James A. HenryVeterans Affairs Medical Center,

Portland, OR, andOregon Health & Science University,

Portland, OR

Kyle C. DennisVeterans Affairs Central Office,

Washington, DC

Martin A. SchechterVeterans Affairs Medical Center,

Portland, OR

General Review of Tinnitus:Prevalence, Mechanisms, Effects,and Management

THEORETICAL/REVIEW ARTICLE

Tinnitus is an increasing health concern across all strata of the general population.Although an abundant amount of literature has addressed the many facets of tinnitus,wide-ranging differences in professional beliefs and attitudes persist concerning itsclinical management. These differences are detrimental to tinnitus patients becausethe management they receive is based primarily on individual opinion (which can bebiased) rather than on medical consensus. It is thus vitally important for the tinnitusprofessional community to work together to achieve consensus. To that end, thisarticle provides a broad-based review of what is presently known about tinnitus,including prevalence, associated factors, theories of pathophysiology, psychologicaleffects, effects on disability and handicap, workers’ compensation issues, clinicalassessment, and various forms of treatment. This summary of fundamentalinformation has relevance to both clinical and research arenas.

KEY WORDS: tinnitus, treatment, hearing disorders, mechanisms, review

T innitus is the perception of sound for which there is no acoustic

source external to the head. It poses a significant clinical problem

for millions of people in the United States and is proportionallyproblematic in countries where epidemiological data have been reported.

Although an abundance of literature concerning tinnitus has been pub-

lished in the last 25 years, there is lack of uniformity with respect to

all aspects of its clinical management. Furthermore, understanding of

pathological mechanisms of tinnitus generation remains in the stage of

hypothesis and conjecture. This article provides an overview of what is

presently known about tinnitus.

DefinitionsMany people may experience transient ‘‘ear noises,’’ which are

often described as a whistling sound, in association with sudden tem-

porary hearing loss (Kiang, Moxon, & Levine, 1970). These transient

auditory symptoms occur periodically and generally resolve within a

few minutes. Consensual criteria that differentiate such normal earnoises from pathologic tinnitus have not been developed. Some authors

have specified that tinnitus must exceed a 5-min duration (Coles,

1984; Davis, 1995; Hazell, 1995). Dauman and Tyler (1992) proposed

that pathologic tinnitus is head noise lasting at least 5 min that occurs

more than once per week. Both of these definitions would constitute

Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005 � In the public domain12041092-4388/05/4805-1204

low-fence criteria to define an internal sound that is

present most or all of the time for the typical tinnitus

patient (Meikle, Creedon, & Griest, 2004).

A distinction is often made between subjective

and objective tinnitus (A. R. Møller, 2003). Subjectivetinnitus refers to an internal sound that is perceived

only by the patient, whereas objective tinnitus is con-

sidered real noise that can be heard by the patient and

the examiner (Ciocon, Amede, Lechtenberg, & Astor,

1995; Lockwood, Salvi, & Burkard, 2002; Perry & Gantz,

2000). Hazell (1995) objected to this distinction on the

basis that tinnitus is, by definition, always subjective.

Hazell distinguished between tinnitus that is generatedeither neurophysiologically or somatically. Somatic tin-

nitus (somatosounds) would usually have a vascular,

muscular, respiratory, or temporomandibular joint

(TMJ) origin. The presence of somatosounds normally

indicates an underlying medical condition that warrants

medical evaluation. Some of the causes of somatosounds

include a variety of vascular lesions, benign intracranial

hypertension, high cardiac output, middle-ear disease,patulous Eustachian tube, and palatal myoclonus (Ciocon

et al., 1995; Hazell, 1995; Perry & Gantz, 2000). Regard-

less of the cause of tinnitus, the signal is eventually

processed by the central auditory nervous system and

consciously perceived in the auditory cortex.

PrevalenceThe prevalence of tinnitus has been estimated on the

basis of data obtained from epidemiologic studies con-

ducted in different countries (Brown, 1990; Davis, 1995;

Hinchcliffe, 1961; Leske, 1981; Office of Population

Census and Surveys, 1983; Sindhusake et al., 2003).

These studies contained at least one question abouttinnitus, either written or conducted by interview, that

was administered to random population samples (Davis

& Refaie, 2000). Unfortunately, the questions used were

not standardized, and they did not always differentiate

normal ear noises from pathologic tinnitus. In spite of

their limitations, these studies indicated that the prev-

alence of tinnitus in adults falls in the range of 10% to

15%. Hoffman and Reed (2004) compared six studies thatobtained age-specific tinnitus prevalence data in adults.

