Tinnitus
Grand Rounds – 1/20/99
Edward D. Buckingham, M.D.
Jeff Vrabec, M.D., Faculty Sponsor
Francis Quinn, M.D., Series Editor
Introduction
Tinnitus is defined as the perception of a sound produced involuntarily within the body. It may be
the most prominent symptom of a disease process which is threatening the patient’s physical well being, or
merely an associated symptom of a benign condition. The psychological effects of benign tinnitus can
severely affect quality of life of the patient and their entire family. In severe cases, the psychological affects
of tinnitus may even precipitate suicide. The physician must be knowledgeable of the causes of tinnitus,
aware of the severe conditions associated with the symptom, able to make the diagnosis, and offer definitive
treatment or symptomatic relief.
Definition and Epidemiology
Tinnitus, as defined above, may be divided into two major categories; objective, or tinnitus
produced by paraauditory structures, usually from vascular or myoclonic sources; and subjective, or tinnitus
generated by the sensorineural auditory system. 1,2 In general, tinnitus prevalence and severity increases
with age mostly affecting those in the 40 to 70 year old age group and with equal sex distribution. A study
by Axelsson and Ringdahl (1987) noted that 337 people with tinnitus were identified in a population of
2378 Swedes 1. Also of note was that the severity of effect on quality of life increased with age. In general,
subjective or sensorineural auditory tinnitus is much more prevalent than objective tinnitus. For the
practicing otolaryngologist these factors have important implications in today’s aging population.
Objective Tinnitus
Strictly, the definition of objective tinnitus is that which is audible to the physician or another
person, but in practice this encompasses all causes which are paraauditory in nature; it may be pulsatile or
non-pulsatile. The differential diagnosis includes; vascular abnormalities such as, neoplasms, arteriovenous
malformations, arterial bruits, and venous hums; and muscle contraction tinnitus such as palatomyoclonus.
The diagnosis of objective tinnitus begins with a thorough history and physical examination. The patient
should be questioned about the nature of the tinnitus and its relation to the heart rate. Asking the patient to
perform light physical activity may confirm the pulsatile nature. Physical exam should include a thorough
otolaryngologic exam paying particular attention to the otoscopic exam looking for retrotympanic mass.
Additionally, a thorough search should be made for an audible bruit with auscultation of the external canal,
orbit, mastoid process, skull, and neck using both the bell and the diaphragm or electronic stethoscope if
available. The remainder of the work-up will be lead by the history, physical findings, and the suspected
diagnosis. All patients should receive an audiogram.
Pulsatile tinnitus
The list of causes of pulsatile tinnitus is extensive. It includes causes of increased intracranial
pressure, carotid artery atherosclerosis, vascular tumors, heart murmers, arteriovenous fistulas, and others
including idiopathic. An algorithm for the diagnosis of pulsatile tinnitus was recently published by
Sismanis.3 The article recommends evaluation first by otoscopy. A retrotympanic mass requires a CT of
the temporal bones looking for glomus tympanicum, aberrant carotid artery, and jugular bulb abnormalities.
Glomus jugulare suspicion requires a CT of the neck and carotid angiography. If no retrotympanic mass is
present, a decision must be made between suspicion of increased intracranial pressure, or carotid
artery/cardiac abnormality. To evaluate suspicion of increased ICP a MRI-MRA and a neuroophthalmology consult should be obtained looking for intracranial abnormality or papilledema. If no
hydrocephalus or other intracranial abnormality is present, lumbar puncture confirms the diagnosis of
benign intracranial hypertension (pseudotumor) if the ICP is greater than 200 mm H 2O. Respectively, if
carotid artery or cardiac abnormality is suspected a duplex ultrasound or echocardiogram should be
performed. These may support the diagnosis of atherosclerotic carotid artery disease (ACAD), carotid
tortuosity, or valvular heart defect with murmur. If a carotid lesion is still suspected and the duplex and
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echo are normal an MRI-MRA or a carotid angiogram may be necessary. In general, the study found that
history and physical examination are the two most important factors in evaluating patients with pulsatile
tinnitus. BIH syndrome, ACAD, and glomus tumors compose two thirds of definable causes. 3
Benign intracranial hypertension (pseudotumor cerebri) syndrome
BIH syndrome was the most common cause of pulsatile tinnitus in Sismanis’s recent study.3 The
condition is characterized by increased ICP without focal neurologic signs, except for an occasional sixth or
seventh nerve palsy. The pathophysiologic mechanism responsible for PT in these patients probably is
