus; subjective and objective. Subjective tinnitus is characterized by an individual's perception of sound in the absence of any physical sound. Subjective tinnitus reflects an abnormality of the ear or the auditory nervous system. Subjective tinnitus is a symptom, not a disease. The cause often cannot be found, and even when a cause is found and treated, tinnitus may persist. Symptomatic treatment may then be the only option. Therapies are directed toward promoting habituation to the tinnitus and suppressing the associated anxiety, depression, and sleep disorder. Objective tinnitus are rare and is not a result of abnormal function of the auditory system but is caused by a physical sound generated in the body and sensed in the normal way. Objective tinnitus is caused by vascular abnormalities (e.g., arteriovenous malformations, glomus tumor, aneurysms, great vessel bruit, benign intracranial hypertension, or high cardiac output), temporomandibular joint disorders, as a result of spontaneous contraction of middle ear muscles, palatal myoclonus, tensor tympani muscle spasm, or a partulous eustachian tube. Tinnitus associated with vascular origins is pulsatile with the frequency of the pulsation being the same as the individual's heart rate. The other tinnitus may present as a clicking sound.

Recent research has proposed that there are two distinct categories of subjective tinnitus, otic tinnitus caused by disorders of the inner ear or the acoustic nerve, and somatic tinnitus caused by disorders outside the ear and nerve, but still within the head or neck. It is further hypothesized that somatic tinnitus may be due to "central crosstalk" within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.

Tinnitus can be distinguished into two distinct types according to the effects reported by the patient. Compensated Tinnitus is that the patient registers the sounds, but can cope with them so that they cause little or no psychological strain and the patient’s quality of life is not substantially affected. Decompensated tinnitus is the most severe form of tinnitus. The sufferer hears sounds caused by "interference" in the brain’s hearing system. The tinnitus has become uncontrollable. This interference is caused by the brain trying to use other sounds to drown out those originating in the inner ear. If emotional overlay and stress cause this "interference" to become excessive, constant activation of the "interference" in sections of the temporal lobe of the auditory cortex and "decompensated tinnitus" will result.

Clinical Manifestations

1, Nature of subjective tinnitus

Subjective tinnitus is perceived as coming from one ear only, from both ears with different or equal intensity, or from inside the head. Left-ear tinnitus occurs more often than right-ear tinnitus, and is also heard in the head. Patients experience more severe tinnitus in the ear with the greater hearing loss. Tinnitus may be constant or may vary in severity from time to time. Tinnitus often associated with hypersensitivity to sound and an exaggerated perception of loudness (hyperacusis). Hyperacusis has been reported to occur in about 40 % of tinnitus patients (Coles, 1996; Jastreboff, 2000). Patients may perceive some sounds as distorted either in time or in pitch, so that one sound is heard as two or painful, which is more troublesome than the tinnitus itself. A cochlear type of hearing loss can be recognized by eliciting the symptom of recruitment and diplacusis. Recruitment is defined as a heightened perception of loudness once the threshold for hearing has been exceeded. Diplacusis refers to a defect in frequency discrimination that is manifest by a lack of clarity of spoken syllables or by the perception that music is out of tune and unpleasant. Patients may complain that their voice sounds hollow or and other sounds are muffled (autophonia). Patients may be disturbed by normal muscular sounds such as chewing, tight closure of the eye, or clenching of the jaws, since the masking effect of ambient noise is lost. Strong sounds can cause tinnitus to increase. The level of annoyance caused by tinnitus is not directly related to its perceived loudness. The complaint of tinnitus does not correlate with the acoustic characteristics of the perceived sound [Hallam R, 1984], but there is a significant correlation with psychological symptoms [McKenna L, 1991]. The most common problems associated with tinnitus is sleep disturbance.

이호기 등(2004)의 조사에 의하면 이명을 느끼는 부위가 한 방향 51 %, 양방향 35 %, 머리 속 또는 위치가 어딘지 모르는 경우가 14% 이었고, 이명을 한 가지 소리로 인식하는 경우는 62 %, 두 가지 이상의 소리로 느끼는 경우가 38 %이었으며,  매미 소리 26 %, 바람 소리 17 %, '윙' 소리가 17 % 였다. 이명이 발생할 당시에 있었던 일은 스트레스 35.6 %, 피로 42 %, 소음노출 21.4 %, 정신적 쇼크 15 % 등이었다. 이명과 관련된 부정적 생각으로는 청력소실에 대한 염려 51.8 %, 이명이 커질 것이라는 염려 51.5 %, 잠들 수 없을 것이라는 생각 17.5 % 등이었다. 저자의 경험에 의하면, 이명은 시작 시점을 모르는 경우가 가장 많았고, 나머지는 주로 낮에 깨어 있을 때 시작하였으며, 수면 중이나 기상 시에 시작하는 경우는 없었다. 유발인자는 정신적 스트레스과 육체적 과로 등이었고. 불면을 극복하는 방법으로 들판에서 우는 개구리 소리를 듣거나, 라디오나 TV 소리를 듣는 방법 등이 있었다.  

2, Sound characteristics of subjective tinnitus

Tinnitus cannot be substantiated of measured objectively. Most patients with tinnitus explain a thrill chirping sound, crickets, or a roaring noise like that made by a jet engine. Matching and masking of the perceived sound can be carried out, but this is also subjective. Validity, reliability of tinnitus pitch and loudness match, and treatment outcomes are difficult to ascertain. Thus, it is of little importance to know the nature of the sound perceived, such as whether the tinnitus resembles a high-frequency or low frequency sound, because no relationship has been established between the these factors and the anatomic location of abnormality. Frequently the patient with a conductive hearing loss has tinnitus which tends to be of low pitch. Tinnitus associated with Meniere's disease is low-pitched and continuous and is described as a hollow seashell sound or very loud roaring. Tinnitus with otosclerosis is low-pitched and is described as a buzzing or roaring sound and may be continuous or intermittent. Tinnitus with acoustic neuroma is a high-pitched ringing or like the sound of steam blowing from a teakettle. Continuous bilateral high-pitched tinnitus often accompanies chronic noise-induced hearing loss, presbycusis, and hearing loss due to ototoxic drug. If the tinnitus is rhythmic, the patient should be asked whether it is synchronous with the pulse or with respiration. A blowing sound that coincides with inspiration, expiration or both can result from an abnormally patent eustachian tube, and this type of tinnitus is particularly common after recent weight loss or debilitating illness. 김성희 등(1995)은 환자가 호소하는 이명의 성상대로 분류를 하였는데 Single continuous sound로는 Humming(윙) 25.0 %, Hissing (쉐) 24,4 %, Buzzing (매미소리) 21.8 %, Rinning (웅) 5.1 % 로 나타났고, Single interrupted sound로는 '앵 앵' 3.2 %, '삐 삐' 2.6 %, '쏵 쏵' 1.3 % 등으로 나타났다. 또한, 이명에 의한 고통은 이명의 크기와 비례하는 것으로 나타났다. 저자에게 호소한 이명의 특징들을 분류하면, (1) High pitch insect: 매미, 귀뚜라미, 여치, 쓰르레기, 벌, 모기, 애기 울음,  (2) High pitch aero: 스프레이, 제트엔진, 폭포, 소나기, 바람.  증기기관차, 바싹 거린다, 낙엽 밟는 소리, (3) High pitch metallic: 쇠 가는 소리, (4) Low pitch mechanical: 형광등, 냉장고 모터, 보일러 모터, 탈곡기 돌아가는 소리, 자동차 엔진 (5) Low pitch beating: 북소리, 쇠젓가락 두드리는 소리, 바늘 시계 소리, 덜거덕, 물 끓는 소리, 등이었다. 큰 소리를 들으면 귀에서 덜거덕 소리가 난다는 환자도 있었다. 

