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8
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Tinnitus, Hyperacusis, and
Auditory Hallucinations
intRoduction
The topics covered in this chapter (tinnitus, hyperacusis, and auditory hallucinations) easily could have been included as
segments in other chapters. However, it
was difficult to determine in which chapter to include these topics as these common auditory disorders can have a number of different etiologies and a variety of
sites of lesion and origins. Given this challenge, as well as the keen general interest
in these disorders, the decision was made
to include a separate chapter for coverage of these three entities. Although these
three entities are often described as disorders, they are actually “symptoms” that
are associated with a variety of underlying disorders. Both terms are used interchangeably in this chapter as they are in
the literature, but the reader should keep
in mind when reading through this chapter
that the three conditions being discussed
are actually symptoms and not disorders.
Tinnitus has been written about for
many years in the fields of otology, psychology, and audiology, and it has been
the focus of considerable research; however, in spite of these efforts, a cure for this
disorder remains elusive. An awareness of
this problem and a better understanding
of the nature and origins of this auditory
symptom have been enhanced by the
many contributions of the late Jack Vernon. His efforts in this area have also led
to the development of interventions that
can help moderate the patient’s tinnitus
and/or the individual’s ability to cope
with this challenging symptom. In addition to these efforts, the fine work of the
American Tinnitus Association has done
much to inform the public about this common and bothersome symptom. In this
regard, public information and education
has played, and should continue to play,
a major role in reducing one of the main
causes of tinnitus (i.e., excessive noise
exposure). Without a doubt, there have
been advances in the understanding of
tinnitus and certain treatments have been
shown to help some individuals. Interestingly, most treatment approaches have
been nonmedical in nature with their
roots anchored in the early approaches
introduced by Jack Vernon.
385
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Hyperacusis, or the increased sensitivity to sounds caused by abnormal loudness perception, is often associated with
tinnitus, but not all individuals with this
auditory condition will report experiencing tinnitus. The abnormal loudness perception noted in hyperacusis frequently is
related to the presence of a sensorineural
hearing loss and the lack of an acoustic
reflex (Møller, 2000). Damage to outer hair
cells in the cochlea has been linked to the
recruitment phenomenon, while the lack
of an acoustic reflex disallows the natural
attenuation of incoming loud sounds. It is
understandable how these two dysfunctions of hearing can be a basis for hyperacusis; however, it should be noted that
not all individuals with hyperacusis have
hearing loss and absent acoustic reflexes.
Hyperacusis has not been studied as
long or as extensively as tinnitus. However, in many patients, tinnitus and hyperacusis coexist and are treated together. As
was the case with tinnitus, no definitive
cure for hyperacusis has been identified,
but through counseling and various treatment approaches (e.g., desensitization
therapy), this disorder can be managed
successfully in many individuals. Procedures such as these can be a critical factor in restoring or establishing the ability
of patients to function normally in their
everyday activities despite the continued
presence of aversions to many common,
everyday sounds.
Auditory hallucinations are new
to audiology here in the United States.
Although new to audiology, this disorder has been studied by psychologists
and psychiatrists for some time as many
individuals with auditory hallucinations
present with psychiatric conditions, such
as schizophrenia. Recent research has
implicated changes in the anatomy of
the central auditory system associated
with hallucinations and has shown that
many people without comorbid diagnoses of psychological and/or psychiatric
conditions also experience auditory hallucinations. These findings have stirred
the interest and attention of audiologists.
The elderly with histories of long-standing severe hearing loss are one group of
patients who seem to be prone to auditory
hallucinations. Another group that experiences auditory hallucinations includes
patients with neurologic damage involving the central auditory structures. As you
will read later in this chapter, the definitions of subjective tinnitus and auditory
hallucinations are quite similar, with both
involving the perception of sound in the
absence of an external auditory stimulus.
