NEURO-OTOLOGY (Continued)

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In the assessment of hearing, one must remember that a dysfunction of the auditory system may be a manifestation of a systemic and possibly life-threatening disorder. Therefore, the examiner, in addition to obtaining a history of the past, present, and familial audiologic and otologic complaints, should also elicit a history of complaints referable to other systems. The first few minutes spent talking with the patient or relatives will help to define the direction the inquiry should take. The examination of the patient, the complaints, and the preliminary audiologic findings determine how inclusive the examination must be and what subsequent tests must be ordered. Be aware that audiologic tests do not always provide an exact diagnosis. Not only should the results from the audiologic test battery be integrated, but also these data should be used with the neurological, otoneurological, and radiological information for the maximum diagnostic accuracy.

TYPES OF HEARING LOSS{Back to Outline}

Hearing loss can result from a lesion anywhere within the auditory system (Nadol 1993). An abnormality within the outer or middle ear results in a conductive loss of hearing due to an inefficient transmission of sound to the inner ear system. When the loss of hearing is due to pathology in the cochlea or along the VIII cranial nerve from the inner ear to the brainstem, the loss is referred to as a sensorineural hearing loss. Patients may exhibit both conductive and sensorineural loss which is referred to as a mixed hearing loss. Central hearing loss (or central auditory dysfunction) is present when a lesion exists in the central auditory pathway beyond the VIII cranial nerve, for instance in the cochlear nucleus in the pons or in the primary or association auditory cortex of the temporal lobe. In addition to these organic types of hearing loss, one should also consider functional hearing loss. The diagnosis of functional hearing loss is made when an individual claims to have a hearing loss, but discrepancies in objective test measures suggest that the loss does not exist, or is exaggerated.

Conductive Hearing Loss{Back to Outline}

Conductive hearing loss occurs with pathology in the outer or middle ear. The bone conduction thresholds are normal, but air conduction results suggest a decrease in hearing sensitivity. The patient with a conductive hearing loss typically demonstrates decreased sensitivity across all frequencies. Sometimes hearing is better for the higher frequencies than it is for the lower ones. (Figure 11):

Another finding of conductive loss is that speech discrimination is relatively unimpaired. A patient with a conductive loss has good discrimination ability provided the speech signal is of sufficient intensity.

Frequently, the patient with a conductive loss of hearing complains of tinnitus, which may be localized in one ear, in both ears, or unlocalized in the head. In the case of a conductive impairment, the tinnitus tends to be of relatively low pitch.

Sensorineural Hearing Loss{Back to Outline}

Sensorineural hearing loss occurs with pathology in the inner ear or along the nerve pathway from the inner ear to the brainstem. Hearing loss from cochlear disorders alone is termed sensory loss. As mentioned elsewhere, there exists some ambiguity among audiologists, neurologists, and otologists concerning what is a retrocochlear and what is a central problem. For the purposes of this discussion, we will define retrocochlear as an abnormality between the cochlea and the brainstem (see below).

The term sensorineural includes both cochlear and retrocochlear disorders. A pure sensorineural impairment exists when the sound-conducting mechanism (outer and middle ear) is normal in every respect, but a disorder is present in the cochlea or auditory nerve. Sensorineural impairment can be congenital or acquired. Congenital sensorineural hearing loss may result from hereditary factors, malformation of the cochlea, inutero viral infections, or birth trauma. The etiology of most sensorineural hearing loss is unknown. Acquired sensorineural hearing loss may be caused by noise exposure, acoustic tumor, head injury, infection, toxic drug effects, vascular disease, or presbycusis.

The configuration of the audiogram demonstrating a sensorineural hearing loss may vary significantly and in some instances may suggest the etiology of the loss. Many people with sensorineural losses experience a loss only in the high frequency region. These individuals have no difficulty understanding speech at normal intensities in a quiet environment since low-frequency hearing is unimpaired. However, they do experience difficulty in understanding speech in a noisy environment. Generally, the low frequencies are defined as the range from 250 Hz to 750 Hz, the middle frequencies as 1,000 Hz to 3,000 Hz, and the high frequencies as 4,000 Hz to 8,000 Hz on the standard audiogram.