secondary to the transmission of systolic pulsations of the CSF to the exposed medial aspect of the dural
venous sinuses and the resulting periodic compression of their walls, which convert the normally laminar
blood flow to turbulent. Diagnosis is made by LP and measurement of CSF pressure after a head imaging
to rule out other etiologies of intracranial hypertension. Patients with BIH tend to be female age 20 – 50
and overweight. Pulsatile tinnitus subsides with light digital pressure applied over the ipsilateral internal
jugular vein of the side with tinnitus. Other symptoms include blurred vision, fronto-occipital headache,
and lightheadedness-disequilibrium. A mild low-frequency hearing loss may be present with excellent
discrimination. The hearing loss normalizes after the elimination of the PT by applying light pressure over
the ipsilateral IJV. Treatment of this syndrome consists of weight loss and administration of acetazolamide
and furosemide. If these fail a subarachnoid-peritoneal shunt may be placed, and some patients have been
relieved by gastric bypass for weight reduction.3
Vascular neoplasms
The classic vascular tumors associated with pulsatile tinnitus are glomus tympanicum and glomus
jugulare. Characteristics of vascular tumors on physical exam and radiography include the following. A
bruit, if found, is not altered appreciably by light pressure on the neck, head position, posture, or Valsalva
maneuver. Tympanometry may be useful showing regular perturbations which when plotting compliance as
a function of time may be compared to the patient’s pulse rate. On otoscopy, a bluish or reddish mass is
highly suggestive of a glomus tumor. Obvious pulsations of the mass and paling when positive pressure is
applied by a pneumatic otoscope support this diagnosis, however, hemotympanum, dehiscent jugular bulb,
and carotid artery abnormality must be considered, and radiographic studies should precede any surgical
procedure such as myringotomy or exploratory tympanotomy. The physician should check the entire head
and neck for masses. Cranial nerve and cerebellar function should be assessed as these tumors may involve
these areas. If a glomus tumor is suspected, a CT scan should be obtained. It may show a mass in the
middle ear space or erosion of the jugular spine. Additionally, arteriography should be performed to
delineate feeder vessels and the tumor’s extent. MRI is also playing an increasingly important role.
Treatment of these lesions is usually surgical.
Arteriovenous malformations
AVMs may be diffucult to differentiate from neoplasms. AVMs are developmental abnormalities
and often are considerably more extensive than their symptoms suggest. These lesions may enlarge rapidly
and tend to recur. They may impinge on adjacent structures, causing deformation by mass effect. The most
common AVMs are those of the posterior fossa between branches of the occipital artery and transverse
sinus. AVMs of the mandible are uncommon, but are notorious for causing tinnitus. Communications
between the carotid artery and cavernous sinus, most often resulting from trauma, are infrequent but have
serious consequences. Pulsatile tinnitus is often the initial complaint of the patient, but other symptoms
include headache, and papilledema. They usually have a bruit and when palpable, exhibits a thrill and is
generally more compressible than a tumor. If associated with a sufficiently large arteriovenous shunt, the
heart rate may actually slow with compression. Treatment is usually surgical preceded by angiography and
selective embolization of feeding vessels. As a general rule the lesion are larger than they appear on
angiography. When adjuvant embolization is used, maximal benefit will be achieved if subsequent surgery
is performed within 72 hours.1
3
Venous hum
This entity results partially from the eddy currents in the jugular vein and are normally heard in the
neck of many children and some adults, most notably, young women. These hums have been attributed to
the transverse process of the second cervical vertebra, and states of increased cardiac output, such as
anemia, thyrotoxicosis, and pregnancy. Often diagnosed when a hearing loss occurs in which external
background noise is attenuated, once diagnosed, they are significant only for the tinnitus they produce.
Placing gentle pressure on the anterior neck that does not occlude the carotid artery may eliminate the
tinnitus. Turning the head toward the uninvolved side decreases the sound and turning toward the involved
side makes it louder, as do deep breathing and Valsalva maneuver. Management consists simply of
reassuring the patient and treating the underlying disorder.1
The complete list of causes of paraauditory tinnitus is quite extensive including atherosclerotic
carotid artery disease, otosclerosis, jugular bulb abnormalites, abnormal condylar and mastoid emissary
veins, and many more. All of these share a common pathphysiology of increased turbulence of blood flow.
