TINNITUS

Definition:  

    -perception of sound without an external acoustic stimulus or

    -perception of a sound produced involuntarily within the body

 Prevalence:

-15-32% of adults have had tinnitus at some point, and about 5 percent are severely disabled by their tinnitus.

-Male/Female ratio = 1, with a peak incidence at 50-70 years.

-Most patients also have hearing loss.

-pitch of tinnitus may correlate with pathology.

 

Classification(s)

One type:

      3 major categories: (1) tinnitus generated by para-auditory structures, (usually vascular or myoclonic)

                                         (2) tinnitus generated by the peripheral sensorineural auditory system.

                                         (3) tinnitus generated by the central sensorineural auditory system.

 

Another type:

      Objective versus Subjective Tinnitus:

                -subjective (audible only to the patient) and objective (audible to the examiner).

 

AETIOLOGY:

(I) PARA-AUDITORY

 Vascular Tinnitus (history of pulsatile tinnitus synchronous with heartbeat)

                -tinnitus is pulsatile & it varies directly with cardiac rate is essential to diagnosing a vascular tumor.

                -this may be confirmed by the history or detected by light exercise.

                -audible bruit.

    Arterial:  -atherosclerotic plaques in the internal carotid artery

                      -AVM (most common is b/w occipital artery and transverse sinus)

                      -Glomus tympanicum & glomus jugulare

                      -aneurysms

                      -persistent stapedial artery

                     -aberrant ICA

    Nonarterial:

                -Venous hums from irregularity of flow in jug veins due to compression from transvs process of C2.

                -jugular bulb abnormalities

                -elevated ICP

                -vascular neoplasms may cause pulsatile tinnitus.

Muscle Contraction Tinnitus: (due to synchronous contractions of muscles of ME, ET & palate).

                -Palatal myoclonus is usually faster than heart rate Þ 60 to 200 per minute - and is objectively audible

                      (Sonotubometry studies Þ sound heard may be the click of the ET walls during relaxation).

                -TMJ dysfunction may also cause tensor tympani spasm.

                -Stapedial and palatal myoclonus may result from multiple sclerosis,

                -intracranial neoplasm, cerebrovascular disease or may be psychogenic.

                -Myoclonus persists during sleep.

External and Middle Ear Tinnitus:    

                -CHL (attenuates background noises, bringing attention to the pulsatile tinnitus)

                                 (e.g. infection, effusion, cerumen, otosclerosis)

                -Cerumen, foreign bodies and hairs may lie against TM and cause tinnitus.

                -patulous ET (patient complains of a rushing or blowing sound with respiration).

                    (Myringotomy and tube, sclerosing agents at tube orifice & diathermy of orifice may be effective)

 

(II) PERIPHERAL SENSORINEURAL TINNITUS:

     -Defn: Peripheral tinnitus is localized to 1or 2 ears, vs central tinnitus (poorly defined,heard all over head).

          -85% of these pts have some form of hearing loss.

     -Hypotheses proposed regarding the pathophysiology of peripheral tinnitus.

                1. Alteration in the spontaneous discharge rate of auditory fibers

                     -auditory system has one of the highest spontaneous discharge rates in the body.

                     -drugs that increase spontaneous discharge rate (e.g. salicylates) => tinnitus in this way.

                2. Alteration in efferent inhibitory neurons firing rate may result in increased firing of adjacent

                     afferent neurons which could be perceived as tinnitus.  (eg acoustic trauma or Meniere's disease)

                3. Tonndorf 1980: decoupling of stereocilia from tectorial membrane=> "noise" from that

                                             area.  This could result from degenerative processes or from noise trauma.

                4. Møller (1984): adjacent auditory nerve fibers could become damaged in such a way that

                                            artificial synapses between them might occur.

                5. Eggermont (1984) : an abnormal displacement of BM twd scala tympani => hyperactivity

                6. Spoendlin (1987) : presence of damaged outer hair cells and normal inner hair cells.

                7. Tonndorf (1987) : chronic tinnitus may be related to deafferentation of nerve fibers.

     -Tinnitus and aging

      -prevalence and severity of tinnitus increases with age.

     -Causes of peripheral tinnitus:

                1. Noise Exposure (most common cause):

                                -typically high-pitched and constant.