Loudness recruitment is usually associated with sensory loss of cochlear origin, which constitutes the majority of sensorineural losses. Recruitment is an abnormally rapid growth of loudness with an increase in intensity (Sanders 1984). The recruiting patient with sensory loss will not hear low-intensity sounds at all, and may just barely hear sounds of moderate intensity, but the recruitment of loudness may cause moderately loud sounds to be perceived as uncomfortably loud. This disruption of normal loudness function may be painful to the individual and require the utilization of variable compression circuitry should the patient pursue hearing aid use.

The patient with sensorineural hearing loss is usually subject to tinnitus of a somewhat different sort from that associated with conductive hearing loss. Generally, the patient with sensorineural loss reports a constant ringing or buzzing noise, which may be localized in either ear or may not be localized. In general, the pitch of tinnitus tends to be higher in sensorineural impairment than in conductive impairment. In addition, the patient may report that tinnitus is only present at night or when background noise is minimal, when in fact it is alway present but the patient's perception is only in quiet environments.

In sensorineural losses, the audiometric Weber test is expected to lateralize to the better hearing ear. Audiometrically, sensorineural loss is characterized by overlapping air and bone conduction thresholds. The tympanogram is typically normal, and acoustic reflexes may be present, elevated, or absent. The audiometric findings for a typical sensorineural hearing loss are displayed in Figure (12).

Contrary to a commonly held misconception, sensorineural hearing loss may be helped by the use of hearing aids. Current technology utilizes full dynamic range compression to significantly increase the effectiveness of amplification.

Mixed Hearing Loss{Back to Outline}

Mixed hearing loss consists of a conductive and a sensorineural component in the same ear. The patient's behavior will reflect attributes of both a conductive and a sensorineural disorder. Causes of mixed hearing loss may be any combination of the conditions described previously for conductive and sensorineural hearing loss. The conductive component of the mixed hearing loss may be corrected by successful medical or surgical treatment, but the sensorineural component is not reversible. The pure tone audiometric pattern for a mixed hearing loss is displayed in Figure 13.

With a mixed loss, both air and bone conduction thresholds are elevated but bone conduction thresholds are better than air conduction thresholds. The difference between the two thresholds is referred to as the air-bone gap and represents the amount of the conductive component present.

Sensory Versus Neural Lesions{Back to Outline}

The problems of differentiating cochlear dysfunction from VIII nerve lesions have received major emphasis during the past several years. In fact, this area has been emphasized to the extent that some audiologists have limited their concept of differential audiology primarily to those tests that assist in localizing the defect within the sensorineural mechanism. The neurologist's interest in sensorineural hearing loss is with regard to the possibility of a cerebellopontine angle tumor. Although many referrals for audiological evaluation are made for this reason, we must emphasize that even the more sophisticated special auditory tests cannot determine the specific pathology underlying the disorder. An MRI may indicate the presence of an abnormality somewhere in the nervous system, but it does not necessarily define the nature of the pathology. The audiological tests, however, highlight patterns of auditory behavior that are generally associated with cochlear or neural involvement.

Routine pure tone and speech testing can yield valuable information on the site of lesion during the initial phase of the differential audiologic study. For example, a pure tone configuration, which is often seen in patients with a presumptive diagnosis of Meniere's disease, is a unilateral hearing loss most pronounced in the low frequency range. In sharp contrast, patients with VIII nerve lesions frequently present a unilateral hearing impairment most evident in the high frequencies and poor speech discrimination. Although such generalizations may describe a substantial number of cases falling into these two categories, numerous exceptions are encountered with either cochlear or neural pathology. Measures, such as tone decay, acoustic reflex measures, acoustic reflex decay, and speech discrimination at high intensity levels must be used to distinguish between VIII nerve, extra-axial and intra-axial brainstem dysfunction.

