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 TITLE:   Tinnitus
 SOURCE:  Dept. of Otolaryngology, UTMB, Grand Rounds
 DATE:    24 November 1991
 RESIDENT PHYSICIAN:      Joseph Bradfield, M.D.
 FACULTY:                 Chester L. Strunk, M.D.
 DATABASE ADMINISTRATOR:  Melinda McCracken, M.S.
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"This material was prepared by resident physicians in partial fulfillment 
of educational requirements established for the Postgraduate Training 
Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and 
was not intended for clinical use in its present form.  It was prepared 
for the purpose of stimulating group discussion in a conference setting.  
No warranties, either express or implied, are made with respect to its 
accuracy, completeness, or timeliness.  The material does not necessarily 
reflect the current or past opinions of members of the UTMB faculty and 
should not be used for purposes of diagnosis or treatment without 
consulting appropriate literature sources and informed professional opinion." 
 
 I.   INTRODUCTION
 
      A. Definition: The perception of sound without an external
 acoustic stimulus.  It may be caused by a wide variety of anatomic
 and pathologic abnormalities.  It should be noted that tinnitus is
 a symptom of a great number of disease processes, therefore all
 patients deserve a full head and neck examination.
 
      B. Prevalence:  It is estimated that from 15-32% of adults
 have had tinnitus at some point, and about 5 percent are severely
 disabled by their tinnitus.
 
      C. Epidemiology:
      1. Male/Female ratio = 1, with a peak incidence in 50-70 year
 olds, declining after that.
      2. Majority report tinnitus is constant.
      3. Over 85% report tinnitus of < 10dB SL.
      4. Most patients also have hearing loss, with 50% of
 profoundly deaf students complaining of tinnitus - usually in the
 better ear.
      5. The pitch of tinnitus may correlate with pathology.
         
 II.   CLASSIFICATION
 
      A.  Objective versus Subjective Tinnitus:  Tinnitus was
 previously grouped into subjective (audible only to the patient)
 and objective (audible to the examiner).  However, it is more
 useful to classify tinnitus by etiology.  Some clues to probable
 origin may be obtained from the patients characterization of his
 tinnitus - with pulsations implying a vascular origin, clicking and
 popping a myogenic origin, and constant noises arising in the inner
 ear.
 
      B.  Otoacoustic Emissions:  This refers to signals thought to
 be generated by the contractile activity of the outer hair cells of
 the cochlea and propagated into the ear canal via the ossicles and
 tympanic membrane.  Otoacoustic emissions may be detected by using
 sensitive microphones placed in the external auditory canal.  The
 level of emission varies up to 35 db SPL, and the signals are
 characteristically narrow band signals between 1.2 and 4.7 KHz.  In
 general, otoacoustic emissions are inaudible to the patient, but
 Penner estimates that in 4% of tinnitus sufferers otoacoustic
 emissions cause the patients tinnitus.  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.
 
      C.  Vascular Tinnitus:  A history of pulsatile tinnitus which
 is usually synchronous with heartbeat suggests vascular origin. 
 Vascular tinnitus may be further divided into:
 
      1. Arterial: Most commonly resulting from atherosclerotic
 plaques in the internal carotid artery.  Other causes include A-V
 fistulae/malformations (the most common AVM causing pulsatile
 tinnitus is between the occipital artery and the transverse sinus),
 aneurysms, persistent stapedial artery and aberrant internal
 carotid artery.  Conductive hearing loss may attenuate background
 noises, bringing attention to the pulsatile tinnitus.
      2.  Nonarterial: Venous hums result from irregularity of flow
 in the jugular veins due to compression from the transverse process
 of C2. In addition, jugular bulb abnormalities, elevated ICP, and
 vascular neoplasms may cause pulsatile tinnitus.
 
      D.  Muscle Contraction Tinnitus:  Results from synchronous
 contractions of the muscles of the middle ear, eustachian tube and
 palate.  Palatal myoclonus is usually faster than heart rate - 60
 to 200 per minute - and is described as an objectively audible
 clicking sound.  Sonotubometry studies indicate that the sound
 heard may be the click of the eustachian tube 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.
          
      E.  External and Middle Ear Tinnitus:   As previously
 mentioned, conductive hearing loss (e.g. from infection, effusion,
 cerumen and especially otosclerosis) may attenuate background noise
 and result in tinnitus.  Cerumen, foreign bodies and hairs may lie
 against the TM and cause tinnitus.  Some place the patulous
 eustachian tube in a separate category of respiratory tinnitus. 
 Here, the patient complains of a rushing or blowing sound with
 respiration.  Myringotomy and tube placement, sclerosing agents at
 the tube orifice and diathermy of the orifice may be effective
 treatment.
          