                                -with continued noise exposure SNHL becomes worse as does tinnitus.

                                -Nb: early in the course there is SNHL at 4 kHz (noise notch).

                2. Presbycusis is commonly encountered in practice.

                                -hearing loss is a downward sloping high frequency, (usually associated c high freq tinnitus).

                3. Head Trauma may Þ tinnitus which is not noticed until some time after injury.

                4. Acoustic Neuroma presents with tinnitus in 10% of the cases.

                         Tinnitus may be constant/intermittent, and may or may not be associated with hearing loss.

                5. Meniere's Dis: (typically low pitched, median 300 hz, rumbling, unilateral, may be intermittent)

                               -generally have more problems, louder, more annoying,more unstable (changes more often).

                6. Otosclerosis may Þ tinnitus both by its conductive component & its involvement in the inner ear.

                                -Typically tinnitus is low-medium pitch.

                                -70-95% of patients with otosclerosis complain of tinnitus.

                7. Drugs - many medications are known to cause tinnitus.

                      a. Aminoglycosides: may be high-pitched and associated mainly with drug-induced hearing loss.

                      b. Quinine: permanent, high-pitched tinnitus. Very rare.

                      c. Salicylates: Temporary tinnitus and mild reversible hearing loss.

                      d. Diuretics: loop-inhibiting agents primarily responsible. May cause "screaming" tinnitus and

                                           significant permanent hearing loss.

                      e. Others include caffeine, cocaine, marijuana and tobacco.

                      f. metabolic diseases (e.g. hyperthyroidism, DM)

                     g. intracranial neoplasms and other CNS lesions (e.g. infections, MS).

 (III)  CENTRAL SENSORINEURAL TINNITUS

          -Defn: is usually described by patient as occurring "all over the head."

         -patients who have undergone labyrinthectomy or VIII section may still complain of tinnitus.

         -mechanism is unknown, but again may lie in the change in firing rates of central inhibitory neurons      

                                            (e.g. in the dorsal cochlear nucleus).

 

 Details on Specific Para-Auditory Conditions

Arteriovenous malformations ......usually present as pulsatile tinnitus

-most common are: those of poster fossa b/w branches of occipital a & trans sinus (Arenberg/McCreary, 1972).

-Communications between carotid artery and cavernous sinus, (mostly from trauma)

-usually have a bruit. The vascular mass, when palpable, exhibits a thrill and generally is more compressible

-AVMs in mandible/maxilla appear with loosening of teeth, periodontal bleeding, & mucosal discoloration.   

             (most common cause of death in these patients is  exsanguination during tooth extraction).

Venous hum

-hum results from eddy currents in jug vn and normally is heard in neck of many children & some adults.

-have been attributed to transverse process of second cervical vertebra impinging on jug vn.

                 and less commonly to increased venous return secondary to AVM & increased intracranial pressure.

-loudness increases in states of increased cardiac output, such as anemia, thyrotoxicosis, and pregnancy.

-they are significant only for the tinnitus they produce.

-may become audible when CHL occurs in which external background noise is attenuated.

-Diagnosis           

                -may have symptoms that are nearly diagnostic.

                -tinnitus may decreased by: 

                                -gentle pressure on anterior neck that does not occlude the carotid artery.             

                                -turning head toward uninvolved side the sound.

                -tinnitus may increased by: 

                                -turning the head toward the involved

                                -deep breathing and Valsalva maneuver.

                -a diagnostic arteriogram still is needed.

-Management

      -reassuring the patient.

      -sound not tolerated by patient or spouse may respond to a high ligation of jugular vein.

      -preoperative angiography is necessary to verify a patent contralateral venous system.

      -level at which an effective ligation may be achieved can be determined by inflation of a Fogarty catheter       

                    balloon at different levels during a retrograde venogram (Ward et al., 1975).

       -this may reveal some pts who still require ablation of their transverse sinus to eliminate the sound.

       -Cary (1961) described the use of a prosthetic device that put gentle, constant pressure on the neck.

Muscle contraction tinnitus

-due to synchronous contraction of fibers of one or more middle ear or palatal muscles.

                  -either voluntary or involuntary, or part of syndrome of palatal myoclonus.

-consists of rapid, repetitive contractions (60-200 /min) of: tensor & levator veli palatini, tensor tympani,

                   salpingopharyngeal, or superior constrictor muscles.