Pulsatile tinnitus should be called idiopatiic only after an extensive workup has been completed and specific
diagnosis has not been reached.
Palatomyoclonus
The myoclonus form of tinnitus is described as an irregular clicking sound heard within the ear.
The sound is rapid (20 to 400 beats per minute) and occurs intermittently. It is caused by the mucous
membranes of the eustachian tube snapping together in response to the movement of the palatal
musculature. Patients may also complain of fullness in the ear and distortion of hearing, and may have
histories of other muscle spasm, including postoccipital spasm, temporomandibular joint problems, and
blepharospasm. Diagnosis is made by auscultating the ear canal with a Toynbee tube for audible clicking.
Tympanogram may show recording movement synchronous with the contraction, and electromyographic
studies of the palatal musculature may confirm the diagnosis. Observable palatal fasciculation is associated
with a CNS lesion in which there is hypertrophic degeneration of the inferior olive; these patients warrant
an MRI to search for this lesion. Palatomyoclonus must be differentiated from tensor tympani spasm, which
will have similar symptoms and findings except without palatal muscle contraction; tensor tympani spasm is
usually transient. Treatment of palatomyoclonus initially consists of medications that include muscle
relaxants such as clonazepam or diazepam, warm liquids, and stress management. Botulinum toxin
injection into the active muscle may help in severe cases.2,4
Idiopathic stapedial muscle spasm
This condition, in contrast to palatomyoclonus, tends to be a rough, rumbling, or crackling noise
often accentuated or triggered by external noises such as voices, rattling of paper, or running water. The
symptoms generally follow this exposure, are brief and intermittent, and rarely become disruptive and
prolonged. Diagnostic studies include variable-intensity tympanometry in an effort to stimulate the spasm
and aid diagnosis, and acoustic reflex testing which may demonstrate a prolonged, continued increased
impedance during and after the sound stimulus.5 Primary treatment consists of muscle relaxants,
clonazepam or diazapam. Because the symptoms may last only 2 or 3 months and then disappear for long
periods, the use of surgery to divide the stapedius tendon should be used very conservatively.4
Subjective Tinnitus
Subjective tinnitus, tinnitus originating within the auditory system, is far more common than
objective tinnitus. As previously mentioned its prevalence increases with age and is related to hearing loss.
Many theories exist and have been published about the underlying physiologic mechanisms that cause
subjective tinnitus, but little is known. Generally, theories involve hyperactive hair cells or nerve fibers
activated by a chemical imbalance across cell membranes or decoupling hair cell stereocilia.1 An alternate
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theory proposes that injury to cochlear integrity from any cause reduces the suppressive influence of the
central nervous system, allowing increased neuronal activity higher in the auditory system. 2 Whatever the
cellular mechanism it appears that tinnitus can be caused by abnormal conditions in the cochlea, the
cochlear nerve, the ascending auditory pathway, or the auditory cortex.
Basic science review topics
Auditory pathway
Sound travels from the cochlear hair cells, which are innervated by the bipolar neurons of the
spiral ganglion in the modiolus of the cochlea. The spiral ganglion cells make up the eighth nerve which
then terminate on the cochlear nucleus. The axons of the cells in the cochlear nucleus stream out along
three pathways: the dorsal acoustic stria, the intermediate acoustic stria, and the trapezoid body. The most
important pathway is the trapezoid body. It contains fibers destined for the superior olivary nuclei on both
sides of the brain stem. Axons arising from the superior olivary nuclei join the crossed and uncrossed axons
from the cochlear nucleus to form the lateral lemniscus. Thus from the outset there is extensive bilateral
auditory input in the central nervous system, so that lesions of the central auditory pathway do not cause
monaural disability. The lateral lemniscus courses through the nuclei of the lateral lemniscus, where some
fibers synapse, once again with crossing from the two sides through Probst’s commissure. All the fibers in
the lateral lemniscus eventually synapse in the inferior colliculus. The inferior colliculus receives binaural
input and its cells are arranged tonotopically. Most of the cells in the inferior colliculus send their axons to
the medial geniculate body of the thalamus in the ipsilateral side of the brain. The cells in the medial
geniculate body then send their axons to the ipsilateral primary auditory cortex in the superior temporal
gyrus (Brodmann’s areas 41 and 42).6
Auditory brainstem response
Auditory evoked responses are electrophysiologic recordings of responses to sound. With proper