The research surrounding tinnitus,
hyperacusis, and auditory hallucinations
is indeed interesting and will be pursued
more in the future. Similarities as well as
differences in these three hearing disorders will likely herald advances in both
the understanding and treatment of these
problems. However, it is important to
keep in mind that not all patients who
experience one or more of these “hearing” symptoms will have an auditory
basis for their disorder. Some will have a
nonauditory basis (e.g., a psychological
or psychiatric condition), and others may
have a comorbid auditory and nonauditory basis. Referrals to other professionals will be critical for those cases where
psychological or psychiatric problems are
suspected either as a primary cause or as
a comorbid condition.
tinnitus
Introduction
Tinnitus can be defined as the perception
of sound in the absence of an environmen-
8. Tinnitus, Hyperacusis, and Auditory Hallucinations 387
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tal stimulus (Chan, 2009). It is derived
from the Latin word tinnire meaning “ring-
ing.” Many people are bothered by tinnitus,
with some experiencing debilitating tinnitus. Despite being a common disorder and
the focus of considerable research, a cure
for this disorder remains elusive. However,
some treatments do provide relief from tinnitus for at least some patients.
Tinnitus generally is classified into
two main categories, subjective and objective. Subjective tinnitus can be heard only
by the person who experiences it. It is
often described as a ringing, hissing, humming, chirping (as in the sounds made by
crickets and/or cicadas), whistling, blowing, or roaring sound. Objective tinnitus,
on the other hand, can be measured if a
probe microphone or stethoscope (even
a hearing aid stethoscope) is placed in the
ear canal or on the pinna. It also may be
heard by others who are in close proximity to the individual if the tinnitus is loud
enough to be perceived. This type of tinnitus is commonly described by sufferers
as being a pulsatile, clicking, or rushing
type of sound (Marion & Cevette, 1991).
Symptoms
As discussed previously, tinnitus is actually a symptom. Hence, this section title
is redundant, but it provides an opportunity to discuss the various characteristics
of tinnitus. The perceptual experience of
tinnitus can be quite diverse, as was mentioned earlier, and in some individuals,
more than one type of sound can be experienced. The tinnitus can be constant, intermittent, fluctuating, triggered by external
and/or internal stimuli, and unilateral or
bilateral. In addition, it may be accompanied by hearing loss or normal hearing, vestibular symptoms, and a variety
of other ear symptoms. The tinnitus and
other aural symptoms may vary in severity
from essentially unnoticeable to intolerable
(Chan, 2009; Marion & Cevette, 1991).
Incidence and Prevalence
Tinnitus is a common disorder of the
auditory system with some reports relating that approximately 10% of the U.S.
adult population, or more than 25 million
Americans, experience tinnitus lasting at
least 5 min (Centers for Disease Control
and Prevention, 2018; National Institute
on Deafness and Other Communication
Disorders, 2016). The incidence does increase with age, and 1 in 200 cases with
tinnitus is considered to be severely bothered by it (Tyler & Erlandsson, 2003).
Etiology and Pathology
Objective tinnitus usually is pulsatile in
nature and often has a vascular basis. This
vascular involvement is usually located
around the temporal bone. Arteriovenous
shunts, venous hum, paragangliomas,
neoplasms, hypertension, and elevated
intercranial pressure are some of the etiologic bases for objective tinnitus (Chan,
2009; Møller, 2000).
Subjective tinnitus is often a result of
noise exposure (18%), trauma (8%), otologic infections or illness (8%), and drugs
(2%) (Henry, Dennis, & Schechter, 2005).
It can be associated with general sensorineural hearing loss, Ménière’s disease,
strokes of the central nervous system, vascular loops, and aging (Henry et al., 2005;
Møller, 2000). In the remainder of the
cases (64%), the subjective experiences of
tinnitus being reported could possibly be
attributed to psychological or nonauditory
factors, such as negative counseling or
other undetermined factors or events.