Each of these studies showed a trend of increasingly

greater prevalence at higher age decades. The studies

also showed a plateau in tinnitus prevalence in either the

60–69 years or the 70–79 years age ranges, with a sub-

sequent decline in prevalence for higher age groups.

SeverityThe term severity in a clinical context refers gen-

erally to the impact of a health condition on quality

of life. With respect to tinnitus, its degree of severity

would reflect the ‘‘nature and extent of patients’

tinnitus-related problems’’ (Meikle, 2003, p. 59). The

prevalence of tinnitus is much higher than the number

of patients who seek treatment (Brown, 1990; Davis,

1995; Hinchcliffe, 1961; Leske, 1981; Office of Popula-

tion Census and Surveys, 1983), thus indicating thatmany individuals who experience tinnitus do not find

it to be a significant or debilitating problem. Tinnitus

becomes a problem when it is perceived as a threat,

appears continually intrusive, or when patients have

difficulty coping with tinnitus as a stress factor (Hazell,

1998b). In many patients, the emergence of tinnitus as

a problem occurs long after the underlying medical con-

dition (most commonly hearing loss). The trigger forthe adverse or intrusive effects of tinnitus is sometimes

unrelated to the associated condition. Emotional stress,

psychological factors, bereavement, unemployment,

or various physical or mental illnesses can trigger in-

trusive tinnitus. In such cases, the patient’s focus and

preoccupation with tinnitus can produce a repeating

cycle of annoyance, mood changes, fear, anxiety, and

depression—all of which are associated with tinnitusseverity.

Use of Questionnaires to Assess SeverityProper methodology for measuring tinnitus sever-

ity has been debated for years (Dobie, 2002; Meikle

& Griest, 2002; Tyler, 1993). There are at least a dozen

published outcome instruments that are used to obtaintinnitus severity ratings, and there is no consensus

regarding their use across tinnitus treatment centers

(Newman & Sandridge, 2004).

Index scores. Most tinnitus questionnaires provide

an index score to quantify the impact of tinnitus on the

patient’s everyday life. For example, individual indexscores for the Tinnitus Severity Index (TSI; Meikle,

Griest, Stewart, & Press, 1995) can range from 0 to

48—from lesser to greater severity. Some tinnitus in-

struments specify different ranges of their index scores

to categorize levels of tinnitus severity. A patient’s score

on the Tinnitus Handicap Inventory (Newman, Sandridge,

& Jacobson, 1998), for example, places the patient into

one of four ‘‘handicap severity ’’ categories (none, mild,moderate, and severe).

Although an index score is generally helpful in

establishing the need for treatment, it can over- or

underestimate tinnitus severity. This point is illus-

trated by a controlled clinical trial that we recently

completed (J. A. Henry, 2004b; J. A. Henry, Schechter,Regelein, & Dennis, 2004). For the trial, it was im-

portant to ensure that study participants had enough

of a problem with their tinnitus to justify 18 months

of individualized management. We carefully screened

Henry et al.: General Review of Tinnitus 1205

about 800 individuals to assess their tinnitus severity,

of which 123 were enrolled (and 111 completed treat-

ment). The mean TSI index score (with a possible range

of 0-48) for the 123 participants was 28.3 (SD = 8.7). The

rigorous screening process ensured that all of these

participants had tinnitus of such severity as to qualify

for long-term treatment. Their TSI scores, however,ranged from 9 to 48—spanning 75% of the possible

range. Participants in our study also completed the

Tinnitus Handicap Questionnaire (Kuk, Tyler, Russell,

& Jordan, 1990; Tyler, 1993) and the Tinnitus Handi-

cap Inventory (Newman, Jacobson, & Spitzer, 1996;

Newman et al., 1998). The baseline index scores for

these instruments showed intersubject variability

comparable with that for the TSI. Clearly, an examinercannot rely solely on an index score to make a clinical

severity judgment.

Impediments to the effectiveness of tinnitus ques-

tionnaires. The objective for any tinnitus questionnaire

is to accurately identify and quantify each patient’s

tinnitus-associated problems. There are two primaryreasons why accomplishing this objective has been so

difficult. First, effects of tinnitus on an individual are

often multidimensional. Tyler and Baker (1983) obtained

lists of difficulties caused by tinnitus from members of

a tinnitus self-help group. These authors commented,

‘‘Perhaps the most striking aspect of these findings is

the diversity and gravity of the difficulties that were

reported’’ (p. 152). Tyler (1993) commented, ‘‘There arethousands of possible questions one could ask about the

distress caused by tinnitus’’ (p. 378).