3, Aural fullness

Aural fullness is frequently associated with tinnitus, and can be due to several different problems. Eustachian tube dysfunction, middle ear fluid and ear infection are only the most obvious possibilities. Less obvious possibilities include hearing loss (for example, sudden sensorineural hearing loss) and a referred sensation of fullness.

In the case of aural fullness, this could be referred from the nasopharynx. Infection or tumor in the nasopharynx could cause a referred sense of fullness in the ear. [Reference; The Medical Consumer's Advocate. Fullness in the ears (aural fullness or pressure). Available URL from:http://www.doctorhoffman.com/wwfull.htm]

Etiology

1, Causes of subjective tinnitus

Tinnitus is a symptom and may have many diverse causes. Tinnitus may be the first symptom of disorder, appearing long before any other symptoms, including hearing loss. Continuous unilateral high-pitched tinnitus often may be the first symptom of an acoustic neuroma, preceding loss of hearing by several years. The most preval‎ent known cause is noise exposure, and idiopathic is about 25 %, while 75 % of people with an acquired profound hearing loss have tinnitus. Auditory damage from excessive noise exposure may be directly related to tinnitus. Long-term noise exposure causes some hair cell damage that cannot be audiometrically measured. The National Study of Hearing (Coles, 1984) found that tinnitus preval‎ence was 7.5 % in people who have had no noise exposure, compared to 20.7 % in people who have had high lifetime noise exposure. There are noises in our lives including traffic noise, concert, airplanes, power tools, etc. However, some patients complain of tinnitus without hearing loss measured on the standard audiometer.

Conditions or triggers are physical or emotional stress, fatigue, aging, ototoxic drugs, Meniere's disease, head or neck trauma, temporomandibular joint disorder, and allergies. The most important predicting factor is hearing impairment. Other predicting factors are a history of childhood otitis media, chronic serous otitis media, and reported difficulty with speech in noise. The onset of tinnitus may be related to direct mechanical injury such as aural syringing or barotrauma, even without obvious trauma. Conductive hearing loss (e.g. from infection, effusion, cerumen and especially otosclerosis) may attenuate background noise and result in tinnitus. Middle ear pathology is rarely associated with tinnitus but may enhance an underlying tinnitus caused by cochlear dysfunction [Hinchcliffe R & King PF, 1992]. Smoking, alcohol, general health factors such as cardiovascular problems, diabetes, thyroid disease and cancer are anecdotally shown to have effects on tinnitus. 저자가 경험한 유발인자들로는 고막을 건드렸을 때, 노래방이나 사격으로 인한 소음, 비행기 여행이나 등산으로 인한 기압변화 등이었다.   

The followings are causes of tinnitus.  

 *Tinnitus with hearing loss

1, Acute acoustic trauma such as intense sound exposure with partial recovery of hearing over a few days.

2. Chronic progressive hearing loss due to presbycusis, chronic acoustic trauma, hereditary hearing loss can be considered together.

3, Autoimmune inner ear disease is like chronic progressive hearing loss except the progression of the hearing loss is measured in weeks or months rather than in years.

4, Medication-related (including withdrawal syndrome) tinnitus with hearing loss is caused by aminoglycoside and loop diuretics.

* Tinnitus without hearing loss

1, Somatic (craniocervical) tinnitus is diagnosed when the patients can somatically modulate their tinnitus by clenching the teeth or pushing on various places on the head. Most commonly the tinnitus gets louder, but many times the tinnitus become quieter, particularly if the tinnitus is unilateral. These include temporomandibular joint syndrome and whiplash injury. 

2, Trauma can be suspected to be the most probable cause if head trauma and tinnitus are chronogically associated. The association with trauma becomes less certain when some or these elements are missing, such as a delay between the trauma and the onset of the tinnitus.

3, Numerous pahrmacologic agents can produce tinnitus without hearing loss, which include salicylates, aminoglycosides, quinidine, indomethacin, propranolol, levodopa, carbamazepine, aminophylline and loop diuretics. The auditory system has one of the highest spontaneous discharge rates in the body. Drugs that increase the spontaneous discharge rate (e.g. salicylates) may cause tinnitus in this way. Food additives such as salt, caffeine, alcohol, monosodium glutamate, saccharin, aspartame, and simple sugars can exacerbate tinnitus. Caffeine and aspirin in usual dosages do not cause or exacerbate tinnitus.

4, Acoustic neuromas invariably are slow growing and rarely present with normal hearing, so it is reasonable to simply follow patients by repeating audiograms every 3 to 6 months (Fig. 1).

2, Causes of objective pulsatile tinnitus

(1) Nonvascular causes

(a) Coarse intermittent sounds coincident with jaw or head movements are typical of a foreign body such as cerumen, water, or hair resting against the tympanic membrane.

(b) Fluttering sound is associated with idiopathic stapedial muscle spasm, especially when the fluttering is associated with facial movements. This condition, in contrast to palatomyoclonus, tends to be a rough, rumbling, or crackling noise often accentuated or triggered by external noises such as voices, rattling of paper, or running water. The symptoms generally follow this exposure, are brief and intermittent, and rarely become disruptive and prolonged. Diagnostic studies include variable-intensity tympanometry in an effort to stimulate the spasm and aid diagnosis, and acoustic reflex testing which may demonstrate a prolonged, continued increased impedance during and after the sound stimulus [Marchiando and Albert, 1983]. Primary treatment consists of muscle relaxants, clonazepam or diazapam. Because the symptoms may last only 2 or 3 months and then disappear for long periods, the use of surgery to divide the stapedius tendon should be used very conservatively [ Schleuning, Alexander J., Tinnitus, In Gates, editor: Current Therapy in Otolaryngology Head and Neck Surgery, 5th ed., Mosby, 1994].