test protocols, the responses can be recorded clinically from activation of all levels of the auditory pathway
from the cochlea to the cortex. The ABR or BAER, brainstem auditory evoked response is applied most
often clinically. ABR wave components arise from the eighth cranial nerve and auditory regions in the
caudal and rostral brainstem. Wave I unquestionably represents the synchronously stimulated compound
action potentials from the distal (cochlear) end of the eighth cranial nerve. Wave II may also arise from the
eighth nerve, but near the brainstem (the proximal end). Waves I and II are generated by structures
ipsilateral to the ear stimulated. All later ABR waves have multiple generators within the auditory
brainstem. Wave III, which is usually prominent, is generated within the caudal pons, with likely
contributions from the cochlear nuclei, the trapezoid body, and the superior olivary complex. The most
prominent and rostral component of the ABR, wave V, is thought to arise in the region of the lateral
lemniscus as it approaches the inferior colliculus, probably on the side contralateral to the ear stimulated. 7
Of note, Ikner and Hassen (1990) found little difference between the auditory brainstem response in tinnitus
and nontinnitus patients matched for hearing loss. Other work in this regard is ongoing. At present no
measurements of sensorineural tinnitus or perceptual descriptions are pathognomonic of a single lesion.1
Evaluation
In evaluating tinnitus patients several etiologic factors should be explored; these include otologic,
cardiovascular, metabolic, neurologic, pharmacologic, dental, and psychological factors. A history of noise
exposure and related symptoms such as hearing loss and vertigo should be obtained including the exact
characterization of the tinnitus quality (buzzing, rushing, ringing, roaring, whistling), and perceptual
location (one ear, both ears, head location). 1 Tinnitus has been related to head injury and whiplash injuries
as well as a past history of meningitis. Multiple sclerosis can also have severe tinnitus in its constellation of
symptoms. Many medications may produce tinnitus most notably aspirin and aspirin-containing
compounds, aminoglycoside antibiotics, nonsteroidal antiinflammatory drugs, and heterocycline
antidepressants. Temporomandibular joint disorders and dental abnormalities are prevalent in tinnitus
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patients and some describe an increase in their TMJ complaints to be concurrent with an increase in their
tinnitus. Psychologic factors play a major role in the patient’s perception of the tinnitus severity, and
tinnitus is a prevalent symptom in somatoform disorder.8 Patients with concurrent depression should be
treated for this disorder as well, which in some cases also shows reduction in tinnitus. 2 Audiometry should
be performed on all patients, and anyone with asymmetrical hearing loss or unilateral tinnitus should
undergo an MRI to rule out posterior fossa tumors. Additionally, the patient should be asked to complete
one or more of the many questionnaires designed to evaluate the perceived severity of the tinnitus.
Measurement of tinnitus
Many tinnitus programs attempt to quantify four aspects of the tinnitus: pitch, loudness, minimum
masking level, and residual inhibition or post-masking effects. The most clinically useful of these is
probably minimum masking level, which may indicate the probability for success of a masking device.
Briefly, although tinnitus does not usually resemble a single tone, most patients are able to equate the pitch
elicited by a pure tone with the most prominent pitch of their tinnitus. However, most patients are unable to
perform this task reliably with a high standard deviation and tendency to choose tones in one octave
difference if tested repetitively. The loudness of tinnitus has been measured by having the subject adjust
the level of a pure tone so that is has about the same loudness as the tinnitus. Most tinnitus is less than 7-db
sensation level. Unfortunately, for some patients disabled by their symptoms, this loudness level may be as
little as 2 dB. A band of noise centered at the pitch-masked tinnitus is presented from threshold to the level
at which the patient’s sound is masked. The number of decibels of sound required to cover the tinnitus is
the minimal masking level. Residual inhibition describes the phenomenon of patients experiencing
periods of decreased or no tinnitus after having been exposed to masking. Post-masking effects published
by Tyer took one of five wave forms: 1) returned to normal loudness immediately, 2) returned immediately
but initially was softer, 3) was absent before gradually returning to normal, 4) was absent before abruptly
returning to normal, 5) was louder before gradually returning to normal. 1
Diagnostic tests
No diagnostic test is yet available to objectively measure or confirm the presence of tinnitus.
However, many investigators have looked at such modalities as ABR, PET, spontaneous otoacoustinc
emissions, and magnetic activity of the auditory system to determine an association with the complaint.