-pts are typically young and often have other associated neurologic disorders (eg brainstem infarct or MS)

-not inhibited by sleep, barbiturate anesthesia, coma, or hemiplegia.

-it continues during phonation and caloric tympanic membrane stimulation,

-may be inhibited by those nonacoustic stimuli that trigger the acoustic reflex.

-audible click heard by some pts is synchronous with relaxation phase of the myoclonus and tubal closure.

Diagnosis

-attempt to hear it.

-auscultate mastoid process, neck, skull, & orbit & determine if sound is:

                 synchronous (vascular) or asynchronous (nonvascular) with the pulse.

-observation of palate is not necessarily diagnostic, as opening the mouth may suppress myoclonus.

-If rhythmic muscle contraction is suggested, tympanometry can be diagnostic.

      -plot of compliance VS time (at ME pressure equal to maximal compliance)

                nb: increasing sensitivity of the instrument sometimes aids in this calculation.

                -can demonstrate a periodic decrease in compliance synchronous with the tinnitus.

                    -has a sawtoothlike waveform and is less periodic than the tracing obtained from vascular tinnitus.

Management   (Management of palatal or tensor tympani myoclonus has taken two forms):

      (1) attempts to decrease the hyperactive motor discharge to the muscles and

                -Diphenylhydantoin (phenytoin), valproic acid and carbamazepineÞ successfully suppress myoclonus.

                -Opening mouth, touching palate, filling mouth with water, blowing cold air on cornea.

      (2) procedures that render the muscle contractions less symptomatic.

                -sectioning tensor tympani muscle, dislocation of the TVP tendon from hamulus, & hamulus fracture

                -myringotomy with ventilating tube placement

 

PATIENT EVALUATION

 A. History:

-Overall history of the patients health is obtained with emphasis on medications and habits.

-The patient should then describe the tinnitus including:

                -1. Quality of tinnitus: pitch, loudness, location, duration pattern (constant, pulsatile, intermittent).

                -2. Other otologic symptoms and history: hearing loss, vertigo, otorrhea, aural fullness, otalgia,

                                infections, head trauma, noise exposure, ototoxic drug use.

                -3. Aggravating factors including fatigue, psychological stress, as well as sleep disturbance and the

                                level of disability created by tinnitus.

Evaluation

Questionnaires can also be useful to better understand patients' problems and to quantify subjective attributes.

-Tinnitus Handicap Scale (Kuk 1991; Tyler, Stouffer, Schum, 1990):

      -Indicate to what degree you agree/disagree with following statements by writing in a number from 0-100.

        0 indicates that you strongly disagree

       100 indicates that you strongly agree

       Numbers between 0 and 100 should also be used to represent your level of agreement with each statement.

      PLEASE ANSWER ALL THE QUESTIONS.

      1. I do not enjoy life because of tinnitus.  ________________

      2. My tinnitus  has gotten worse over the years.     ________________

      3. Tinnitus interferes with my ability to tell where sounds are coming from.       ________________

      4. I  am unable to follow a conversation during meetings because of tinnitus.   ________________

      5. Tinnitus causes me to avoid noisy situations.     ________________

      6. Tinnitus interferes  with my speech understanding when talking with someone in a noisy room____            

      7. I feel uneasy in social situations because of tinnitus.         ________________

      8. The general public does not know about the devastating nature of tinnitus. ________________

      9. I cannot concentrate because of tinnitus.             ________________

      10. Tinnitus creates family problems.         ________________

      11. Tinnitus causes me  to feel depressed.                ________________

      12. I find it difficult to explain what tinnitus is to others.        ________________

      13. Tinnitus causes stress.           ________________

      14. I am unable to relax because of tinnitus.              ________________

      15. I complain more because of tinnitus.    ________________

      16. I have trouble falling asleep at night because of tinnitus.                ________________

      17. Tinnitus makes me feel tired. ________________

      18. Tinnitus makes me feel insecure.          ________________

      19. Tinnitus contributes to a feeling of general ill health.       ________________

      20. Tinnitus affects the quality of my relationships.                ________________

      21. Tinnitus has caused a reduction in my speech understanding ability.          ________________

      22. Tinnitus makes me feel annoyed.          ________________

      23. Tinnitus interferes with my speech understanding when listening to the  television____________

      24. Tinnitus makes me feel anxious.            ________________

      25. I think I have a healthy outlook on tinnitus.       ________________

      26. I have support from my friends regarding my tinnitus.     ________________

      27. I feel frustrated frequently because  of tinnitus.                ________________

      To obtain total score, subtract 100 from questions 25 and 26, add scores from all questions & divide by 27.