(c) Clicking tinnitus may be due to contraction of the middle ear muscles such as tensor tympani or stapedius, or the nasopharyngeal muscles controlling the patency of the eustachian tube. If the clicking is heard bilaterally and irregularly, it is usually associated with palatomyoclonus. These contractions can range between 10 and 240 per minute. This disorder is seen in young patients, mostly within the first 3 decades of life. Brainstem infarctions, multiple sclerosis, trauma, and syphilis have also been reported in association with palatal myoclonus. Patients may also complain of fullness in the ear and distortion of hearing, and may have histories of other muscle spasm, including postoccipital spasm, temporomandibular joint problems, and blepharospasm. Diagnosis is made by auscultating the ear canal with a Toynbee tube for audible clicking. Palatal myoclonus may not be observable on intra-oral examination, and may be inhibited with the mouth open.

Myoclonic contractions of the tensor veli palatini, levator veli palatini, salpingopharyngeus, and superior constrictor muscles can result in objective pulsatile tinnitus. Stapedial myoclonus has also been reported as a cause of pulsatile tinnitus. Myoclonus persists during sleep.

If no sound or tympanic movement can be detected and the clicking is strictly unilateral, then this subjective form of clicking tinnitus can always be suppressed with carbamazepine. The clicking is irregular and the clicks sometimes run together, so that some patients describe as sounding like a typewriter. Pulsatile tinnitus may result from otosclerosis and may respond to stapedectomy.

OBJECTIVE NONPULSATILE TINITUS

Objective tinnitus can also produced by high-level spontaneous otoacoustic emissions (SOAEs) which can be heard by others but the patient often cannot hear these noises. The normal cochlea produces low-intensity sounds called otoacoustic emissions (OAEs). These sounds are produced specifically by the cochlea and, most probably, by the cochlear outer hair cells as they expand and contract. When present in humans, SOAEs usually occur in the 1000- to 2000-Hz region; amplitudes are between -5 and 15 dB SPL. Otoacoustic emissions may be detected by using sensitive microphones placed in the external auditory canal. Some individuals have multifrequency SOAEs over a broader frequency range. Although, spontaneous otoacoustic emissions (SOAEs) are not usually associated with tinnitus, high-level SOAEs may occur which can be heard by others but the patient often cannot hear these noises. Such emissions are very uncommon but may coexist with sensory hearing loss. High-level SOAEs are more common in children than in adults. Identification of these patients is considered important in that aspirin can abolish these emissions - and may relieve tinnitus if a non-ototoxic dose can be established.

(2) Vascular causes

If tinnitus is pulsatile, the next step is to determine if it is related to the cardiac cycle. One of the most common forms of objective tinnitus is a self-audible bruit, the origin of which is the turbulent flow of blood in large vessels of the neck. Sismanis A and Smoker WR (1994) reported that, in 100 cases of pulsatile tinnitus, intracranial hypertension, glomus tumor, and carotid disease were found to be the most common causes. An associated fluctuating hearing loss raises the possibility of microvascular compression of the auditory nerve causing the pulsatile tinnitus. A purple coloration of the tympanic membrane is diagnositic of a glomus tumor (Fig. 2). A red mass behind the tympanic membrane is evidence for an aberrant carotid artery, dehiscent jugular bulb, or a vascular tumor. A unilateral conductive hearing loss with ipsilateral pulsatile tinnitus suggests otosclerosis. High cardiac output states such as anemia or hyperthyroidism can cause bilateral pulsatile tinnitus. Pulsatile tinnitus is also result from antihypertensives such as enalapril or verapamil.

 (a) ARTERIAL CAUSES

Atherosclerotic carotid artery diseases are common causes of tinnitus. Intracranial vascular abnormalities such as dural arteriovenous fistulae are uncommon causes of tinnitus. A dural arteriovenous fistula (AVF), also called a dural arteriovenous malformation, is an abnormal direct connection between a meningeal artery and a meningeal vein or dural venous sinus (Fig. 3). A dural AVF is usually become symptomatic during the fifth or sixth decade of life. Pressure on the site of AVF obliterates the tinnitus (Fig. 4). The transverse and sigmoid sinuses are the most common dural sinuses involved, followed by cavernous sinus. AVFs are usually acquired and thought to result from dural venous thrombosis which may be caused by trauma, obstructing neoplasm, surgery, or infection, or it may occur spontaneously. As the thrombosed segment recanalized, ingrowth of dural arteries takes place and artery-to-sinus anastomoses are formed. Mortality from hemorrhage of a dural AVF is 10 to 20 % .In case with retrograde drainage into the cortical veins, the chance of subarachnoid or parenchymal hemorrhage is much higher.

(b) VENOUS CAUSES

Pseudotumor cerebri syndrome is the most common cause of venous pulsatile tinnitus in obese female patients. Although headache or visual disturbance are the classic presentations, pulsatile tinnitus alone or in association with hearing loss, dizziness, and aural fullness has been reported as the main manifestations of this syndrome. Light digital compression over the ipsilateral internal jugular vein results in immediate cessation of this tinnitus. Auditory brainstem evoked responses (ABR) may present prolonged interpeak latencies.

venous diverticulum with stricture,
 transverse sinus stenosis.
transverse sinus venous diverticulum
dominant  sigmoid sinus
dominant jugular vein

(3) Idiopathic pulsatile tinnitus

Idiopathic or essential pulsatile tinnitus and venous hum are synonymus used interchangeably in the literature to describe patients with pulsatile tinnitus of unclear cause. The most common age group of patients with idiopathic pulsatile tinnitus is between 20 and 40 years, and there is marked female preponderance. A possible cause of idiopathic pulsatile tinnitus is believed to be turbulent blood flow produced in the internal jugular vein as it curves around the lateral process of the atlas. Venous hums are worsened by Valsalva's maneuver, deep breathing and turning away from the afflicted ear, and lessened by turning toward the side affected. If the patient can obliterate the tinnitus with localized pressure in the periauricular region, an emissary vein is probably accounting for the tinnitus (venous hum) (Fig 5). Management consists simply of reassuring the patient and treating the underlying disorder.