Central Auditory Disorders{Back to Outline}

As would be anticipated, lesions within the central auditory system are difficult to detect or localize. In fact, many central auditory dysfunctions will not be demonstrated by conventional audiologic measurements. Individuals with known lesions in the central auditory tracts may not manifest any significant hearing loss when tested by conventional pure tone audiometry (Benjamin and Troost 1988). Total removal of one hemisphere of the brain in humans has not resulted in any major change of auditory sensitivity in either ear. Central disorders of hearing are quite unusual. When accompanied by other neurologic signs and symptoms, a central diagnosis is suggested. Normal measures mentioned previously, such as tone decay or acoustic reflex, strongly suggest an eighth nerve lesion. One excludes eighth nerve lesions as a separate category and concentrates on the central auditory brainstem and hemispheric pathways. Neuroimaging procedures such as MRI may help to localized the abnormality.

TINNITUS{Back to Outline}

Ear and head noises, the most common complaints presented to the audiologist or otolaryngologist, are frequently seen by the neurologist. As many as 32% of the adult population have tinnitus, with 20% of the population rating their condition as severe (Vernon 1994). Tinnitus may be considered a significant symptom when its intensity so overrides normal environmental sounds that it invades the consciousness. The patient experiencing tinnitus may describe the sound as ringing, roaring, hissing, whistling, chirping, rustling, clicking or buzzing, or other descriptors. Although most patients report the presence of tinnitus to be constant, others report it to be intermittent, fluctuating, or pulsating. Tinnitus may be perceived as a high - or low - pitched tone, a band of noise, or some combination of such sounds.

The perceived loudness of tinnitus in any patient may be intense enough to be highly debilitating. Most patients with sensorineural hearing loss report tinnitus to be a high-frequency tone, but tinnitus associated with conductive hearing loss tends to be low in frequency. However, knowledge of the pitch of the tinnitus is of little diagnostic benefit other than allowing for the gross dichotomy of conductive versus neural pathology.

The majority of tinnitus sufferers have a concomitant loss of hearing, which may be either conductive or sensorineural. Only a minority of tinnitus patients have audiometrically hearing sensitivity. Tinnitus may precede or follow the onset of a loss in hearing, or the two may occur simultaneously.

Tinnitus is a symptom of an underlying disease or specific lesion when it is perceived above the intensity levels of environmental sounds. It may be the first symptom that brings the patient to a neurologist. The complaint may be an early symptom of a tumor in the internal auditory meatus or in the cerebellopontine angle, a glomus tumor, or a vascular abnormality in the temporal bone or skull. Because tinnitus may be a characteristic symptom of a number of disorders, a complete medical and audiological evaluation is an important initial step in the management process.

Classification of Tinnitus{Back to Outline}

Subjective tinnitus{Back to Outline}

Subjective tinnitus is a auditory sensation heard only by the patient. It may be present in one or both ears or localized within the head. For most patients, tinnitus is a subjective sensation. This type of tinnitus can result from a lesion involving the external ear canal, tympanic membrane, ossicles, cochlea, auditory nerve, brainstem, and cortex. The most common cause is cochlear disease. Tinnitus associated with Meniere's syndrome is often low-pitched and continuous, and is described as a hollow seashell sound or very loud roaring. Tinnitus with otosclerosis is also low-pitched, is described as a buzzing or roaring sound, and may be continuous or intermittent. Continuous bilateral or unilateral high-pitched tinnitus often accompanies chronic noise-induced hearing loss, presbycusis, and hearing loss due to ototoxic drugs. A number of drugs such as aminoglycosides, quinidine, salicylates, indomethacin, carbamazepine, propranolol, levodopa, aminophylline, and caffeine, may produce tinnitus with or without associated hearing loss (Baloh 1984).

Objective tinnitus{Back to Outline}

Objective tinnitus is far less frequent than subjective tinnitus. It is perceived not only by the patient, but by the examiner as well. Objective tinnitus may be vascular (an arteriovenous malformation or fistula) or mechanical in origin. Objective mechanical tinnitus is due to abnormal muscular contraction of the nasopharynx or middle ear, as may occur in palatal myoclonus. Objective tinnitus of vascular origin may also be a referred bruit from stenosis in the carotid or vertebrobasilar system.

Tinnitus may be classified as mild, moderate, or severe. Mild tinnitus is usually noticed only in quiet environments or at bedtime. It is usually not very disturbing, and the patient can easily be distracted from the tinnitus by other stimuli. Moderate tinnitus is more intense and is constantly present; the patient is conscious of the tinnitus when attempting to concentrate or when trying to sleep. Severe tinnitus may disable individuals to the extent that they are is unable to concentrate on little other than the tinnitus itself.