The second primary factor hindering the develop-

ment of a universally effective tinnitus questionnaire is

the need to properly weight the different problematic

aspects of tinnitus. A question may be irrelevant to thepatient’s circumstances, yet the question may receive

equal weight when calculating the index score (Newman

& Sandridge, 2004). If a questionnaire addresses mostly

irrelevant items for a particular patient, the index score

might be spuriously low. For example, a patient’s only

reported problem may be difficulty falling asleep. The

questionnaire used might focus more on emotional con-

sequences of tinnitus, in which case this patient’s indexscore would be low, even though an individual question

about sleep disturbance might indicate a severe prob-

lem. Another patient might report being generally both-

ered by tinnitus most of the day. This patient’s problem

would affect most life activities, which would result in a

correspondingly high index score. These two hypothet-

ical patients each have a severe problem with tinnitus.

The latter patient would provide an index score reflectingsevere tinnitus, whereas the former patient would not.

Individual outcome questions. Another option for

assessing overall tinnitus impact is to use a single out-

come question that is global in nature. In our clinical

trial, we asked global-severity questions such as, ‘‘How

much of a problem is your tinnitus?’’ and ‘‘How annoy-

ing is your tinnitus?’’ Responses were based on 0–10

analog scales. The mean responses for the 123 en-

rolled participants were 6.5 (SD = 2.0; range = 2–10)

and 6.4 (SD = 2.2; range = 0–10) for the two questions,respectively. These mean responses are what might

be expected for a group of patients such as these who

require intensive rehabilitative management. The

ranges of individual responses, however, indicate that

a single overall response is often not an accurate gauge

of severity.

Intake interviews. The use of written, self-

administered questionnaires is important for any tin-

nitus assessment, but they should be used with an

awareness of the above-mentioned caveats. Determina-

tion of the severity of tinnitus is a very complex issue.

It requires an astute examiner to identify specifically

how tinnitus is a problem for a patient, and to what

degree. Written questionnaires, which have been doc-umented for response validity (such as the TSI), are

generally helpful in this process. In addition, an intake

interview is helpful and should be conducted. We have

published two in-depth interviews that can be used for

this purpose, one specific to management with tinnitus

masking (Schechter & Henry, 2002) and one for use

with tinnitus retraining therapy (TRT; J. A. Henry,

Jastreboff, Jastreboff, Schechter, & Fausti, 2003). Aproperly conducted interview is informative for the ex-

aminer in revealing each patient’s concerns, which will

need to be addressed in managing the problem. The in-

terview also can serve to provide the clinician opportu-

nities to answer a patient’s questions about the tinnitus

condition.

Quality of LifeIt is largely unknown why about 80% of the people

with chronic tinnitus suffer little or no treatment-seeking effects from their tinnitus, whereas about 20%

manifest a clinically significant condition (Davis &

Refaie, 2000; P. J. Jastreboff & Hazell, 1998). Assess-

ing the effects of tinnitus on an individual’s quality of

life is a complex issue than is due to a variety of fac-

tors: (a) Tinnitus, like pain, is an entirely subjective ex-

perience that can only be described by patient report

(Jacobson, 2000; Meikle, 2003); (b) results of psycho-acoustic testing of tinnitus perception have been

shown repeatedly to have little if any correlation with

the degree of tinnitus impact (Coles, 2000; J. A. Henry

& Meikle, 2000; Sullivan et al., 1988); (c) as with

chronic pain syndromes, psychological factors may play

a critical role in determining an individual’s reactions

1206 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

to tinnitus (e.g., some people are accustomed to solving

their own problems whereas others need a great deal

of support; Erlandsson, 2000; Sullivan et al., 1988);

(d) women are more likely to report emotional reactions

to their tinnitus than men (Dineen, Doyle, & Bench,

1997; Hallberg & Erlandsson, 1993; Meikle & Griest,

1989); (e) the rate of personality disturbances is greaterfor male than for female tinnitus patients (Erlandsson,

2000); and (f) there are individual differences in daily

lifestyle, as well as individually distinct acoustic envi-

ronments, that may make some patients more prone to

intrusive tinnitus.