3, Pathophysiology of subjective tinnitus

One theory is that cochlea may produce tinnitus. The auditory system has one of the highest spontaneous

 discharge rates in the body. Drugs that increase the spontaneous discharge rate (e.g. salicylates) may cause tinnitus in this way. Others have suggested that an alteration in efferent inhibitory neurons firing rate may result in increased firing of adjacent afferent neurons which could be perceived as tinnitus. Such could be the case where acoustic trauma or Meniere's disease has resulted in an area of local hair cell damage. In an effort to improve sound detection, efferent inhibitory neurons might decrease their firing in an effort to increase local sound reception. Because the area of dis-inhibition is spread over an adjacent area the hyperactivity of hair cells adjacent to the damaged area could be percieved as tinnitus - in a frequency close too the area of damage

 ( the so-called edge effect). Zenner HP and Ernst A (1993) mentioned about the functional alteration of ion channels of outer and inner hair cell membrane with blockage of sodium through apical membrane channels. This impairs the cochlear electromechanical transduction [Haginomori S, 1995] and results in an overshoot in the cochlear nerve fibers [Martin WH, 1993]. An alteration in efferent inhibitory neurons firing rate may result in increased firing of adjacent afferent neurons which could be perceived as tinnitus.

The outer hair cells and the apex of cochlea may be more vulnerable to ischemia than the inner hair cells and the base of the cochlea because of the proximity of the blood vessels (Fig. 6).

Another theory is that tinnitus is triggered by damage to the cochlea but is generated by the central nervous system. A feedback loop resulting from the central auditory system attempting to compensate for a peripheral hearing loss may result tinnitus.

Jastreboff and Hazell (1993) hypothiesized that tinnitus results from discordant damage to the inner and outer hair cells. When the outer hair cells are damaged, the inner hair cells are deprived of information that they had been receiving from the outer hair cells, and that deprivation can affect the neural output from the inner hair cells that is sent up to the brain. The altered output can create a pattern of nerve fiber discharges, and the brain interprets as a tinnitus. Moller (1999) and Lagner and Wallhauser-Franke (1999) reported evidence that while the initial site of lesion might be within the cochlea, the tinnitus itself is created centrally in the auditory cortex and the limbic system. Even when the cause in the ear ceases to exist, the central closed-loop continues. This kind of tinnitus is also known as “centralised tinnitus“, and it works on the same principle as the “phantom pain” which is often experienced by amputees. This pathophysiology also has many similarities with central neuropathic pain.

Kaltenbach JA (2006) reported that tinnitus-related hyperactivity in the dorsal cochlear nucleus (DCN) has been found to correlated with damage to outer hair cell and DCN is a possible source of tinnitus-generating signals. This hypothesis was originally developed on the basis of evidence that the DCN becomes hyperactive following exposure to intense noise.

Diagnosis

1, Initial eval‎uation of tinnitus patients

The initial task of the examining physician is to obtain a detailed description of the nature of the tinnitus. The features that must be ascertained are (1) its quality, particularly whether or not it is pulsatile, (2) its location, whether it is heard in one ear or not, (3) its variability, whether it is intermittent or constant, and (4) its pitch, whether it is predominantly low or high frequency in character. The eval‎uation of a tinnitus complaint include any association with medications, psychosocial stressors, a concurrence medical illness, other auditory, vestibular, or neurological complaints, or a head, neck, or dental disorders.

Exacerbating and remitting factors should be sought including diurnal variations in the tinnitus. The tinnitus exam should include inspection of the teeth for evidence of bruxism, listening around the ear and neck for sounds similar to their tinnitus, and palpation of the cranio-cervical musculature for muscle tension and tenderness with special attention to any asymmetries.

(2) Basic office examination of hearing

Whether or not the patients' complaint is one of hearing loss, a basic assessment of hearing should be preceded. A patient with a conductive hearing loss has good discrimination ability provided the speech is made loud enough. The patients with a sensorineural impairment may speak with excessive loudness of voice in situations where a loud voice is inappropriate. People with a hearing loss in the high frequency region have difficulty in understanding speech in a noisy environment. The hearing ability for high frequency is often lost in the elderly, and the ability to discriminate speech sound is decreased. Thus, it is important to use lower voice tone in speaking to an elderly person.

It the external canal is occluded by cerumen, it can be removed with warm water lavage using a syringe (without needle) with a piece of rubber tubing affixed to the end. Before irrigation, mineral oil, baby oil, or glycerin can be used to soften wax in the ear. Hydrogen peroxide may aid in the removal of wax.

Tuning fork test of air and bone conduction is performed with the Weber and Rinne test (Fig. 7). Turning forks at a frequency of 256 or 128 Hz produce the vibration which the patient may mistake for sound. Thus, the 512 Hz tuning fork is preferred. Normal subjects can hear the fork about twice as long by air as by bone conduction. Weber test is performed by placing the stem of a tuning fork on the forehead, nasal bone or a central incisor, and the patient is asked where he or she hears the tone. In unilateral hearing losses, lateralization to the poorer-hearing ear indicates an element of conductive impairment in that ear. Lateralization to the better-hearing ear suggests that the problem in the opposite ear is sensorineural. Rinne test is performed by placing the stem of a tuning fork on the mastoid process for testing bone conduction, and holding the turning fork about 2.5 cm lateral to the tragus for air conduction. The patient's eyeglasses should be removed. A positive Rinne is defined by that air conduction is heard better than bone conduction, which means normal hearing or sensorineural hearing loss. A negative Rinne is defined by that bone conduction is heard better than air conduction, which means conductive hearing loss.

(3) Basic audiometry

Most tinnitus patients also have some degree of hearing loss. Assessment of hearing sensitivity, loudness tolerance, and tinnitus should be routinely performed. Audiometry which is consists of a battery of test: 1, Pure tone thresholds; 2, Speech recognition or reception thresholds (SRT); 3, Tinnitus pitch and loudness matching; 4, Minimum masking levels (MMLs); 5, Residual inhibition; 6, Loudness discomfort levels (LDLs) to speech and pure tone.

Pure tone thresholds are established for frequencies of 250-8000 Hz. Although the ear of a young person with normal hearing is able to detect sound waves with frequencies varying from about 20 to 20000 Hz, the range of greatest sensitivity is between 2000 and 3000 Hz. The intensity of sound is measured in units called decibels (dB). The decibel scale begins at 0 dB, which is the intensity of the sound that is least perceptible by a normal human ear. The decibel scale is logarithmic, so that a sound of dB is 10 times as intense as the least perceptible sound. A whisper has an intensity of about 40 dB, and heavy traffic produces about 80 dB. Hearing is considered normal when threshold sensitivity is 0-25 dB for frequencies of 250-8000 Hz. Responses at 500 Hz, 1000 Hz, and 2000 Hz are averaged together to compute the pure tone average. Responses greater than 25 dB are classified by degree as mild (25-40 dB), moderate (40-55 dB), moderately severe (55-70 dB), severe (70-95 dB) and profound (>95 dB).