      F.  Peripheral Sensorineural Tinnitus:  Peripheral tinnitus is
 localized to one or both ears, while central tinnitus is more
 poorly defined and may be heard all over the head.  Eighty-five
 percent of the patients with tinnitus have some form of hearing
 loss.  Many hypotheses have been proposed regarding the
 pathophysiology of peripheral tinnitus.  Two of the most commonly
 accepted are:
 
      1.  Alteration in the spontaneous discharge rate of auditory
 fibers - 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).  This is supported by the observation
 that patients with high pitch, noise induced hearing loss usually
 have high pitched tinnitus, and that patients with Meniere's
 disease often complain of low pitched tinnitus.
      2.  Tonndorf proposed in 1980 that decoupling of the
 stereocilia from the tectorial membrane could result in an increase
 in "noise" from that area.  This could result from degenerative
 processes or from noise trauma.  
 
      Multiple pathologic processes may cause peripheral tinnitus:
 
      1.  Noise Exposure may be the most common cause.  In Vernon's
 study tinnitus associated with noise exposure is typically
 high-pitched and constant.  With continued noise exposure SNHL
 becomes worse as does tinnitus.  Early in the course there is SNHL
 at 4 kHz (noise notch) but recovery at higher frequencies. This is
 lost as condition worsens.
      2.  Presbycusis is commonly encountered in practice.  The
 hearing loss is downward sloping high frequency, usually with
 associated high frequency tinnitus.  
      3.  Head Trauma may result in tinnitus which is not noticed
 until some time after injury.  It may be on the side of, or on the
 side opposite to trauma.  It frequently increases in intensity
 initially and then gradually resolves.
      4.  Acoustic Neuroma presents with tinnitus in 10% of the
 cases.  Tinnitus may be constant or intermittent, and may or may
 not be associated with hearing loss.
      5. Meniere's Disease - Tinnitus one of the three cardinal
 symptoms of disease.  It is typically low pitched (median 300 hz)
 and rumbling, unilateral, and may be intermittent especially early
 in course.  Typically it is associated temporally with attacks of
 vertigo and hearing loss.  Later in disease the tinnitus may become
 constant.
      6. Otosclerosis may cause tinnitus both by its conductive
 component as well as by its involvement in the inner ear. 
 Typically the tinnitus is low-medium pitch as in other conductive
 problems.  70-95% of patients with this disorder complain of
 tinnitus.
      7. Drugs - many medications are known to cause tinnitus.  It
 should be remembered that tinnitus is a common disorder, and may be
 related only temporally to medications.
           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.
      8. Other causes of peripheral tinnitus include metabolic
 diseases (e.g. hyperthyroidism, Diabetes), intracranial neoplasms
 and other CNS lesions (e.g. infections, MS).
 
      G.  Central sensorineural tinnitus is usually described by
 patient as occurring  "all over the head."  Evidence for the central
 generation of auditory signals is found in the observation that
 patients who have undergone labyrinthectomy or eighth nerve section
 may still complain of tinnitus.  The mechanism for central tinnitus
 is unknown, but again may lie in the change in firing rates of
 central inhibitory neurons (e.g. in the dorsal cochlear nucleus). 
 Tumors of the central nervous system - especially the temporal
 lobe, and generalized head trauma are implicated.  
  
 III.  PATIENT EVALUATION
 
      A. History:  An 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.  
 
      B. Physical Examination:  All patients recieve a general head
 and neck examination with particular attention to neurologic and
 cardiovascular systems.  The pinna, external canal and drum are
 inspected for clues to the origin of tinnitus.  The mastoid, orbit,
 neck, skull and external auditory canal are auscultated with a
 stethoscope.  Any sounds should be correlated with the patients
 pulse.  Additional procedures:
      
      1.  The physician should determine if the tinnitus changes
 with head position.  Venous hums are more common in younger women,
 and may be eliminated by gentle pressure on the internal jugular. 
 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
 examination, and may be inhibited with the mouth open.  If
 suspected, the palate may be observed with  a flexible fiberoptic
 nasopharyngoscope.  If careful search must also be made for other
 neurologic symptoms.
      4.  The TMJ should be palpated and auscultated, and a search
 made for other evidence of TMJ disease.
 
      The history and physical examination should give a good idea
 of the source of tinnitus, and the remainder of the workup may be
 tailored accordingly.   In a patient with bilateral symmetric
 hearing loss and an appropriate history, limited additional workup
 would be indicated.      
 