The effects of tinnitus on quality of life are highlyindividualized, and personality characteristics may

predispose a person to experience tinnitus as a ‘‘dis-

tressing’’ symptom (J. L. Henry & Wilson, 2001).

Subjectively loud tinnitus can, however, be an intru-

sive and challenging condition for anyone so afflicted.

Quality of life is most certainly reduced to some degree

for anyone with chronic tinnitus, as its mere presence

precludes the serenity that many associate with a quietenvironment. Accordingly, the notion of peace and quiet

is no longer an option for many tinnitus patients. It

is not surprising, therefore, that sleep disturbance is

reported by about one half of those individuals who

complain of tinnitus (Erlandsson, 2000; Jakes, Hallam,

Chambers, & Hinchcliffe, 1985; Meikle & Walsh, 1984;

Tyler & Baker, 1983).

Sleep deprivation is one of the primary effects of

tinnitus, along with the effects on cognition, emotional

status, and hearing (Dobie, 2004b; Tyler, Noble, Preece,

Dunn, & Witt, 2004), and can manifest as a single

independent problem. These primary effects of tinni-

tus, however, are not mutually exclusive and there is

overlap for most patients. For example, chronic sleepdeprivation caused by tinnitus may result in trouble

focusing attention (effects on cognition) and give rise to

associated frustration and anger (effects on emotional

status). These kinds of effects can be self-perpetuating,

with the potential to affect every aspect of life. A

comment is in order concerning patients’ common

complaint that tinnitus affects their hearing. Although

this is certainly possible, tinnitus is generally not asignificant factor contributing to an audiometric deficit

(Coles, 1995; Dobie, 2004b; Zaugg, Schechter, Fausti, &

Henry, 2002).

One’s reaction to tinnitus can affect further the

ability (or desire) to interact normally with otherpeople and can result in a state of chronic stress that

can impact such basic activities as eating, driving,

and performing any kind of chore. Sahley and Nodar

(2001) have proposed a model to explain how stress

can exacerbate tinnitus. Their idea is that glutamate

activity at the synaptic bases of inner hair cells is

enhanced in response to opioid dynorphins that are

released into the synapses during stressful situations.

Clinical depression and anxiety are additional poten-

tial sequelae for patients who are most affected by tin-

nitus (Dobie, 2003; Halford & Anderson, 1991; Kirsch,

Blanchard, & Parnes, 1989).

Conceptualization of Tinnitus ImpactThe need to provide uniform and reliable clinical

measures for defining the negative impact of tinnitus

has been recognized for many years. One approach

that has been suggested for meeting this need is to use

the concepts of impairment, disability, and handicap,

as defined by the World Health Organization (WHO;1980; see also, Newman et al., 1996; Shulman, 1991;

Tyler, 1993). Meikle (2003) described a uniform concep-

tual framework for assessing tinnitus severity on the

basis of the WHO method for categorizing the negative

effects caused by chronic conditions. Meikle argued that

such standardization would provide a rational basis for

stratifying tinnitus patients into different groups and

would further enable meta-analyses and other types ofcomparisons among treatment centers.

WHO (2001) now uses a new International Classi-

fication of Functioning, Disability and Health (ICF).

The new model conceives of a person’s disability as a

dynamic interaction among health conditions and

personal factors and is referred to as the ICF inter-active model. Using this model, disability is an um-

brella term covering three levels of reduced function:

impairment of body structure or function (body level),

limitation in activities ( person level), or restriction in

participation (society level; Australian Institute of

Health and Welfare, 2002). Each of these levels should

be addressed when treating any form of disability.

A health condition can cause three hierarchical

levels of life impact, which are shown in Figure 1. At

the lowest level, the condition would cause a ‘‘problem

in body function such as significant deviation or loss’’

(Australian Institute of Health and Welfare, 2002,

p. 3). A problem in body function can lead to activity

limitation, which refers to difficulties an individualmay have in executing activities. Activity limitation

can further lead to participation restriction, which re-

fers to problems an individual may experience being

involved in life situations. There also are environ-

mental and personal factors that can be either barriers

to, or facilitators of, the person’s ability to function.

Tinnitus impact on function can be conceptualized

for a typical patient using the ICF interactive model

shown in Figure 2. The ‘‘health condition’’ is tinnitus,

and the ‘‘problem in body function’’ for the patient

is the perception of tinnitus as a loud ringing sound.