Symbols being used for audiometry are are right air conduction:O, left air conduction:X, right bone conduction:<, left bone conduction:>, right bone masking:[, and left bone masking:] (Fig. 8). With conductive hearing loss, air conduction is impaired but bone conduction remains normal, producing air-bone gap on the audiogram (Fig. 9). Measurement of bone conduction always requires masking of the nontest ear. With sensorineural hearing loss, both air and bone conduction are impaired. Typical audiogram patterns seen in patients with sensorineural hearing loss are notched pattern of noise-induced hearing loss (type A), downward-sloping pattern of presbycusis (type B), low-frequency trough of Meniere's syndrome (type C), and V-pattern of congenital hearing loss (type D) (Fig. 10). 김성희 등 (1995)에 의하면, 이명을 호소하는 환자들 중에 순음청력검사에서 장상청력을 가진 환자가 47.3 % 였으며, 난청을 동반한 환자는 52.5 % 였다.

Speech reception thresholds (SRT) is the lowest intensity at which an equally weighted two-syllable word (e.g.,학교, 감자) is understood approximately 50 % of the time. The pure tone average and speech recognition threshold should be within 7 dB. A patient with a conductive hearing loss has good discrimination ability provided the speech is made loud enough. Frequently the patient with a conductive hearing loss has tinnitus which tends to be of low pitch. The patients with a sensorineural impairment may speak with excessive loudness of voice in situations where a loud voice is inappropriate. People with a hearing loss in the high frequency region have difficulty in understanding speech in a noisy environment. Recruitment is an abnormally rapid growth of loudness with an increase in intensity, and cause intense sounds to be perceived as uncomfortably loud. The alternate binaural loudness balance (ABLB) test provides a direct measurement of loudness recruitment if the hearing loss is unilateral. A short-duration tone is presented alternately to each ear. The intensity of the tone to one ear is fixed, while the intensity to the other ear is adjusted until the listener perceived the loudness of the two tones to be equal. Recruitment is usually associated with sensory loss of cochlear origin, which constitutes the majority of sensorineural hearing losses. Obtaining a Tinnitus pitch and loudness match is an attempt to quantify the patient's tinnitus. Most patients have tinnitus in the 4000-8000 Hz range, so that most patients perceive 1000 Hz as lower in pitch than their tinnitus frequency. Initial testing level is 10-20 dB SL at normal-hearing frequencies, and 5-10 dB SL at hearing-loss frequencies. The patient with sensorineural hearing loss reports a constant ringing or buzzing noise, and the pitch of tinnitus tends to be higher than in conductive impairment. The degree of hearing loss of a patient cannot determine the severity of tinnitus.

Nodar RH and Graham JT (1965) remarked that the pitch of tinnitus associated with a conductive hearing loss is of low frequency (median of 490 Hz, with a range of 90 to 1450 Hz). That which accompanies sensorineural hearing loss is higher (median of 3900 Hz, with a range of 545 to 7500 Hz). This rule does not apply to Meniere’s disease, in which the tinnitus is described as a low-pitched whoosh, buzz, or roar (median frequency of 320 Hz, with a range of 90 to 900 Hz).

김성희 (1995) 등에 의하면, pitch match에 있어서 순음양상 (pure tone nature)이 88.8 % 였으며, 협대역잡음양상 (narrow band noise)이 10.4 % 였다. 주파수별로는 4000-6900 Hz 사이가 49.6 %로 가장 많았고, 0-1900 Hz 사이가 21.7 %, 2000-3000 Hz 사이가 21.7 %, 7000 Hz 이상은 6.8 % 였다. Loudness match에서는 0-3 dBSL가 42.1 %로 가장 많았으며, 4-6 dBSL 사이가 19.5 %, 7-9 dBSL 사이가 3.0 %, 10-12 dBSL 사이가 13.5 %, 13-15 dB 사이가 7.5 %, 16 dBSL 이상이 14.4 % 였다.

Obtaining the Minimum Masking Levels (MMLs) determines the minimum level of broadband noise that will mask a patient's tinnitus. The lower MML, the more likely the patients will achieve success with masking. With tinnitus retraining therapy (TRT), MMLs have been shown to become smaller over time in association with treatment efficacy (Jastreboff, Hazell, 1994). It is recommended the use of a 2-12 KHz band of noise for determining MMLs. Many central auditory lesions are not be demonstrated by conventional audiologic measurements. Residual inhibition test consists of presenting the noise at 10 dB above the MML for 60 seconds. After turning off the noise, the majority of patients will report that their tinnitus is reduced in loudness lasing 45-60 seconds. 김성희 등 (1995)에 의하면, Residual inhibition 에 의하여 이명이 소실되거나 감소하는 경우는 85.4 % 였고, 크기의 변함이 없거나 오히려 증가하는 경우는 14.5 %였다. 고의경 (1990) 은 순음보다는 대역잡음이나 백색잡음에서 Residual inhibition의 출현율이 높았으며, 차폐역치보다 30 dB 큰 소리를 이용하였을 때 70 % 이상의 출현율을 보고하였다.

Loudness discomfort levels (LDLs) is to determine the level of each sound just below its level of physical discomfort. LDLs testing is achieved by presenting a 1000 Hz tone at the approximate most comfortable level for about 2 seconds, and the patient indicates if the tone can be made louder. Each successive level is raised 5 dB until the patient signals that the tone can only be listened to comfortably for a few seconds. That level is recorded as the LDL for 1000 Hz. For each subsequent test frequency, the starting level should be about 20 dB below the previous frequency's LDL. Many tinnitus patients have difficulty tolerating the loudness of sounds that the average person can tolerate without difficulty. Minimum testing should establish pure tone LDLs at octave frequencies between 1000 and 8000 Hz. Patients with normal loudness tolerance do not experience discomfort when listening to short-duration audiometer pure tone up to about 100 dBHL. The LDLs can be plotted on the audiogram, which should be done along with an explanation of the concept of dynamic range. The location of the tinnitus match on the audiogram closer to the threshold curve and farther from the LDL curve will provide further evidence that the tinnitus is a weak signal. In addition, if sound tolerance is a problem, plotting the LDLs on the audiogram will quantify the problem (Fig 11).