EXAMINATION OF HEARING{Back to Outline}

Basic Office Examination of Hearing{Back to Outline}

Whether or not the patient's complaint is one of hearing loss, a basic assessment of auditory function should be part of the neurological examination. The external ear should be inspected with an otoscope to determine the patency of the external ear canal and the integrity of the tympanic membrane. If the external canal is occluded by cerumen, simple tests of hearing may be invalidated. The cerumen should be removed, if possible, with warm water lavage using a syringe with a 5 to 8 cm piece of rubber tubing affixed to the end to avoid injury to the ear. If water lavage has not removed impacted cerumen, a neurologist should refer the patient to an otolaryngologist for removal.

Assuming there is no cerumen in the external ear canal, the tympanic membrane should be inspected. The neurologist should be able to recognize an inflamed, bulging, or scarred drum, and should note whether there is perforation of the tympanic membrane; blood behind the eardrum; or a pulsating blue mass, which may be indicative of a glomus jugulare tumor. Excellent descriptions of tympanic membrane findings may be found in modern texts of otology. At times it may be helpful to inspect the mobility of the eardrum by increasing pressure within the external canal, using a hand-held pneumatic bulb, attached by tubing to an outlet in the otoscope. Little or no mobility of the tympanic membrane suggests fluid or a mass behind the drum, or a fixed ossicular chain.

The office examination of hearing loss may include tuning fork tests of air and bone conduction. Tuning forks at a frequency of 256 or 128 Hz should not be used due to the vibrations they produce by bone conduction, which the patient may mistake for sound; the 512 Hz is the lowest useful frequency. Two standard tuning fork tests are the Weber and Rinne tests.

Weber Test{Back to Outline}

The Weber test is based on the principle that the signal, when transmitted by bone conduction, will be localized to the better hearing ear or the ear with the greatest conductive deficit. The test can determine the type of hearing impairment when the two ears are affected to different degrees. The stem of a vibrating tuning fork is placed on the skull in the midline, and the patient is asked to indicate in which ear the sound is heard. The usual location described is for placement on the forehead; but better locations are the nasal bones or teeth when a stronger bone conduction stimulus is required. 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{Back to Outline}

The Rinne test is probably the most commonly used tuning fork test, but the name is usually mispronounced: It is German, not French, and is accentuated on the first syllable (Rin'neh). The Rinne test is a comparison of the patient's hearing sensitivity by bone conduction versus air conduction. A normal individual will perceive the air conducted sound as louder or the same as bone conducted sound. Proper placement of the tuning fork in each situation is important. When testing by bone conduction, the stem fork should be placed firmly on the mastoid, as near to the posterosuperior edge of the ear canal as possible. The stem should not touch the auricle of the external canal, which should be held to the side by the examiner's fingers. Touching the external ear itself could give false results due to vibration of the auricle. When testing by air conduction, the fork is held about 2.5 cm lateral to the tragus. In the Rinne test, when the conduction mechanism is normal in an ear (that is, in individuals with normal hearing and in those with sensorineural hearing impairment), air conduction will be heard better than bone conduction as it is a more efficient means of sound transmission. This finding is termed a positive Rinne. Bone conduction will be heard better than air conduction when there is a deficit in the conduction mechanism and is referred to as a negative Rinne. A conductive deficit of more than 15 db reverses the tuning fork responses (that is, bone conduction is better than air conduction) at 512 Hz. When testing by bone conduction, the examiner should not forget to have the patient remove his or her eyeglasses: the earpiece can interfere with proper placement of the stem of the tuning fork or give inappropriate conduction or vibratory information. Although tuning fork tests allow the examiner to identify a conductive versus a sensorineural loss, and in some cases lateralize the symptomatic ear, it does not evaluate the degree of impairment or the effects of that impairment on speech understanding.