Henry et al.: General Review of Tinnitus 1207

The patient’s main tinnitus-related problem is that the

tinnitus makes it difficult to concentrate (i.e., activity

limitation), and, in turn, the concentration difficulty

hinders work performance (i.e., participation restric-

tion). The main environmental factor influencing the

patient’s tinnitus-related problem is that the family is

unsympathetic toward the tinnitus condition and does

not provide emotional support. The main contributing

personal factor is the patient’s predisposition to anx-

iety. The model clarifies how these different compo-

nents and factors interact with each other to determine

the degree of impact on human function.

On the basis of the ICF interactive model, 100% of

individuals with permanent tinnitus have an impaired

body function because of the condition. For the 20% of

individuals with clinically significant tinnitus (Davis

& Refaie, 2000; P. J. Jastreboff & Hazell, 1998), the

associated problems impact to some degree at the

activity-limitation and participation-restriction levels.

Impact on SocietyWorkers’ Compensation

Workplace noise can be a significant hearing-

health hazard (Gabriels, Monley, & Guzeleva, 1996),

not only in causing hearing loss but also in precipitat-

ing tinnitus (Axelsson & Barrenas, 1992). Severe

tinnitus is frequently more disabling than hear-ing loss, but tinnitus has not typically been monitored

in noise conservation programs (Gabriels et al., 1996).

Tinnitus that is associated with noise-induced hearing

loss can severely affect or even end a person’s occupa-

tion (Coles, 2000). In spite of these realities, workers’

compensation boards are inconsistent in how they ad-

dress tinnitus claims (Tyler, 2003). In some cases, com-

pensation boards will not accept a claim for tinnitus byitself; rather, they assign impairment secondary to hear-

ing loss. Tinnitus is, however, becoming increasingly the

primary or only complaint, and awards for tinnitus can

greatly exceed those for hearing loss (Coles, 2000).

Workers’ compensation programs in 29 of the 50

United States compensate workers for tinnitus (Dobie,2001). In 13 of these states, tinnitus is compensated

only if hearing impairment is also present. In most

states, statutes of limitations (which define the period

within which legal action can be taken) range from 1 to

5 years. In some states, the statute of limitations is

only 30–200 days.

Vernon (1996) and Tyler (2003) have noted that

tinnitus litigation involves establishing the presence,

etiology, and severity of tinnitus. Vernon also noted the

necessity of establishing the permanency of tinnitus,

and Dobie (2001) stressed the importance of historic

documentation. Because tinnitus is by nature subjec-

tive, there is no objective measure to prove its existence

or to verify the reported severity. Tinnitus assessment,like pain assessment, depends on subjective scaling,

self-report, and medical history. Thus, any litigation in-

volving tinnitus must rely on the reliability of tinnitus

psychoacoustic measures, consistency of verbal responses

Figure 1. The International Classification of Functioning, Disabilityand Health (Australian Institute of Health and Welfare, 2002)interactive model to describe human functioning. From DisabilityData Briefing No. 20: The International Classification of Functioning,Disability and Health (p. 1) by the Australian Institute of Healthand Welfare, 2002. Available from http://www.aih.gov.au/publications/dis/ddb20/ddb20.pdf. Copyright 2002 by theAustralian Institute of Health and Welfare. Adapted with permission.

Figure 2. Conceptualization of tinnitus-related problems based onInternational Classification of Functioning, Disability and Healthinteractive model (Australian Institute of Health and Welfare, 2002).From Disability Data Briefing No. 20: The International Classificationof Functioning, Disability and Health (p. 1) by the Australian Instituteof Health and Welfare, 2002. Available from http://www.aih.gov.au/publications/dis/ddb20/ddb20.pdf. Copyright 2002 bythe Australian Institute of Health and Welfare. Adapted withpermission.

1208 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

and medical records, and sufficient duration of the tin-

nitus condition to establish permanency (minimum of

2 years duration was proposed by Vernon; Henry, 2004a).

Economic ImpactThe U.S. Department of Veterans Affairs (VA)

regards tinnitus as a disabling condition (J. A. Henry,

Schechter, et al., 2004). U.S. military veterans can

submit claims for tinnitus that they believe was caused

by exposure to noise during their military service.

Approved claims usually result in a monetary benefit

as compensation for the disability. As of September

2004, 289,159 veterans had received a disability award

for their tinnitus, and most of these individuals wereentitled to receive monthly compensation benefits for

their service-connected disability. The total yearly com-

pensation amount was estimated at $345,495,552. Every

veteran who is service-connected for tinnitus (whether

they receive compensation benefits) is eligible for clin-

ical services at VA medical centers.