      C. Audiometric evaluation:  A 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, as well as 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 and residual inhibition may also be
 estimated.  In general tinnitus is matched at about 3 - 4 db above
 threshold.  About half of patients say their tinnitus is a single
 tone - in the other half the tinnitus resembles a narrow band
 noise in the 3000 - 5000 Hz 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.  
 
      D. Laboratory studies:  Patients with sensorineural tinnitus
 require routine laboratory studies to determine the source of their
 hearing loss.  Studies include CBC, ESR, electrolytes, urinalysis,
 thyroid function and glucose tolerance tests, and serology for
 syphilis and collagen vascular diseases (ANA, Lupus prep,
 rheumatoid factor, and complement).
 
      E. 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.  
 
 IV.  TREATMENT
 
      A. Surgical Therapy:  Once the etiology of tinnitus is
 established, specific therapy may be instituted.  Surgical therapy
 is most effective in vibratory tinnitus and neoplasms:
 
      1. Correction of lesions in vascular abnormalities
 sometimes affords relief e.g. jugular vein ligation, embolization
 of AVM, resection of glomus tumors.
      2. Tensor veli palatini section, myringotomy and tube
 placement and ostium sclerosis has been advocated for patulous
 eustachian tube with mixed results and 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.  However House reports in 500 translabyrinthine removals
 of acoustic neuromas with eighth nerve section that 50% remain the
 same or improve, and 50% worsen.
            
      B. Medical Therapy:  Surgery has little place in the
 management of tinnitus in the absence of other pathologic
 conditions requiring treatment.  Many medical therapies have been
 tried: 
      
      1. Anticonvulsants: Carbamazepine, primidone and phenytoin
 have been advocated 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 and Local anesthetics: Up to 80% of
 patients respond to IV lidocaine with decrease or disappearance of
 tinnitus. A very small percentage have reported complete relief.
 Tocainide, an oral analog, is advocated by Shea who reports 46%
 improved.  However, the drug has significant side effects at the
 required doses - CNS excitation and nausea, vomiting and anorexia.
 Flecainide has also been evaluated with disappointing results -
 only 23% of the patients reported improvement.
      3.  Vasodilators have been used to combat supposed local
 ischemia.  Niacin family most widely used, but now falling into
 disfavor.  Cerebral vasodilators such as carbon dioxide, histamine
 and papaverine have also been used without much success.
      4. Antidepressants: Help some patients with clinical evidence
 of depression. May also have activity at neuronal level.
 
      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: provides good masking especially for those
 with tinnitus pitch in speech range.
      2. Tinnitus masker: 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 reported in from 5-50% of patients in different
 studies.  Some concern has been raised because 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.  
 
      D. Biofeedback:  House reports that biofeedback training is
 effective in improving tinnitus in 80% of the patients who complete
 a training course.  Biofeedback is effective in reducing anxiety
 and stress which may exacerbate tinnitus, and increases the 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.  Portmann and Shulman initially had some
 success with stimulation of round window and transcutaneously but 
 this not confirmed by recent studies.  McKerrow, and House and
 Thedinger have used cochlear implant as analog for tinnitus
 instrument with some success.
      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:  Otolaryngic allergy affecting the inner,
 outer, or middle ear could possibly contribute to tinnitus. 
 Allergy management in Meniere's disease patients brought on symptom
 relief in 30%.  Other dietary constituents - notably coffee, tea,
 red wine, alcohol, cheese and chocolate have on occasion been
 implicated.  The role of zinc in tinnitus generation has also been
 suspected by some.
 
 VI.  SUMMARY AND CONCLUSIONS
 
      A.  It is crucial that the physician bear in mind that
 tinnitus is a symptom and not a disease.  Each patient requires a
 full evaluation for the etiology of his tinnitus.  Specific disease
 entities identified should be treated, and patients must be given
 as much information as possible about the cause and potential
 treatment of their tinnitus.  Extensive counseling is often
 required in those with disabling tinnitus.  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.
      B.  Finally, patients should be encouraged to contact:
  
                     The American Tinnitus Association
                     P.O. Box 5
                     Portland Oregon 97207
 
 -------------------------------------------------------------------------------
                          BIBLIOGRAPHY
 
 Alleva, M, Loch, WE, and Paparella, MM.  Tinnitus. Primary Care.  
 1990. 17:289-97.
 
 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.
 
 Fox, GN, and Baer, MT.  Palatal Myoclonus in Children.  Western 
 Journal of Medicine.  1991. 154:98-102.
 