Otoacoustic emissions
OAEs are low-intensity sounds produced by the cochlea in response to an acoustic stimulus. Outer
hair cell motility affects basilar membrane biomechanics, resulting in a form of intracochlear energy
amplification, as well as cochlear tuning for more precise frequency resolution. The outer hair cell motility
generates mechanical energy within the cochlea, which is propagated outward, via the middle ear system
and the tympanic membrane, to the ear canal. Vibration of the tympanic membrane then produces an
acoustic signal, which can be measured by a sensitive microphone. The two most studied subcatagories of
OAEs in relation to tinnitus are spontaneous otoacoustic emissions (SOAE), and distortion product
otoacoustic emissions (DPOAE).
SOAEs, measurable in the external ear canal without stimulation, are present in only about 60% of
persons with normal hearing, and are found twice as commonly in females as in males. Because tinnitus
represents a spontaneous perception without any stimulus, it was quite reasonable to search for a direct
correlate of the tinnitus that was emitted into the ear canal. Unfortunately, at present the relationship
between spontaneous emission and tinnitus is unclear.1
DPOAEs, which are produced when two pure-tone stimuli at different frequencies are presented to
the ear simultaneously, are present in all normal hearing individuals. When outer hair cells are structurally
damaged or at least nonfunctional, OAE cannot be evoked by acoustic stimuli. For example, up to 30 % of
a population of outer hair cells may be damaged without substantially affecting the simple audiogram. In
such cases the evoked OAEs invariably are abnormal and can be used to detect this damage. While no
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correlation between tinnitus patients and DPOAEs has been observed, many clinical applications for
DPOAEs currently exist, and hope exists for a correlation to tinnitus. Norten et al have observed an
oscillating or prolonged evoked emission in five of six tinnitus subjects, but none in two subjects without
tinnitus. They suggested that “...the evoked emission and the tinnitus might be related to the same
underlying pathology, but the former is not the cause of the latter.” 1,2
Treatment
Counseling
Initially, a general discussion with the patient regarding all the etiologic factors connected with the
tinnitus should take place. The patient is reassured after the workup as to the unlikelihood of tumor or lifeendangering disease. The patient is told that in 25 percent of cases symptoms improve significantly or go
away. In 50 percent of patients the symptoms decrease over a period of months, in only 25 percent do the
symptoms persist at the same level, and reassurance is given that only a very small portion will have
increased symptoms. Patients should be advised to avoid loud noise, or if unavoidable, to wear appropriate
ear protection. They should restrict caffeinated beverages or any stimulants. Coffee, tea, colas, and
chocolate are excluded or reduced. They should quit smoking as many patients report a decrease in their
tinnitus with smoking cessation.4
Medications
Medications the patient is currently taking may be the cause of the tinnitus; these should be
reviewed. Aspirin-containing compounds, non-steroidal anti-inflammatory medications, and heterocycline
antidepressants should be limited, reduced in dosage, or changed to attempt relief of tinnitus.
The use of medication for the treatment of tinnitus has been largely ineffective. Drugs such as
nicotinic acid (vitamin B6), carbamazepine, baclofen, and others have been tried and some even tested in
double-blind placebo-controlled trials. None has been shown to be beneficial.1,9,10 Lidocaine has been
studied in several carefully controlled double-blind studies and shown to be beneficial, however, lidocaine
must be given intravenously, has a very short half-life, and is sometimes accompanied by undesirable side
effects. Oral analogs of lidocaine such as tocainide and flecainide acetate were also attempted for relief
without benefit. Melatonin, 3.0 mg qhs, was recently studied in a double-blind placebo-controlled trial and
found to be no better than placebo at relieving tinnitus. However, among patients reporting difficulty
sleeping attributable to their tinnitus, 46.7% reported an overall improvement after melatonin compared
with 20.0% for placebo (p=0.04). Benzodiazepines also may be beneficial; clonazepam, oxazepam, and
alprazolam; may all provide benefit, especially for patients with concurrent depression. In recent study
76% of patients taking alprazolam had a reduction in the loudness or their tinnitus while only 5% of the
placebo group showed benefit.12 Overall, medication should not be the major strategy for the treatment of
tinnitus, however for certain sufferers medication may provide some benefit in conjunction with other
therapy.