Tests of Auditory Function{Back to Outline}

An audiologic assessment is comprised of pure tone air and bone conduction testing, speech threshold and word discrimination measures. Threshold is defined as the lowest intensity (measured in decibels) an individual can detect a pure tone or speech signal more than fifty percent of the time. Pure tone air and bone thresholds are established for frequencies from 250 Hz to 8,000 Hz. This frequency range is important to the detection and understanding of the speech signal. Hearing is considered normal when threshold sensitivity is between 0 and 25 dB for frequencies of 250 Hz to 8000 Hz (Figure 14):

Responses greater than 25 dB are classified by degree as mild, moderate, severe, moderately severe, and profound (Figure 14). Responses at 500 Hz, 1000 Hz, and 2000 Hz are averaged together to compute the pure tone average (PTA).

In the measurement of bone conduction thresholds, pure tones are transmitted via a bone oscillator, usually placed on the mastoid. This signal directly stimulates the cochlea, bypassing the external and middle ear. The presence of decreased air conduction thresholds and normal sensitivity by bone conduction suggests abnormality in the external ear or middle ear system and is termed a conductive hearing loss.

Speech reception threshold (SRT){Back to Outline}

A speech reception threshold is the lowest intensity and equally weighted two syllable word is understood approximately fifty per cent of the time. The pure tone average and speech reception threshold should be within 7 dB of each other. Comparison of the speech reception threshold and the pure tone average serves as a check on the validity of the pure tone thresholds. Discrepancies between these measures may suggest a functional or non-organic hearing loss.

Speech discrimination{Back to Outline}

Speech discrimination is a tool used to assess an individual's ability to understand a speech signal at normal or above normal conversational levels. Most commonly, a phonetically balanced word list of fifty one-syllable words is presented to the patient at a supra-threshold level. The patient's score is represented as a percentage of the number of words correct. Generally, discrimination ability decreases proportionately with an increase of hearing impairment. However, there is an exception in conductive hearing loss where discrimination ability remains relatively good because the inner ear system is normal. Poor discrimination ability in the presence of relatively good hearing sensitivity may suggest retrocochlear pathology such as acoustic neuroma and should be aggressively pursued by the clinician.

Immittance Test Battery{Back to Outline}

Tympanometry, static acoustic immittance and acoustic reflex threshold measures comprise the acoustic immittance test battery.
Tympanometry{Back to Outline}

Tympanometry is a measure of middle ear mobility when air pressure in the external canal is varied. Results are graphically represented with a pressure along the X axis and compliance along the Y axis. Normal tympanograms have a pressure peak point of 50 mm H2O.(Figure 15):

Static compliance{Back to Outline}

Static compliance refers to the ease of flow of acoustic energy through the middle ear. Immittance measures are obtained at +200 mm H2O (first point of compliance, or C1) and again at the point the tympanic membrane is most compliant (second point of compliance, C2). The point at which the tympanic membrane is most compliant allows maximum transmission of energy through the middle ear cavity. Compliance of the tympanic membrane is derived by subtracting C1 from C2. Values less than 0.25 cm3 of equivalent volume indicate a stiff or non-compliant middle ear system. Values greater than 2.5 cm3 suggest an overly compliant system. Abnormalities associated with reduced mobility of the tympanic membrane in associated middle ear structures include otitis media, otosclerosis and large cholesteatomas. Ossicular chain discontinuity is the most common cause of excessive tympanic membrane mobility. Examples are shown in Figure 15. Extremely high equivalent middle ear volume and low static compliance suggests tympanic membrane perforation.

Acoustic reflex threshold{Back to Outline}

The acoustic reflex threshold is the lowest intensity needed to elicit a contraction of the stapedius and tensor tympani muscles using a pure tone stimulus. The introduction of an intense sound into the ear canal results in a temporary increase in middle ear impedance. This phenomenon occurs bilaterally, however, it is typically measured in one ear at a time. Contralateral reflexes are measured by stimulating one ear and measuring the reflex from the contralateral ear. Ipsilateral reflexes are measured by stimulating and recording from the same ear. Reflexes occur between 70 and 100 dB SPL (Sound Pressure Level) in normal ears. Middle ear abnormalities or significant sensorineural hearing losses may elevate or obliterate the acoustic reflexes. Retrocochlear pathology and facial nerve disorders may also affect contralateral and ipsilateral acoustic reflexes.