Quality

-Patients' descriptions of tinnitus (eg buzzing, rushing, ringing, roaring, and whistling).

-nb: pulsing or popping soundsÞ vascular or muscular tinnitus, but may also occur with sensorineural tinnitus.

Perceptual location

-one ear; in both ears; at the back, middle, side, or front of the head; and occasionally outside of the head.

 Pitch

-most pts are able to equate the pitch elicited by a pure tone with the most prominent pitch of their tinnitus.

-Several techniques are available to estimate tinnitus pitch.

      -patient may be asked which of two tones has a pitch closer to the tinnitus.

      -patient manipulates frequency of a tone until its pitch is ~ equal to most prominent pitch of tinnitus.

-pitch matching reliability varies widely among patients.

-one in every two patients with tinnitus, pitch varies from day to day or within a day.

Loudness

-measured by having subject adjust level of a pure tone so that it has about the same loudness as the tinnitus.

-Several researchers, Þ level of this pure tone of equivalent loudness was only 3 or 4 dB above threshold,

      even when the patients complained that the tinnitus was very loud.

 B. Physical Examination:

                 -General H&N examination with particular attention to CNS & CVS systems.

                -Pinna, external canal are inspected for clues to the origin of tinnitus.

                -Tympanic membrane:

                        -bluish or reddish mass is highly suggestive of a glomus tumor.

                             (pulsation of mass & paling when positive P with pneumatic otoscope support this diagnosis).

                       -hemotympanum.

                -Mastoid, orbit, neck, skull and external auditory canal are auscultated with a stethoscope.

                      -Any sounds should be correlated with the patients pulse.

                    -When a bruit is found, a palpable thrill is sought.

                -Additional procedures:

                     1.determine if the tinnitus changes with head position.

                              (Venous hums are more common in younger women, may be eliminated by gentle P on IJV).

                              (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.

                     2. AVMs in the mandible and maxilla may cause discoloration of the overlying skin or mucosa.

                     3. Palatal myoclonus may not be observable on intra-oral exam, may be inhibited with mouth open.

                                   If suspected, the palate may be observed with a flexible fiberoptic nasopharyngoscope.

                     4. TMJ should be palpated and auscultated.

                     5. small, sensitive microphone (Villchur/Killion1975) in the closed ear canal and use

                         amplification to listen to even the softest sounds.

  

INVESTIGATIONS:

 Audiometric evaluation:

      -standard audiometric battery:

                -puretone air and bone conduction, speech reception and discrimination,

                                reflex testing (including decay) and impedance should be performed.

                -tympanometry may identify negative pressure associated with conductive losses,

                                & to identify fluctuations in pressure associated with muscle twitching or pulsations.

     -ABR may be indicated when retrocochlear pathology is suspected.

     -Tinnitus matching:

                -allows a more precise definition of loudness and pitch - masking

                -residual inhibition may also be estimated.

                -in general tinnitus is matched at about 3 - 4 db above threshold.

                -50% pts say tinnitus is a single tone - others tinnitus resembles a narrow band noise in 3-5kHz range.

                -Masking involves adjusting the intensity of external sound until it drowns out the tinnitus.

                -Residual inhibition is the cessation of tinnitus after a sufficient masking stimulus.

                        The usual length is 25 to 45 seconds.

Masking

-in ~90% of patients the presentation of a pure tone or noise can mask tinnitus completely.

-this suggests that tinnitus and response to acoustic stimulus share same neural channels somewhere in CNS.

Patterns

-A tinnitus-masking pattern can be measured by determining the minimal level required to mask tinnitus at     several tone frequencies (Bailey, 1979; Formby and Gjerdingen, 1980; Fowler, 1940; Mitchell, 1983).