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The pathophysiology of tinnitus is
not well understood, and although interesting theories abound, only a few of these
will be mentioned here. It is well known
that if tinnitus is present, there is likely to
be damage or a substantial change to the
auditory system’s function. This damage
may not be measurable or diagnosed as
the compromise may be subclinical (i.e., it
is not detected by routine audiologic procedures), but the damage still is present
and is likely the generator or the origin
of the tinnitus. One commonly accepted
theory posits that tinnitus is caused by
increased spontaneous auditory activity
involving the “in phase” firing of a sufficient number of nerve fibers to result in the
perception of sound (Møller, 2000; Tyler
& Erlandsson, 2003). Also advanced is the
theory that damage to the auditory system
results in an alteration of the normal firing
rates of the inhibitory and excitatory fibers
within the auditory nerve or the brain. In
this case, the firing of excitatory fibers that
are normally suppressed by the inhibitory
circuits results in the experience of tinnitus (Møller, 2000). A third theory suggests
that the decoupling of hair cells secondary
to damage of the cochlea and/or related
structural damage to other inner ear structures involving the hair cells (e.g., a collapsing tectorial membrane) could cause
the hair cells to fire without sound stimulation (Tonndorf, 1980). It also has been
proposed that defects in the reticular lamina may cause a random depolarization
of hair cells resulting in the perception of
tinnitus (Feldmann, 1988). Finally, Eggermont (2007) advances the notion that the
pathophysiology of tinnitus depends on
the particular disorder associated with
it. He discusses how ion channel alteration for particular disorders could trigger
the tinnitus response. He also discusses
various neurotransmitters and drugs that
can affect the auditory system and how
these could play a role in tinnitus. In a
more recent article, Sahley, Hammonds,
and Musiek (2013) have postulated that
dynorphins and other lateral efferent
neurotransmitters can serve to exacerbate
tinnitus. All of these theories are based on
the concept that there is structural or biochemical damage to the cochlea and/or
the auditory nerve, which in turn creates
improper function of the structures within
the organ of Corti, giving rise to the tinnitus. In other words, when the auditory
system is damaged, there are multiple
sites at which processing changes can
occur. This in turn can result in various
types of dysfunction, which may lead to
the experience of tinnitus.
Due to the likely presence of multiple pathophysiologic factors in many tinnitus sufferers, it is difficult to determine
which one actually triggers the tinnitus.
It may be possible that a constellation of
factors needs to exist to create the perception of tinnitus. Although the previous
discussion has focused on pathophysiologic alterations or compromise in the
cochlea and/or the auditory nerve, it also
is important to realize that involvement
of the auditory pathways in the brain can
additionally result in tinnitus (Lockwood,
Salvi, & Burkard, 2002; Møller, 2000).
Site of Lesion
Objective tinnitus is most often related to
dysfunction of the middle ear or its immediate area (Chan, 2009). Muscular or vascular problems in this region of the head
often give rise to pulsatile or clicking-type
sounds that are heard by the patient. Seldom does this type of tinnitus originate
from the cochlea or more central auditory
structures.
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For many years, subjective tinnitus
was believed to be primarily a cochlear
problem. However, periodic reports have
suggested that this may not always be the
case. Most startling were reports of individuals with severe tinnitus and hearing
loss who underwent surgical sectioning
of the auditory nerve only to have the
tinnitus either remain or become worse
(see Møller, 2000). For example, it has
been documented that 33% of patients
undergoing eighth nerve sections for
Ménière’s disease, a peripheral problem,
do not demonstrate relief or improvement in their tinnitus following surgery.
This seems to indicate that although there
may be a cochlear problem initiating the
tinnitus, the source of the tinnitus changes
over time.
This type of finding would suggest
that the central auditory pathways may
be responsible for the generation and/or
persistence of tinnitus in some cases. This
is not to say that cochlear damage cannot cause tinnitus. It is highly likely that
damage to the cochlea from insults such
as high intensity noise or Ménière’s disease will result in the cochlea generating
subjective tinnitus. However, a study by
Lockwood et al. (2002) indicates that neural activity within the brain also can generate tinnitus (at least some of the time).