There are no known studies that have attempted

to estimate the economic impact of tinnitus on the

general population. Reich (2002) addressed this issue

and concluded, ‘‘It isn’t possible to assign a specific

cost figure to tinnitus’’ (p. 18). To conduct such a study

would require obtaining estimates of (a) loss of job

productivity, (b) medical costs associated with tinni-tus, (c) costs of litigation associated with tinnitus, and

(d) compensation awards and payments for tinnitus.

These costs must be substantial, as evidenced by the

cost to the Veterans Health Administration. Moreover,

the overall costs are expected to increase as the public

becomes better educated about tinnitus and as noise

exposure increases as a problem in our society.

Factors Associated With TinnitusMany factors are known to be associated with

tinnitus. These factors are often considered ‘‘causes’’ of

tinnitus when a connection between the two is estab-

lished. An event, such as impulse noise, may indeed

cause the onset of tinnitus. The mechanism responsi-

ble for sustained tinnitus, however, remains unknowneven when the causal event is unequivocal. The present

understanding of cellular events and other pathologic

mechanisms that underlie tinnitus onset is insufficient

to enable their identification even when a tinnitus-

causing event seems obvious. We therefore use the terms

cause and etiology in the context of events leading to the

onset of tinnitus.

It is often reported that the most common cause of

tinnitus is noise exposure (Axelsson & Barrenas, 1992;

Penner & Bilger, 1995). Medications are frequently as-

sociated with permanent or temporary tinnitus. More

than 300 prescription and over-the-counter medications

list tinnitus as a side effect (DiSorga, 2001). Less known

are the complex interactions between multiple medica-

tions that may contribute to the etiology of tinnitus.

Other factors associated with tinnitus include aging,

head and neck injuries, vascular and cerebrovasculardiseases, systemic disorders, infectious disease, auto-

immune disorders, ear conditions, and TMJ disorders

(Perry & Gantz, 2000; Vernon & Møller, 1995).

In many cases, the cause of tinnitus is identified

as idiopathic (Meikle & Griest, 1989). Patients from

the Oregon Tinnitus Clinic (OTC) complete extensivequestionnaires, including a description of what they

believe has caused their tinnitus. In a sample of 2,369

of these patients, 40% reported no known events as-

sociated with their tinnitus onset. Patients who could

identify a precipitating event revealed four general cat-

egories of tinnitus etiology: (a) noise-related, (b) head

and neck trauma, (c) head and neck illness, and (d) other

medical conditions. The percentages by category of theassociated condition (and subcategories of each condi-

tion) for the OTC patient sample are shown in Table 1.

Hearing Loss and AgingThere is a clear relation between hearing loss and

tinnitus (Axelsson & Barrenas, 1992; Davis & Refaie,

2000; Meikle, 1991), and the majority of tinnitus

patients have some degree of hearing loss (Axelsson

& Ringdahl, 1989; Davis & Refaie, 2000; J. L. Henry &Wilson, 2001; Vernon, 1998). Vernon and Meikle (2000)

reported that 70% to 80% of tinnitus patients have

‘‘significant hearing difficulties’’ (p. 327).

Approximately 34 million Americans are hearing

impaired (Blackwell, Collins, & Coles, 2002). Because

hearing loss and tinnitus are so closely related, popula-tions with more prevalent hearing loss have a corre-

spondingly greater prevalence of tinnitus (Hoffman &

Reed, 2004). The prevalence of hearing loss increases

with age, especially after age 65 (Axelsson & Barrenas,

1992; Beck et al., 2002). Thirty percent of all individuals

between the ages of 65 and 74 years and 50% of those

persons 75 years and older have hearing loss (Blackwell

et al., 2002).

Although tinnitus is commonly associated with hear-

ing loss in older patients, other medical factors become

increasingly prevalent and must be considered as poten-

tial causes of tinnitus. These factors include conditions

such as vascular disease, middle-ear disease, diabetes,

hypertension, autoimmune disorders, and degenerativeneural disorders, with or without concomitant hearing

loss (Perry & Gantz, 2000). Furthermore, these medical

conditions are accompanied by increasing use of medi-

cations, which may also cause tinnitus emergence or

Henry et al.: General Review of Tinnitus 1209

exacerbation. Two percent of a sample of 1,630 OTC

patients reported medications as the cause of their

tinnitus (Meikle et al., 2004).