(4) Brainstem Auditory Evoked Potentials (BAEP)

 The auditory nerve in human is approximately 2.5 cm long. The absolute latency of the BAEP waves is dependent on the intensity of the click stimulus. The BAEP reflects excitation mainly of the brainstem auditory pathways on the stimulated side. For clinical purpose, wave I, III, and V have been used to localize lesions to the area between acoustic nerve and upper brainstem (Fig. 12). Wave V is most robust, often being identifiable at only 10 dB above hearing level. At 70 dB above hearing level, all waves are identifiable (Fig.13). Interpeak latencies (IPLs) are relatively immune to peripheral hearing loss, they are preferred to measurements of peak latencies in neurologic studies. BAEP measurements are particularly useful for early detection of acoustic neuroma. The most common abnormality of acoustic neuroma is absence of all waves beyond wave I (Fig. 14). For small tumors with minimal or no detectable hearing loss, prolongation of the IPL I-V is the most common finding. A long latency of wave V with normal interpeak latency (IPL) I-V is suggestive of a peripheral lesion. However, interpeak latencies (IPLs) I-III and I-V can be increased when the delay starts with wave II (Fig. 15). The wave V and wave III must be used instead of IPLs if wave I and other waves preceding wave V can not be distinguished. Absence of all BAEP waves or increased latency of all BAEP waves with normal IPLs may be due to a reduction in stimulus intensity caused by technical problems, hearing loss, or a distal acoustic nerve lesion. Severe lesions of the acoustic nerve may abolish the BAEP entirely or leave only wave I intact. Less severe lesions of the acoustic nerve may increase the latency of BAEP wave, starting either with wave I or with wave II. Absence of all waves beyond wave I or wave II provides clear evidence for a lesion involving the proximal acoustic nerve or the pontomedullary region of the brainstem. Lesions of the lower brainstem reduce and delay BAEP waves starting with wave II or III which may increase IPLs I-III and I-V. Lesions of the upper brainstem reduce and delay wave IV and V which may increase IPLS III-IV and I-V but spare IPL I-III. Bilateral absence of all waves after wave I may be seen in brain death.

(5) Work-ups for pulsatile tinnitus

Complete blood count and thyroid funciton tests should be obtained in cases of suspected anemia and hyperthyroidism which are high cardiac output states. Duplex carotid ultrasound should be obtained in suspected cases of atherosclerotic carotid artery disease.

For patients with normal otoscopy, MRA/MRV(magnetic resonance venography) in conjunction with MRI should be obtained. Small ventricles or empty sella are findings of pseudotumor cerebri syndfome. Dilated cortical veins on MRI is suggestive of an AVM. Dural venous sinus thrombosis can be diagnosed with MRV.  In patients with normal MRI/MRA/MRV associated with objective arterial pulsatile tinnitus or head bruit, carotid angiography should be considered to exclude dural AVF and fibromuscular dysplasia. For patients with a retrotympanic mass, high resolution temporal bone CT should be obtained. This can detect glomus tympanicum, aberrant internal carotid artery, or jugular bulb abnormalities. For patients with glomus jugulare tumors, CT examination of the neck should be obtained to assess for additional chemodectomas along the carotid arteries.

Treatment

When a specific cause is not identifiable, it is generally considered that one form of treatment for tinnitus is not enough, leaving several approaches: psychological support, medical treatment, alternative medications, and audiologic treatment.

(1) Initial counseling and psychological support

 Explanation of test results is critical to patient care. In audiogram, loudness matches are usually less than 10 dB SL sensation level. Patients can be counseled that tinnitus is a weak signal by plotting the tinnitus match on the audiogram. Loudness discomfort levels (LDLs) can be effective in showing that tinnitus is a weak signal. All tinnitus patients must be countered by an explanation of tinnitus together with reassurance that most cases improve with time.[Coles RRA, 1987] The patients should understand the tinnitus does not cause hearing loss and vice versa. Giving attention to patient's problem, explaining the pathophysiology of tinnitus, discussing hearing problems, and giving reassurance are helpful for many patients. Tinnitus patients generally have an improvement resulting from the awareness of treatment although counseling for tinnitus can be effective simply because of the Hawthorne effect. The Hawthorne effect is a phenomenon in industrial psychology first observed in the 1920s that refers to improvements in productivity or quality resulting from the mere fact that workers knew they were being studied or observed. The purpose of the tinnitus questionnaire is to give the patient an opportunity to talk, to quantify the subjective loudness of tinnitus the patient experiences, and to help determine treatment outcomes. 이호기 등(2004)은 이명 재훈련 치료에서 지도 상담의 효과를 다음과 같이 설명하였다. 상담을 통해서 이명에 대한 불필요한 공포를 없애고, 이명현상에 적응할 수있는 계기를 마련해 주며, 이명에 대하여 자율신경계와 감정의 반응을 긍정적으로 변화시켜서 궁극적으로는 변연계와 자율신경계의 습관화 (habituation)를 유도하고, 나아가서 이명에 대한 인식(perception)을 습관화한다.

초기 면담 때 이명에 대한 주관적 평가를 환자로 하여금 하게 한다. 다음은 이명의 정도를 평가하는 항목들이다.

이명의 정도 평가항목

(1) Loudness of tinnitus  0~10

(2) Awareness of tinnitus  0~100 %

(3) Annoyance of tinnitus  0~10

(4) Effect of tinnitus on life (tinnitus handicap questionnare)

호전: 4 항목 중 2 항목 이상에서 2점 이상 또는 20 % 이상 감소된 경우. 악화:2 항목 이상이 나빠진 것

TInnitus scoring scale (Ohsaki et al,1988)

1, 시끄러운 곳에서도 이명(耳鳴)이 들립니까? 항상(1), 가끔(0.5), 아니오(0)

2, 주무실 때 방해될 정도로 크게 들립니까?  항상(1), 가끔(0.5), 아니오(0)

3, 잠은 쉽게 못 드십니까? 항상(1), 가끔(0.5), 아니오(0)

4, 조용한 곳에서는 이명이 들립니까? 항상(1), 가끔(0.5), 아니오(0)

5, 일상 생활 하실 때에 이명이 들립니까?  항상(1), 가끔(0.5), 아니오(0)

6, 직장생활에 방해가 됩니까? 항상(1), 가끔(0.5), 아니오(0)

7, 일 할 때 이명을 잊어버릴 수 없습니까? 항상(1), 가끔(0.5), 아니오(0)

Jastreboff PJ et al (1996) suggested categorization for treatment of the patients with TRT (Table 1).

(2) Medical treatment for tinnitus

Medications are readily relieve troubling symptoms associated with tinnitus such as insomnia, depression, and anxiety. Medications rarely abolish the tinnitus but often they can quiet the tinnitus. The follwoing medications can provide relief for some tinnitus patients.

Alprazolam was found to help reduce the anxiety associated with tinnitus and promote sleep, and quiet the tinnitus. Clonazepam outperformed the antihistamines. However tinnitus recurred when taking alprazolam or clonazepam was stopped [Busto U, 1988. Johnson RM, 1993]. Diazepam and flurazepam caused no significant change in tinnitus [Murai K, Tyler RS. 1992]. Benzodiazepines are the drug of choice in anxious patients, but they may make a depressed patients worse.