Brain Stem Auditory Evoked Potentials{Back to Outline}

Brainstem auditory evoked potentials (BAEPs) are also known as brainstem auditory evoked responses (BAERs) or auditory brainstem responses (ABRs). These physiological measures can be used to evaluate the auditory pathways from the ear to the upper brainstem (Picton 1990). In addition, ABR threshold testing may be used to determine behavioral threshold sensitivity in infants or uncooperative patients. The most consistent and reproducible potentials are a series of five submicrovolt waves that are seen within 10 msec of an auditory stimulus. These potentials are recorded by averaging 1,000 to 2,000 responses from click stimuli by use of a computer system and amplifying the response (Figure 16).

Figure 16. Brainstem auditory evoked potential (BAEP) in a normal adult. Responses were recorded between electrodes on the vertex and the ipsilateral mastoid. Waves I, III and V are labeled. ms/div = milliseconds per division, V/div = microvolts per division.

The anatomical correlates of the five reliable potentials have only been roughly approximated. Wave I of the BAEP is a manifestation of the action potentials of the VIII nerve and is generated in the distal portion of the nerve adjacent to the cochlea. Wave II may be generated by the VIII nerve or cochlear nuclei. Wave III is thought to be generated at the level of the superior olive, and waves IV and V are generated in the rostral pons or in the midbrain near the inferior colliculus. The complex anatomy of the central auditory pathway (Benjamin and Troost 1988), with multiple crossing of fibers from the level of the cochlear nuclei to the inferior colliculus, makes interpretation of central disturbances in the evoked responses difficult. Excellent reviews of the generation of the potential, and interpretation of abnormality, are found in recent contributions.

The brainstem auditory evoked potential (BAEP) is a sensitive, noninvasive diagnostic test for the diagnosis of cerebellopontine angle tumors (Picton 1990). This test is used to differentiate cochlear from VIII nerve hearing defects and, on some occasions, demonstrates an auditory abnormality when behavioral audiometric testing is still normal. The majority of patients with acoustic tumors had abnormal responses (Baloh and Honrubia 1990).

The absence of waves III and V has been seen in some patients with vestibular schwannoma and in cerebellopontine angle meningiomas. Such patients often have marked hearing deficits with poor discrimination on behavioral testing, suggesting retrocochlear disease. The absence of all waves should not occur unless a severe hearing loss exists. The most specific evoked potential abnormality is the presence of an increase in interwave intervals. Abnormal interwave latencies (I-III or I-V) are the most specific and sensitive abnormalities seen with cerebellopontine angle tumors. The abnormal prolongation or absence of wave V at increased click rates is also characteristic of retrocochlear pathology. Increased absolute latencies of all waves, when compared to responses from the other ear or to clinical normative data may signify a conductive deficit.

Electrocochleography{Back to Outline}

Electrocochleography (ECochG) is a method of recording the stimulus-related electrical potentials associated with the inner ear and auditory nerve, including the cochlear microphonic, summating potential (SP) and the compound action potential (AP) of the auditory nerve. This measure is beneficial in the differential diagnosis of certain types of sensory disorders, such as Ménière's disease or cochlear hydrops. The amplitude of the SP and AP is measured and is of primary interest when evaluating an ear for increased endolymphatic pressure.

THERAPY FOR AUDITORY DISORDERS{Back to Outline}

Therapy for auditory disorders is largely the province of the otolaryngologist and the audiologist. The neurologist interested in neuro-otology however, should have some knowledge of therapy to promote appropriate referrals. The nature of the treatment program depends, of course, on the exact diagnosis, that is the type of hearing loss and the age of the patient. Both medical and surgical therapies are appropriate depending upon the nature of the disorder. Medical or surgical therapy is used in coductive losses due to otitis media. Surgery is the primary therapy for hearing loss caused by otosclerosis, usually manifest as a conductive type of hearing loss, as described earlier. A discussion of surgical therapy of otosclerosis is beyound the scope of this chapter. The interested reader is referred to textbooks of Otology. However, almost every type of non-conductive hearing loss may be helped by a variety of amplification devices and/or counselling.