Environmental masking
For cases of mild tinnitus, especially in individuals where the tinnitus is only bothersome in quiet
situations, such as reading or sleeping, home environmental masking techniques may prove beneficial. This
usually involves music or broad-band masking by placing the dial on the radio between FM stations at a
loudness level to mask the tinnitus. This is particularly useful at night. The sound required to mask the
tinnitus is soft and not necessarily disturbing to the patient or other family members.4
Hearing aids and maskers
Because an external noise can render tinnitus inaudible in many patients, it seems reasonable to
introduce such a noise to provide temporary relief. Saltzman and Ersner (1947) observed that a hearing aid
amplified background noise that could successfully mask the tinnitus. Hearing impaired patients with
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tinnitus probably 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.1 Commercially available tinnitus maskers are also available either alone or in combination
with a hearing aid. When using these devices the noise can either completely mask the tinnitus or partly
mask it, so that both noise and tinnitus are heard, but the tinnitus is reduce in loudness. There are no clear
guidelines for selecting the spectrum characteristic of the masking noise and no indications that
measurements of pitch, loudness, or postmasking characteristics can be used to select an appropriate
spectrum for the tinnitus masker. Narrwband noises (less than a half-octave bandwidth) have a tonal
character, and those with a prominent tonal component are more annoying than broadband noise. A
conservative approach would be to urge the patient to use the lowest level masker that provides adequate
relief and to inform the patient that the masker need not be worn continuously. Additionally, there is no
available protocol for deciding which ear to fit with a masker, and any combination, unilateral or bilateral
may be affective.
Electrical stimulation
In the past several experiments were conducted on the use of electrical current to reduce tinnitus.
Several authors have demonstrated that the use of direct current applied to the round window or promontory
could reduce tinnitus. Unfortunately, direct currents (DC) may produce permanent damage and, therefore,
cannot be used clinically. Other work has focused on using alternating current from an external stimulator
with electrodes placed on the tympanic membrane, transtympanically on the promontory, and
transcutaneously in the preauricular and postauricular regions of the ear. The results from these studies
were mixed, but with some promising results even leading to one extracochlear wearable device to reduce
tinnitus being marketed in the U.S. in 1985. However, Dobie et al. (1986) demonstrated that only 1 patient
out of 20 clearly received benefit from the device. The product has been removed from the market.1
Fewer investigators have explored the use of intracochlear electricity to suppress tinnitus. Most of
these reports have been observations that some cochlear-implant patients report a reduction in their tinnitus
while listening to speech. A few patients have received a cochlear implant explicitly for tinnitus reduction
and not to improve their hearing ability. JW House (1984) reported that WF House implanted devices in
five severe-to-profoundly-hearing-impaired patients for tinnitus relief. No special stimuli were
administered to these patients, and only one reported a reduction in tinnitus while listening to speech
through the cochlear implant. Hazell et al. (1989) reported on six totally deaf patients who had received an
intracochlear implant and additional experimental trials with sinusoidal stimuli. They were able to reduce
the tinnitus in all six patients using a 100-Hz sinusoid. At least two of the patients elected to forego their
speech processors and to use their implant to suppress their tinnitus. One reported that turning on the
current turned off his tinnitus “like a light switch.”1
Surgery
While surgery is effective in treating conditions for which tinnitus is an associated symptom, such
as otosclerosis, acoustic neuroma, and glomus jugulare, destructive surgical lesions into the peripheral
auditory system are mostly ineffective. Case reports exist in the literature describing successful selective
cochlear neurectomy in patients who have lost all serviceable hearing in the affected ear, fail to respond to
medical management, and accept the fact that their tinnitus may persist despite surgery. Additionally,
microvascular decompression of the cochlear nerve has reported success in certain cases. A recent study by
Vasama in patients with severe hearing loss, severe tinnitus, abnormal brainstem auditory evoked potentials,
and in some abnormal acoustic middle ear reflex response claims in 22 patients: 7 had relief of their
tinnitus, 8 were slightly improved, 4 did not change, and 2 worsened. This procedure, if performed, at all
should be kept in the hands of surgeons experienced in the technique.14 Results from either of these
techniques are at best inconsistent, and few otologists advocate their usage; validating the hypothesis that
somehow tinnitus generators are centralized and are not consistently relieved by uncoupling the end organ. 1
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Neurophysiological approach to Tinnitus and Habituation
The neuorphysiological model of tinnitus has not been discussed previously and has been reserved
until now because of its differences with the other theories of tinnitus production and how to treat it. The
previously discussed theories share the beliefs that processes resulting in tinnitus were restricted to auditory
pathways, and more-over, in the dominant majority of models, to the cochlea; and all models were focused
on and concerned only with tinnitus generation, treating auditory pathways as passive, unchangeable
transmitters of the signal to the auditory cortex. Consequently, diagnostic efforts were concentrated on
psychoacoustical descriptions of tinnitus (its loudness, pitch, and maskability). Psychoacoustical
characterization of tinnitus, however, did not turn out to be of any help in predicting treatment outcome, or
explaining why people with similar descriptive characteristics had drastically different annoyance levels.