Functional imaging studies have demonstrated that tinnitus activates the auditory cortex on only one side of the brain,
whereas an external tonal stimulus activates both cortices. In addition, changes
in functional imaging measures have been
documented for individuals who can
increase the loudness of their tinnitus by
gazing in a certain direction or by clenching their teeth. In these cases, the changes
in functional imaging measures revealed
increased cortical activity that correlated
with the tinnitus provoking maneuvers
(see Lockwood et al., 2002, and Møller,
2000, for reviews).
An additional observation that is
worth mentioning relates to what appears
to be a disconnect between the apparent
anatomic site of abnormality and the site
of physiologic abnormality. This “disconnect” could add to the difficulty of interpreting the triggers and nature of tinnitus
in many patients. Additional research is
needed to delineate the nature and exact
site of physiologic abnormalities in individuals for whom there may be a discrepancy between the apparent anatomic site
of pathology and the actual physiologic
site of abnormality.
At this point in time, it is probably
best to keep an open mind and entertain
the possibility that subjective tinnitus
can be localized in the cochlea, the auditory nerve, and/or the central pathways.
Currently, there is little in terms of test
procedures that allow the accurate localization of tinnitus within the peripheral
and/or central auditory system. Tinnitus
often can be localized by the patient to
one ear, both ears, or to an area more centrally located in the head. If localized to
one or both ears, it is commonly assumed
that the tinnitus arises from a peripheral
auditory structure. On the other hand, it
is inviting to think that tinnitus located in
the head or midline may have a central
origin; however, currently there is a paucity of evidence to support a precise locus
of this symptom.
Medical and Audiologic
Evaluation
One of the most important steps in the
medical evaluation of tinnitus is obtaining a thorough history from the patient
in order to begin the process of making
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a correct diagnosis of the etiology (Perry
& Gantz, 2000). However, it should be
noted that the etiology cannot always be
determined, but the medical evaluation
can help rule out a more serious medical
involvement (i.e., a retrocochlear lesion).
Closely listening to the patient’s reported
symptoms is key. It is important to determine if the reported tinnitus is the chief
complaint, or if this symptom is secondary to other issues (hearing loss, vertigo,
etc.). In addition, the characterization of
the tinnitus, such as whether it is symmetric (often reported to be “in the head”) or
lateralized to one ear or the other, is of the
utmost importance.
Following a thorough case history, a
full head and neck examination is necessary. Included in this examination should
be a comprehensive otologic examination,
including otomicroscopy. Additionally,
each cranial nerve should be examined as
some otologic disorders (such as a mass
lesion) may affect primarily the auditory
nerve, resulting in tinnitus, but they also
may affect one or more of the adjacent
nerves. An examination of all of the cranial nerves can provide insight as to the
basis of the underlying problem (Fortune,
Haynes, & Hall, 1999). An audiologic
evaluation is also warranted to determine
if a hearing loss is present and to rule out
significant retrocochlear involvement
as a contributory factor to the symptom
if a hearing loss is identified. Although
nonpulsatile, bilateral tinnitus often does
not require any further medical examination, individuals who present with unilateral tinnitus or pulsatile tinnitus, as well
as those with asymmetric hearing loss,
should be seen for a magnetic resonance
imaging (MRI) with gadolinium contrast
procedure (Schwaber, 2003). In particular, the internal auditory canals should
be examined. For those patients who
cannot undergo an MRI, an auditory
brainstem response (ABR) evaluation or
computed tomography (CT) scan should
be considered. In addition to traditional
imaging, patients with objective pulsatile
tinnitus should be evaluated for a variety
of disorders including neoplasms, vascular lesions, benign intracranial hypertension, great vessel bruits, and high cardiac output (Perry & Gantz, 2000). These
individuals should undergo additional
examinations as appropriate, which may
include magnetic resonance angiography
(MRA) or arteriograms. The benefit of
MRA is that it is essentially noninvasive,
and it is additionally helpful in determining both arterial and venous involvement. Laboratory testing also may be indicated for some patients. Patients may be
evaluated for a variety of disorders, which
may include endocrinopathies, metabolic
disorders, autoimmune diseases, and
syphilis (House & Derebery, 1995).