Nortriptyline improved sleep interference especially in the female patients [Dobie RA, et al. 1993]. Amitriptyline was also effective with respect to interference with sleep or activity [Podoshin L, et al, 1995]. Musculoskeletal problems in the head and neck such as temporomandibular disorder predicted lack of response to nortriptyline, and massage and stomatognathic therapies might be useful for tinnitus [Dobie RA, 1999]. Goodey RJ (1981) reported that in cases where tinnitus was reduced by a tricyclic drug, tinnitus also could be suppressed with lidocaine.  

Lidocaine is the only drug that has shown to be effective in repeated controlled study. It was hypothized that lidocaine might reduce the spontaneous cochlear activity and modulate neural transmission in patients with tinnitus [Covino BG, 1983]. Lidocaine cannot be used clinically because it must be injected, its effects are short lasting, and it frequently produces side effects. The lidocaine test was performed through IV injection of 2 % lidocaine chloridrate without epinephrine at a dose of 1 to 2 mg/Kg in period of 3 to 30 min. [Sanchez TG, et al 1999. Kalcioglu MT, et al 2005. Baloh RW, 1998]. Common reactions include drowsiness, dizziness, and mild confusion for short duration. Sanches et al (1999) reported that lidocaine test showed favorable results in 76 % of patients, especially those with bilateral tinnitus, and mentioned that there is a close association between lidocaine snd carbamazepine. Martin FW and Colman BH (1980) noticed that tinnitus patients with normal hearing were least responsive to lidocaine and the patients with Meniere's syndrome had the most consistent response. Duckert LG and Rees TS (1983) reported that there was no consistent response to lidocaine for patients with noise-induced hearing loss, and that there was no consistent relationship between audiometric patterns and lidocaine response. Majumdar B et al (1983) reported that lidocaine response was more pronounced in patients with high-pitched tinnitus compared to those with low-pitched tinnitus. There was tendency of favorable response in patients of chronic tinnitus. Sanches TG et al (1999) reported 50 % of the tinnitus patients had relief, 29.4 % unchanged, and 5.8 % aggravated, and 14.7 % had side-effects.  

저자가 170명의 이명환자에게 리도케인 검사를 한 바에 의하면 83 %에서 양성반응이 나타났고 이명억제 효과는 5분에서 최고 3일 까지 있었으며, 부작용으로는 어지럼, 입에서 약 냄새가 나는 현상, 이명이 잠시 악화되는 증상 등이 있었다.   

Carbamazepine can be used for the treatment of tinnitus when the patient achieves improvement of tinnitus after the lidocaine test. Carbamazepine can inhibit the hyperactivity of the auditory pathways [Melding PS, 1978], despite side effects and long-term risk of bone marrow suppression [Marks NJ, 1981]. The maximum dose of carbamazepine is 200 mg three times a day. Side effects were nausea, sedation, gate ataxia, and confusion [Lechtenberg R, Shulman A. 1984]. Unilateral irregular clicking tinnitus with no detectable sound from the ear canal can be suppressed by carbamazepine. Holshof JH and Vermeij P (1986) reported beneficial effects from flunarizine in patients who had both tinnitus and dizziness. Eperison is a skeletal muscle relaxant that, when added to an antidepressant/vitamine B12 regimen, reduced loudness more than the antidepressant/vitamine B12 regimen alone [Kitano H and Kitahara M, 1987]. Ohsaki K et al (1988) reported that combination of betahistine mesilate, vitamine B complex, and diazepam was effective after 5 weeks of administration. Azevedo AA and Figueiredo RR (200) reported that acamprosate, a drug used in the treatment of alcoholism, resulted 86.9% of success in the relief of tinnitus with low incidence of side effects. Acamprosate has a dual mechanism action, which decreases the Glu transmission (afferent-excitatory) and increases GABA (efferent-inhibitory), with excellent tolerability. Allain H and Bentue-Ferrer D (1998) and Meyer B (1986) reported the efficacy of almitrine-raubasine in improving vertigo and tinnitus.

(3) Alternative medications for tinnitus

Adapted from; [Seidman MD, Babu S, Alternative Medications and Other Treatment for Tinnitus: Facts From Fiction. Otolaryngologic Clinics of North America 2003;359-381], [Blumenthal M, et al (1998). German Fedral Institute for Drugs and Medical Divices Commission, American Botanical Council, Integragive Medicine Communications (editors). The complete German Commission E monographs. 1st ed. Integrative Medicine Communications. Boston]

The B complex vitamines have interrelationships in their function within human enzyme system. Deficiency in these vitamines has been shown to result in tinnitus. The B vitamines, are water soluble and easily absorbed except vitamine B12. Vitamine B-1 (Thiamine) has a critical role in maintaining a healthy central nervous system. Thiamine levels can be affected by ingestion of caffeine, antacids, oral contraceptives, and a diet hign in carbohydrate. The mechanism which relieves the tinnitus seems to be by a stabilization effect on the nervous system of the inner ear. Dosage ranges from 25 to 500 mg/d. Vitamine B-3 (Niacin) aids in the functioning of the central nervous system. Niacin may provoke migraine or cause a flush lasting 5 to 60 minutes which is harmless but can be uncomfortable. Niacin dosage tinnitus is not established but 50 mg twice a day is recommended with increasing dose by 50 mg at every two weeks to a maximum dose of 500 mg twice a day. Vitamine B-12 (Cobalamin, cyanocobalamin) is stored for up to 9 months in the liver and kidneys. It has been estimated that 5-10 % of persons over the age of 65 years are deficient in vitamine B12. Vitamine B12 is found in pork, eggs, clams, seafood, and milk. Because of relatively poor gastric absorption, vitamine B12 should be taken as a sublingual tablet or by injection. Supplements range from 50 mcg to 2 mg. Folic acid is a vital coenzyme required for RNA and DNA synthesis and seems to have a stabilization effect on the nervous system. The dosage ranges from 400 to 800 mcg per day and requires 2 to 3 months of trial to achieve results.

The human cochlea has the body's greatest concentration of zinc. It has been demonstrated that supplementation with doses of 34 to 68 mg of zinc over 2 weeks decreased tinnitus. The recommendation dietary intake of zinc for adults is 15mg. Some patients have experienced improvement in their tinnitus after starting a regimen that included calcium. Absorption of dietary calcium can be drastically reduced by consuming large amounts of cocoa, spinach, kale, almonds, and whole wheat products. Alcohol, sugar, coffee, tetracycline, or aluminum-containing antacids can also result in lower absorption of calcium. The recommendation dietary intake of calcium is 800 mg for adults, 1200 mg for premenopausal women, and 1500 mg for postmenopausal women unless they are taking estrogen. Calcium dosage for tinnitus ranges from 1000 to 1500 mg/day for several months. Magnesium was shown to prevent hearing loss. Animal studies have shown that noise exposure causes magnesium to be excreted from the body. Ginkgo biloba is recommended 240 mg twice per day to treat tinnitus and vertigo. A positive response can occur within weeks, but can take up to four months.