Feldmann (1971) classified masking patterns into five broad categories:

      1. Congruence, in which the tinnitus was masked just above threshold throughout the frequency range

      2. Distance, in which the tinnitus was masked at high levels throughout the frequency range

      3. Persistence, in which the tinnitus could not be masked

      4. Convergence, in which the tinnitus could be masked at high SLs at low frequencies and low SLs at

            high frequencies in subjects with a precipitous high-frequency hearing loss

      5. Divergence, in which the tinnitus could be masked at low SLs at low frequencies and high SLs at

            high frequencies in subjects with mild-to-moderate hearing loss

Psychoacoustic tuning curve

-may be useful to establish site of tinnitus.

-In the normal ear:

      -A low-level, pure-tone signal excites a small region of the basilar membrane.

      -A second pure tone  (a masker) with freq similar to above, can be introduced to masks the orig stimuli.

      -When this masking occurs, it is assumed that the excitation pattern of the masker has overlapped that

            of  the signal.

      -As the masker frequency moves further away from the signal frequency, greater masker intensities are   

            required for the excitation patterns to overlap.

      -The minimal level required to mask the signal VS masker frequency => plot called a psychoacoustic tuning

             curve (PTC) is obtained.

      -This curve represents, the spatial extent of the displacement pattern of signal along the basilar membrane.

            -tinnitus patients usually exhibit abnormal PTCs.

    -Tyler and Conrad-Armes (1984) used tinnitus loudness and pitch matches to determine the signal level and

            frequency for the PTC.

    -observations suggest that the tinnitus does not originate in a single place on BM in most cases.

    -the diversity of responses also affirms likelihood that tinnitus originates in many places in auditory system.

Noises of different bandwidths

-masking by noises of different bandwidths is another technique used to measure frequency resolution.

-In normal listeners:

-the overall level of noise band required to mask a tone is independent of its width at narrow bandwidths.               

-as the masker bandwidth is widened, some critical bandwidth is reached, beyond which the overall level   must be increased to mask the tone.

-nb: When fitting a tinnitus masker based on the lowest level to mask the tinnitus, careful tailoring of the         masker spectrum may be desirable.

 Ipsilateral and contralateral masking

-Normal-hearing;  pure tone presented to one ear can be masked easily by a noise presented to the same ear.

      -If a noise < 40-50 dB SPL is presented to opposite ear, the signal threshold can be increased by a small

          amount, usually less than 5 dB. This is called central masking because the interaction is presumed to occur

          between the excitation produced by the signal and masker in the central nervous system.

      -If noise>40-50dB SPL is presentd to opp ear, the noise can mask the tone in contralat ear by bone

            condctn  => this  is called cross-over.

-Minimal masking levels of broadband noise required to mask the tinnitus:

      -masker levels required in the contralateral ears were similar to the levels in the ipsilateral ears,

                =>  cross-over masking was not occurring.

      nb: In some patients, once unilateral tinnitus is masked, a tinnitus of a similar quality suddenly appears in

                the opposite ear, as if the tinnitus were present in both ears all the time but was lateralized to one ear

                because of its greater loudness.

Adaptation of tinnitus masking

-If a continuous noise is presented at levels that initially masked the tinnitus, in some patients the tinnitus

         will  reappear after several seconds or minutes.

-cause: ?? the adaptation of the masker, whereas the tinnitus, being processed differently, did not adapt.

        or ??  the masker is exacerbating the tinnitus, and the tinnitus magnitude is increasing over time.

Postmasking effects

-when a masking noise is turned off,  in many cases the tinnitus remains inaudible.

Spontaneous otoacoustic emissions

-spontaneous acoustic emissions most likely indicate an active mechanism within the cochlea.

-At present the relationship between spontaneous emission and tinnitus is unclear.

Auditory brainstem response

-Ikner&Hassen (1990) Þ  little difference between (ABR) in tinnitus & nontinnitus patients matched for HL.

  

Laboratory studies:

   Patients with sensorineural tinnitus require routine laboratory studies to determine source of HL

    FBC, ESR, EUC, UA, TFT, and glucose tolerance tests, syphilis serology,  collagen vascular diseases (ANA,

        Lupus prep, rheumatoid factor, and complement).

Radiologic evaluation:

-CT and MRI are useful in evaluation of neoplasms and other soft-tissue lesions.