A complete audiologic evaluation is
an important early step in the diagnosis
and treatment of tinnitus. Classic puretone and speech audiometric procedures
along with immittance testing and otoacoustic emissions should be completed.
If indicated, a workup for auditory nerve
or central involvement should be carried
out (Marion & Cevette, 1991). For puretone thresholds, the use of pulsed tones
may make it easier for the patient to identify the stimuli accurately. It also is helpful
to have the patient indicate how much the
tinnitus bothers him or her by determining
what percentage of the time the patient is
aware of the tinnitus versus what percentage of the time they are actually disturbed
by it. Møller (2000) advocates using three
categories for this purpose. These catego-
ries include (1) mild — does not interfere
with daily living; (2) moderate — annoying
and unpleasant; and (3) severe — interferes
8. Tinnitus, Hyperacusis, and Auditory Hallucinations 391
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with daily living in major ways. A number
of self-assessment scales have been developed for the purpose of documenting the
effects of tinnitus on the patient’s daily
activities. A listing of some of the more
common self-assessment scales is provided later.
An audiologic, or sometimes termed
psychoacoustic, assessment of tinnitus
can prove valuable in a number of ways
and should be included in the evaluation
of the patient who presents with tinnitus.
Tyler and Erlandsson (2003) mention five
ways that the evaluation of tinnitus can
be used. These include: (1) to confirm
that the patient has tinnitus, (2) to monitor
changes in the tinnitus over time, (3) to
provide insights as to underlying mechanisms, (4) to help in the fitting of devices
for tinnitus treatment, and (5) to render
a determination of the reliability of the
patient’s report of tinnitus, which may
be important, especially in legal cases.
Although such testing is often desirable,
many patients will find tinnitus assessments to be challenging and often difficult to complete. Therefore, it is important
that the audiologist’s rationale for conducting the psychoacoustic testing be well
thought out and made clear to the patient.
The evaluation of tinnitus is indeed difficult and not as accurate or precise as
most would like it to be. This fact should
be understood by those undertaking this
challenging task. Despite various psychoacoustic strategies that have been invoked
to complete tinnitus matching procedures
in the clinical setting, the results remain
quite variable as tinnitus has many components and it often changes quickly in
pitch and loudness, rendering it difficult
to measure.
The key aspects of tinnitus assessment center around pitch and loudness
matching (see Marion & Cevette, 1991;
Tyler & Erlandsson, 2003). In tinnitus
matching procedures, the patient is asked
to match the pitch and loudness of his or
her tinnitus to external sounds presented
under earphones. Multiple replications
are usually required to reach stable values. In cases of unilateral tinnitus, matching can be performed with the external
sound presented to the ipsilateral ear (ear
with the tinnitus) or the contralateral ear
(ear without the tinnitus). If bilateral tinnitus is present, each ear must be evaluated separately, which can be challenging.
In addition to the matching procedure, a
masking procedure can be used. In the
masking procedure, the sound pressure
level (SPL) of a broadband noise needed
to mask out perception of the tinnitus is
determined. This procedure, as well as the
loudness matching procedure, can give
some indication of the perceived loudness
of the tinnitus. It has been reported that
most people match their tinnitus to an
external stimulus that is in the 10 to 30 dB
sensation level (SL) range (Møller, 2000).
However, a more recent study has shown
that the average intensity match for tinnitus was under 10 dB SL for patients
with histories of noise exposure (Nageris,
Attius, & Raveh, 2010), and clinical experience has also shown that the intensity
match for the majority of patients is below
10 dB SL (Vernon & Meikle, 2000). It is
important to note that the measurement
of tinnitus loudness is affected considerably by the frequency at which the measure is obtained. The SL values typically
are lower when loudness is measured at
the pitch (i.e., the frequency) of the tinnitus than when it is measured at a lower
frequency (see Vernon & Meikle, 2000,
for additional information on loudness
matching procedures and findings).
In regard to pitch-matching proce-
dures, tinnitus is usually matched to high
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