(4) Audiologic treatment and management

Sound therapy includes hearing aid, masking and tinnitus retraining therapy. Hearing aids have been reported to provide masking relief to the patients with hearing loss. Hearing aids amplify environmental sounds and make tinnitus less noticeable. Amplification of ambient sounds can mask the tinnitus to some degree. The degree of hearing loss of a patient cannot determine the severity of tinnitus and correcting a conductive hearing problem cannot eliminate the tinnitus. However, without counseling and continued support, hearing aids alone are not effective. Masking is achieved by providing external sound to help the patients learn to ignore their tinnitus. The primary purpose of tinnitus masking is to provide palliative relief from tinnitus, not completely to mask tinnitus nor provide a distraction from tinnitus. Maintaining an enriched sound environment keeps the tinnitus embedded in a background of sound. Maskers emit an acceptable 3000-12000 Hz broadband sound, like the "shhh" of running water. Minimum masking level may be predictive of efficacy of treatment with tinnitus masking and may be reduced over time when treatment is effective with TRT. The way to predict masking effect is achieved by checking whether the static sound covers tinnitus while tuning a radio between stations. Or if a shower drowns out tinnitus, it can be predicted that masker would be effective. The effect is probably because a broad band noise is less irritating to the patient than their narrow band tinnitus.

Tinnitus retraining therapy (TRT) utilizes sound generators and takes 1-2 years. The primary purpose of TRT is to achieve long-term habituation to tinnitus, not for patient acceptance of sound enrichment. Habituation to tinnitus by reducing the contrast between the tinnitus and the background sound is the ultimate treatment goal with TRT. Patients wear ear-level sound generators similar to maskers. Depending on the patient's needs, hearing aids or combination devices (hearing aid and sound generator combined) are used. The recent digital sonic technology produces sound devices for relieving tinnitus. Quiet and restful sounds such as rainfall produced by sound devices using CDs, MP3 players, or softwares may be helpful to the patients with sleep disturbance.

Prevention of tinnitus

Dietary and lifestyle modification such as elimination of caffeine, salt, alcohol, simple sugars, nicotine, monosodium glutamate (MSG) and aspartame may be of some benefit to some patients with tinnitus. Noise has negative effects on hearing loss and tinnitus. Some people develop hearing loss from being exposed to noise - either long-term continuous noise or a sudden blast of noise. A sound of 140 dB, such as that emitted by a jet plane at takeoff cause pain. Frequent or prolonged exposure to sounds with intensities above 90 dB is likely to cause permanent hearing loss. For prevention of hearing loss and tinnitus, excessive nose should be avoided. If someone has to shout to be heard from a distance of three feet, it is too loud. The Occupational Safety and Health Act (OSHA) guidelines designed to prevent noise-induced hearing loss are as followings: Rock concert (100-110 dB) should be allowed less than 13 minutes per week, and headphone set (85-120 dB) should be used less than 2 hours per week.

Conclusion

Tinnitus should be regarded as a symptom with multiple causes and mechanisms. Although the best method for treating tinnitus would be medical treatment, none of the specific treatments for subjective tinnitus has been shown to eliminate tinnitus more frequently than placebo. Identification and treatment of patients experiencing anxiety, insomnia or depression are vital components of an effective tinnitus management. Shulman A (1991) described in his book that it is generally considered that one form of treatment for tinnitus is not enough. Ohsaki K (1998) mentioned that 5 weeks is considered to be minimum period necessary to eval‎uate the effectiveness of medical treatment. Outcome measurement should be eval‎uated by reliable tools. The most obvious tool for measurement of response to therapy would be the severity of impact of tinnitus on activity of daily life. Loudness and pitch of tinnitus are very poorly correlated with impact and thus are poor choices as outcome variables. Utilization of acoustic therapy combined with counseling contributes to relief of tinnitus. Tinnitus Retraining Therapy (TRT) is one of the new procedure for managing tinnitus.

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Figure legends

Figure 1. Acoiustic neuroma. Transverse thin-section T2-weighted MR image (4,000/108, one signal acquired) shows a small, hypointense tumor (arrow) in the fundus of the left internal acoustic canal.

Figure 2, Tympanic membraine glomus tumor.

Figure 3. Dural arteriovenous fistula. A dural arteriovenous fistula, also called a dural arteriovenous malformation, is an abnormal direct connection between a meningeal artery and a meningeal vein or dural venous sinus.

Figure 4. Obliterating pulsatile tinntus of dural arteriovenous fistula. Pressng against the site of AVF with enough pressure for stopping arterial flow may obliterate the tinnitus.

Figure 5. Obliterating pulsatile tinntus of venous hum. Localized pressure in the periauricular region obliterates the tinnitus resulted from venous hum.

Figure 6. Simplified anatomy of cochlea. The outer hair cells and the apex of cochlea may be more vulnerable to ischemia than the inner hair cells and the base of the cochlea because of the proximity of the lood vessles.

Figure 7. Weber and Rinne test. Weber test is performed by placing the stem of a turnig fork on the forehead, nasal bone or a central incisor, and the patient is asked where he or she hears the tone.

Figure 8. Symboles in audiometry. Symbols are right air conduction:O, left air conduction:X, right bone conduction:<, left bone conduction:>, right bone masking:[, and left bone masking:].

Figure 9. Audiogram of conductive hearing loss. Air conduction is impaired but bone conduction remains normal, producing air-bone gap on the audiogram. Meaurement of bone conduction always requires masking of the nontest ear.

Figure 10. Typical four audiogram patterns seen in patients with sensorineural hearing loss. (A) Notched pattern of noise-induced hearing loss (type A); (B) Downward-sloping pattern of presbycusis (type B); (C) Low-frequency trough of Meniere's syndrome (type C); and (D) V-pattern of congenital hearing loss (type D).

Figure 11. Hearing threshold, loudness math and LDLs. The LDLs can be plotted on the audiogram, which should be done along with an explanation of the concept of dynamic range.

Figuer 12. NoOrmal BAEP. For clinical purpose, wave I, III, and V have been used to localize lesions to the area between acoustic nerve and upper brainstem.

Figure 13. Wave V is most robust, often being identifiable at only 10 dB above hearing level. Increasing to 70 dB above hearing level makes all waves are identifiable.

Figure 14. The most common abnormality of acoustic neuroma is absence of all waves beyond wave I.

Table 1. Jastreboff PJ et al (2000) suggested categorization for treatment of the patients with TRT. kindling: prolonged sound-induced exacerbation of tinnitus or hyperacusis when the effects persist to the following day. NR: not relevant; NG: noise generator;  HA: hearing aid