-Angiography and CT with contrast may be useful when tinnitus is thought to be due to vascular abnormalities.

-Arteriography is performed on most patients to delineate feeder vessels and the tumor's extent.

-MRA/MRV.

 MANAGEMENT

 A. SURGICAL THERAPY:

-Once the etiology of tinnitus is established, specific therapy may be instituted.

 -Surgical therapy is most effective in para-auditory tinnitus.

      1. Correction of vascular abnormalities.( jugular vein ligation, embolization of AVM, resection of glomus)

      2. TVP section, myringotomy + tube placement and ostium sclerosis for patulous ET & palatal myoclonus.

-Surgery is less effective in sensorineural tinnitus:

      1. Results best in otosclerosis surgery: 75% of patients report improvement in tinnitus.

      2. Various nerve sectioning procedures have been performed - retrolabyrinthine vestibular neurectomy,         tympanosympathectomy, translabyrinthine cochleovestibular neurectomy, with variable results.

      3. House reports in 500 translabyrinthine removals of acoustic neuromas with eighth nerve section

            that   50% remain the same or improve, and 50% worsen.

      4. House and Brackmann (1981), Þ 25% chance of improving tinnitus when a cochlear nerve section

             was added to a vestibular nerve section for Ménière's disease; tinnitus worsened in 1 of 17 (6%)

            patients.

      5. Stellate ganglia block or section (based on the ischemia theory) ?? Þ  increased blood flow to cochlea.

      6. Warrick (1969).66ptsÞ (+)’ve response in 56% of pts with Ménièr’s & 27% of pts with idiopath tinnitus

      7. Other procedures directed toward tinnitus: tonsillectomy, excision of the tympanic plexus, and section

             of   the vestibulofacial anastomoses (McFadden, 1982).

B. MEDICATION

-nb: Murai et al., 1992 a recent review of pharmacologic treatment of tinnitus.

 1. Anticonvulsants: (Carbamazepine 100 to 400 mg/day....??? good to reasonable results )

                                     (primidone and phenytoin ....less favourable results)

      -based on theory that they will decrease neural hyperactivity.

      -limited by lack of effectiveness and side effects (bone marrow depression and hepatotoxicity).

2. Anti-dysrythymics & LA’s:

      -IV lidocaine: up to 80% of patients respond with decrease or disappearance of tinnitus.

                -very small percentage have reported complete relief.

      -Tocainide, an oral analogof lignocaine, is advocated by Shea who reports 46% improved.

                -but drug has significant side effects at the required doses (ie CNS excitation, N&V, anorexia).

      -Flecainide Þ  disappointing results - only 23% of the patients reported improvement.

3. Vasodilators Þ  to combat supposed local ischemia.

      -Niacin family most widely used, but now falling into disfavor.

      -Nicotinic acid (vitamin B6), a peripheral vasodilator

      -Cerebral vasodilators such as carbon dioxide, histamine and papaverine Þ  without much success.

4. Antidepressants: Help some patients with clinical evidence of depression.

                                    May also have activity at neuronal level.

5. BZ’s: (Lechtenberg & Shulman 1984)

      -12 of 23 (52%) patients receiving oxazepam reported benefit,

      -18 of 26 (69%) receiving clonazepam reported benefit.

                Clonazepam is an anticonvulsant, well absorbed GIT & metabolized in the liver.

C. MASKING:

-Hippocrates noted masking effects of noise in 400's B.C. The effect is probably for two reasons:

      1. A broad band noise is less irritating to the patient than their narrow band tinnitus.

      2. Patients have control over the masking.

-Many tinnitus sufferers have developed their own masking techniques

      •running fans, faucets, air conditioners, or a poorly tuned radio.

-Several types of hardware available:

      1. Hearing aid (Saltzman and Ersner 1947):

                -provides good masking especially for those with tinnitus pitch in speech range.

                -hearing aid amplifies background noise that could successfully mask the tinnitus.

                -Hearing-impaired patients with tinnitus should try a hearing aid before trying a tinnitus masker.

                -A hearing aid interferes less with speech, does not produce an intense noise that could

                     produce  damage, and can improve speech understanding.

      2. Tinnitus masker (Jones and Knudsen 1928): worn like hearing aid but produces only masking noise.

      3. Tinnitus instrument: combination aid and masker with independently adjustable controls.

                Good for patients with hearing loss in same frequency range as their tinnitus.