Amplification{Back to Outline}

Contrary to a commonly held misconception, sensorineural hearing loss may be helped by the use of a hearing aid. It should be recognized, however, that hearing aids only compensate for loss of sensitivity, but the matter in which increased loudness is achieved may reduce distortion and significantly increase discrimination in certain situations. Modern hearing aids use the latest microcircuitry and signal-processing techniques, such as digital filtering, to improve significantly the effectiveness of amplification.

In addition to hearing aids, devices such as telephone amplifiers, television/radio access systems, personal listening systems, and alerting devices are designed to improve communication in difficult listening situations. There are many assistive devices on the market and new systems and modifications are appearing at an accelerating rate.

We note that the hearing aid is the most important rehabilitative tool available for the management of sensorineural hearing loss, however, counseling should represent a central focus of any management strategy for the hearing-impaired adult. In addition, the hearing-impaired should receive counseling both before and after the provision of amplification. Lastly, cochlear implants have proven to be extremely beneficial for those individuals with severe to profound hearing loss who receive minimal benefit from amplification.(Waller and Roland, 1996)

Management of Tinnitus{Back to Outline}

The complete evaluation of the tinnitus patient should be approached from a dual perspective. The patient with tinnitus, regardless of location, type, or severity, must first have a thorough otologic and audiologic examination. If there are accompanying symptoms, a complete neurological examination may be appropriate. The patient with an isolated symptom of a persistent, yet unexplained, tinnitus should receive follow-up examinations at definite intervals when initial medical, otologic, and neurological studies reveal no evidence of disease. Tinnitus may be the first symptom of disorder, appearing long before any other symptom, including hearing loss. When medical and otologic examination fail to disclose a remediable cause for the tinnitus, or when a diagnosis is ascertained for which no known medical therapy is presently available at present, the tinnitus patient should undergo further evaluation to determine the most appropriate nonmedical avenue for rehabilitation.

When a specific otologic cause for the tinnitus is identified, otologic management is indicated. When a lesion or disease process is not identifiable, however, then tinnitus management is more difficult. Given no underlying otologic disease, there is at present no effective surgery or medical therapy for the treatment of tinnitus.

Research on the effectiveness of pharmacological therapy for tinnitus, although certainly encouraging, involve medications, such as carbamazepine, lidocaine, and intravenous barbiturates, whose potentially serious side effects limit their usefulness. There is some suggestion that relatively low doses may prove effective in tinnitus management.

Masking{Back to Outline}

The use of masking as a management tool in the treatment of the tinnitus patient has met with mixed success over the years. The audiologist should remain cognizant of factors such as the patient's perception of the pitch and loudness and the overall spectral intensity of the masking signal. The referring neurologist should be aware of these issues as well.

Tinnitus maskers are designed to provide relief to the tinnitus sufferer by introducing an external masking sound into the effected ear or ears, thereby minimizing or eliminating the perception of the tinnitus. Although the use of tinnitus maskers has not proved universally successful, masking is still a feasible technique that cannot be ignored. The actual efficacy of tinnitus maskers in the average tinnitus patient is probably less than 30%. The use of a hearing aid may be more beneficial by addressing the primary hearing problem.

Biofeedback{Back to Outline}

Experience with tinnitus patients reveals that many have relatively high levels of anxiety, tension, or other symptoms of chronic stress. There is a significant correlation between tinnitus and tension. Biofeedback as a treatment in the management of tinnitus was first reported in the literature in the mid-1970s. These early studies reported the use of biofeedback as effective in the relief of tinnitus or the associated annoyance produced by it. Biofeedback is quite effective for enhancing relaxation, as are traditional relaxation procedures. When used together, muscle tension and general life stresses are reported to be reduced.

Counseling{Back to Outline}

The need for effective counseling is one important aspect of tinnitus management regardless of the management approaches taken with a given patient. Many patients are frightened by the presence of tinnitus and need a careful and clear explanation of the disorder, coupled with firm reassurance from both the neurologist and the audiologist. In light of the various effects tinnitus may have on a given patient counseling must be directed toward all of the patient's difficulties, not this specific problem in isolation.

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