The neurophysiological model postulates that tinnitus emerges as a result of the interaction of a
number of subsystems in the nervous system. Auditory pathways play a role in the development and
appearance of tinnitus as sound perception, whereas other systems, predominantly the limbic system are
responsible for the tinnitus annoyance. The problem occurs when the perception of tinnitus is associated
with negative emotions, induces fear, and has qualities of threat. Typical fears are expressed as, “I have a
brain tumor; I am going deaf; etc.” The limbic system in turn activates the autonomic nervous system
resulting in the feeling of annoyance. Because annoyance evoked by tinnitus in this model is primarily
dependent on the activation of the limbic system, which is a perception by the individual and an associated
emotional state, the psychoacoustical characterization of tinnitus is irrelevant.
Habituation is traditionally defined as: the disappearance of reactions to sensory stimulus because
of repetitive exposition of a subject to this stimulus and the lack of positive or negative reinforcement
associated with this stimulus. In ordering tasks to be performed, the brain uses the following principles: 1)
the importance of the signal, particularly if a signal has a negative connotation indicating danger; and 2) its
novelty. If a signal has not been associated with any significant event or does not indicate danger, and is
not new, it gradually undergoes habituation, and after a number of repetitions, a person does not
consciously perceive its presence. This is accomplished by directive counseling aimed at educating the
patient of the potential mechanisms of tinnitus, presented within a background of the physiology of the
auditory nervous system. As part of the counseling, the results of all audiologic and medical tests are
presented, and their relevance discussed. Once the patient feels that he or she understands the mechanisms
of tinnitus and its impact, the level of annoyance decreases and by repetitive, less intensive counseling
during follow-up visits, it is possible to eliminate the negative associations initially evoked by tinnitus.
Beginning the process of habituation by directive counseling is an essential step of the treatment,
but it is not sufficient to achieve permanent habituation. To facilitate the habituation to tinnitus perception,
it is advisable to enhance the level of auditory background surrounding the patient, ie. partial masking,
particularly when he or she is in a quiet environment. This procedure increases the background level of
spontaneous and evoked activity within the auditory pathways, and by reducing the contrast of the tinnitus
signal versus background, the process of habituation is facilitated. It is of utmost importance, however, to
avoid masking tinnitus completely. By definition, once a tinnitus signal is masked it cannot be habituated
to. This supposition reflects the fact that habituation is basically a reconditioning of connections within
subcortical centers, and this process cannot occur if the stimulus (tinnitus) is absent. An example of this is a
patient who had undergone tinnitus masking for fifteen years without any changes in his tinnitus, any
indications of habituation of tinnitus perception, or tinnitus-induced annoyance. After about a year of
habituation therapy with the use of low- level broad-band noise, this patient is only aware of tinnitus for a
small percentage of the time, and the annoyance induced by tinnitus decreased significantly as well.
Patients are fitted binaurally with broad-band noise generators, which have a reasonably stable
amplitude of sound and allow for a smooth increase of sound from the zero level. The patients are advised
to use the devices for at least 6 h per day, particularly when they are in a quiet environment. In patients
with hearing loss, hearing aides are also used with instructions on how to create the proper auditory
environments (to use the hearing aid not as an aid in communication, but as a tool for enhancing the
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auditory input to the brain). The process of habituation typically requires 12 months and Jastreboff insists
that the patients continue for another 6 months to ensure that plastic changes within the brain are firmly
established. After that time period use of the noise generators is no longer necessary. He reports
approximately 83% of patients exhibit significant improvement with this combined therapy .15
Summary
It is important to differentiate between the different types of tinnitus. A physician must recognize
when tinnitus is a symptom of a potentially life threatening condition verses a problematic annoyance for
the patient. Patience and understanding of what the patient is experiencing, including their fear is essential.
Tinnitus produced by paraauditory structures is usually treatable through accepted medical therapy. The
treatment of sensory neural tinnitus is less clear, but recent advances in theory and management are
encouraging.
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References
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