-As noted, inhibition of tinnitus sometimes persists even after masking noise removed (residual inhibition).

-Improvement and continued use Þ in 5-50% of patients in different studies.

-Concern has been raised b/c some maskers are powerful enough (>85 db) to produce additional hearing loss.

-No data are currently available, so patients should use the lowest setting which provides relief.

-masking data of Feldmann (1971), Shailer et al. (1981), and Tyler and Conrad-Armes (1984) =>

             noise spectrum of the masker need not be centered on the frequency of the tinnitus.

-No protocol is available for deciding which ear to fit with a masker.

Tyler and Conrad-Armes (1983a) showed that in many patients the tinnitus can be masked equally well in both

 ears; therefore, the clinician always should try to fit the tinnitus masker on each ear separately.

 D. Biofeedback:

-House: biofeedback training is effective in improving tinnitus in 80% of pts who complete a training course.

-Biofeedback is effective in reducing anxiety and stress which may exacerbate tinnitus, and increases ability

     of  the patient to cope with his symptoms.

 

E. Miscellaneous Treatments:

1. Electrical stimulation initially proposed in 1801 when Grapengiesser applied current to external canal.

      -A positive DC current is most effective - especially when applied at the promontory or round window

      -but ultimately destroys hair cells and spiral ganglion cells.

      Extracochlear stimulation

                -Hatton et al. (1960), using direct current, produced a reduction in tinnitus in 15 of 33 (46%) patients.

                          -electrical current was most effective in suppressing tinnitus in profoundly hearing-impaired pts

                -Portmann (1983) were able to reduce the magnitude of tinnitus in 66% of 72 patients with tinnitus

                            (no selection criteria reported) by presenting a positive current to the cochlear round window.

                                The tinnitus was reduced throughout the stimulation.

                                After current was terminated, tinnitus reappeared louder than before in several patients

               -Graham& Hazell (1977);  Hazell (1983), =>transtympanic stimulation of the promontory in

                               totally deaf patients,  reduce tinnitus in 2 of 13 (15%) and 7 of 12 (58%) patients,

                                respectively.

                -Chouard et al. (1981) electrodes on tragus and behind ear lobe.

                                Þ 64 ears Þ reduced tinnitus in 30 (47%).

                -Vernon and Fenwick (1985) Þ  transcutaneous electrodes in preauricular and postauricular regions.

                                -5 of 23 (22%) Þ  reduction in their tinnitus.

                -Kuk et al. (1989) Þ  eardrum electrode.

                -Theraband (Shulman, 1985),

                                -an extracochlear wearable device to reduce tinnitus, marketed in the United States.

      Intra-cochlear stimulation

                -House and Brackmann (1981) reported that 23 of 29 (79%) 3M/House cochlear-implant patients

                         with tinnitus reported relief of tinnitus while using their cochlear implant.

2. Acupuncture: Multiple authors have found no benefit over placebo.

3. Hypnotherapy: Has been demonstrated to be a useful adjunct to relaxation training in some patients.

4. Allergy and Diet: ?????

 

F. Counselling:

Stouffer recommends the following be covered with patients:

1. Tinnitus is a common condition usually associated with benign disease.

2. Tinnitus may increase with time.

3. It is unlikely the patient will become less annoyed by his tinnitus.

4. A log of times, places, and conditions which affect the tinnitus may be useful in managing the condition.

5. Ear/noise protection is important.

6. Patients with Meniere's disease may have more difficulties coping with tinnitus than others.

 

Bibliography:

Cummings, C. Otolaryngology. Vol. IV. Ch. 172. pp. 3201-3217.

English, GM. Otolaryngology. Vol. I. Ch. 53.

Fortnum, HM, and Coles, RRA. Trial of Flecainide in the Management of Tinnitus. Clinical Otolaryngology. 1991. 16:93-96.

 Glasscock, ME, et al. An Analysis of the Retrolabyrinthine vs. the Retrosigmoid Vestibular Nerve Section. Otolaryngology, Head and Neck Surgery. 1991. 104:88-95.

Paaske, PB, et al. Zinc in the Management of Tinnitus. Annals of Otology, Rhinology and Laryngology. 1991. 100:647-649.