 Glasscock, ME, et al.  An Analysis of the Retrolabyrinthine vs. 
 the Retrosigmoid Vestibular Nerve Section.  Otolaryngology, Head 
 and Neck Surgery.  1991. 104:88-95.
  
 Hazell, JW, and Jastreboff, PJ.  Tinnitus I:  Auditory Mechanisms: 
 a Model for Tinnitus and Hearing Impairment.  Journal of 
 Otolaryngology. 1990. 19:1-5.
 
 Hazell, JW.  Tinnitus II:  Surgical Management of Conditions 
 Associated with Tinnitus and Somatosounds.  Journal of Otolaryngology. 
 1990. 19:6-10.
 
 Hazell, JW.  Tinnitus III:  The Practical Management of Sensorineural 
 Tinnitus.  Journal of Otolaryngology. 1990. 19:11-18.
 
 House, JW. Tinnitus: evaluation and treatment. AJO. 1984.  5:472-475.
 
 House, JW.  Therapies for Tinnitus.  American Journal of Otology.  
 1989. 10:163-165.
 
 Levine, SB and Snow, JB. Pulsatile tinnitus. Laryngoscope. 1987.  
 97:401-405.
 
 Mattox, DE and Richtsmeier, WJ. Tinnitus: the initial evaluation.  
 OHNS. 1987. 96:172-174.
  
 Mattox, DE, and Wilkins, SA.  Tinnitus.  American Academy of 
 Otolaryngology-Head and Neck Surgery Instructional Package.  
 Washington, DC. 1989.
 
 McKerrow, WS, et al.  Tinnitus Suppression by Cochlear Implants.  
 Annals of Otology, Rhinology and Laryngology.  1991. 100:552-558.
 
 Penner, MJ.  An Estimate of the Prevalence of Tinnitus Caused by 
 Spontaneous Otoacoustic Emissions.  Archives of Otolaryngology, Head 
 and Neck Surgery.  1990. 116:418-423.
 
 Paaske, PB, et al.  Zinc in the Management of Tinnitus.  Annals of 
 Otology, Rhinology and Laryngology. 1991. 100:647-649.
 
 Spektor, Z, et al.  Otoacoustic Emissions in Normal And Hearing 
 Impaired Children and Normal Adults.  Laryngoscope. 1991. 
 101:965- 976.
 
 Stouffer, JL, et al.  Tinnitus as a Function of Duration and 
 Etiology: Counseling Implications.  American Journal of Otology.  
 1991. 12:188-194.
 
 Thedinger, BS, et al. Cochlear implant for tinnitus. Annals of 
 Otology, Rhinology and Laryngology. 1985. 94:10-13.
 ---------------------------END-------------------------------------------


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1.  Which of the following statements abouttinnitus is FALSE?
    a.  It is the perception of sound without an external acoustic stimulus
    b.  it is an only an annoying symptom that really needs no workup.
    c.  It is a symptom of a great number of a number of disease 
        processes and patients deserve a careful evaluation
    d.  Subjective tinnitus is audible only to the patient

2.  Which of the following is NOT  associated with tinnitus?
    a.  otosclerosis
    b.  head trauma
    c.  penicillin toxicity
    d.  acoustic neuroma

3.  Vascular causes of tinnitus are mostly associated with 
    a.  aberrant subclavian arteries
    b.  berry aneurysm
    c.  temporal arteritis
    d.  plaques in the internal carotid artery

4.  Which points are mostly important to elicit in the patient with tinnitus?
    a.  pulsatile or steady character
    b.  previous noise exposure
    c.  hearing loss
    d.  all of the above
  
5.  Which of the following is not really essential to the examination for
    tinnitus:
    a.  checking for postauricular lymphadenopathy
    b.  auscultation of the common carotid arteries
    c.  inspection of the pinna and ear canal
    d.  listening to the mastoid bone, orbit, ear canal, and skull with
        the stethoscope

6.  The most common pathologic process associated with peripheral tinnitus is
    a.  liver disease
    b.  industrial or military noise exposure
    c.  cerebrovascular accident
    d.  pituitary adenoma

7.  The medications most likely to cause tinnitus are
    a.  aminoglycosides
    b.  loop diuretics
    c.  salicylates including aspirin in large doses
    d.  all of the above

8.  The most effective treatment of persistent tinnitus is
    a.  anti-arrythmics
    b.  acupuncture
    c.  stimulus masking agents
    d.  anti-cholinergics


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==================================================================
   Francis B. Quinn, Jr., M.D.    
   University of Texas Medical Branch
   Dept. of Otolaryngology
   Galveston, TX 77555-0521      Internet addresses:
     409-772-2706, 772-2701        fbquinn@UTMB.edu
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