There are also changes in life that occur withaging. These changes, such as illness, retirement, loss

of function, loss of spouse or friends, or reduced social

activity may bring on changes in mood, depression, and

anxiety. These stressful life events have the potential

to increase the perceived loudness of tinnitus or to

exacerbate tinnitus reactions (J. L. Henry & Wilson,

2001). Some patients report stress as the precipitating

factor for their tinnitus (Meikle & Griest, 1989).

The increase in tinnitus prevalence in older patients

does not necessarily mean that tinnitus as a separate and

distinct symptom will increase with age (Hoffman &

Reed, 2004). The International Work Group on Hearing

Problems and the Elderly (Salamon, 1986) concluded

that the incidence of tinnitus was not greater than thatexpected for older patients with hearing loss and other

age-related diseases; in addition, the pathophysiology of

tinnitus in older patients was the same as that in youn-

ger patients. Others have argued that age-related tin-

nitus exists as a distinct pathology and is related to de-

generation at all levels of the auditory system (McFadden,

1982). For the aged population, tinnitus may go un-

reported or may be given less importance in the context

of other significant medical problems.

Psychological Aspects of TinnitusPain and tinnitus may cause emotional and psycho-

logical distress that is out of proportion to the magnitude

of the injury. Because both conditions are subjective

phenomena, which are most reliably measured by self-

report, standardized scales can be helpful in quantifying

the associated psychological reactions (Farrar, Portenoy,

Berlin, Kinman, & Strom, 2000; Newman & Sandridge,2004). Moreover, both pain and tinnitus are associated

with dysfunctional, inappropriate coping strategies or

ideations (Sweetow, 2000). In this regard, tinnitus is

similar to other phantom sensations such as phantom

pain and phantom limb (P. J. Jastreboff, 1990, 1995).

Not all patients experience tinnitus in the sameway, and intrinsic and extrinsic factors such as per-

sonality, psychosocial factors, and environment contrib-

ute to the patient’s tinnitus reaction (P. House, 1981).

Some patients barely notice tinnitus, whereas others

are severely affected by difficulty with concentration,

sleep disturbances, anxiety, depression, or despair (Tyler

& Baker, 1983). Hallam, Rachman, and Hinchcliffe

(1984) noted that the ‘‘majority’’ of people with tinnitusgenerally develop a tolerance to the symptom and that

the great majority of patients learn to accept tinnitus

as ‘‘part of their environment’’ within a year (Hazell,

1979, p. 88). Furthermore, the number of problems peo-

ple associate with their tinnitus is greatest when tin-

nitus has been present for only a short period of time

(Tyler & Baker, 1983). Hallam et al. surmised that an

adaptation effect seems to take place that causes tin-nitus to become less of a problem over time. On the

basis of these, and a number of other observations, the

authors proposed ‘‘an habituation model of tolerance

for tinnitus’’ (Hallam et al., 1984, p. 44) that was de-

signed to explain this apparent adaptation effect. It is

important that they postulated that habituation to tin-

nitus is the ‘‘normal’’ state, whereas the inability to ha-

bituate occurs far less frequently and is due primarilyto certain psychological factors.

Sound carries meaning. Sound can evoke strong

emotional reactions because of its importance to sur-

vival and because it is the primary medium for spoken

language (Hallam et al., 1984; Hazell, 1999; Iversen,

Kupfermann, & Kandel, 2000; Sweetow, 1995). Ourears are always searching the world around us for

meaningful or threatening sounds. Most sounds that

have little meaning or are not interpreted as a threat

are quickly habituated (not reacted to) by the central

Table 1. Conditions associated with tinnitus, as reported froma group of 2,369 Oregon tinnitus clinic patients.

Total %

Category of associatedcondition

% (as singlecause)

As singlecause

As one ofmultiplecauses

Noise related 18% 22%Long-duration noise 10%Explosion 5%Brief intense noise 3%

Head and neck trauma 8% 17%Head injury 4%Whiplash/cervical trauma 3%Concussion G1%Skull fracture G1%

Head and neck illness 8% 10%Ear infection, inflammation 3%Cold/sinus infection 3%Other ear problems 2%Sudden hearing loss 1%Allergies/hay fever 1%

Other medical conditions 7% 13%Other illnesses 2%Drugs, medications 2%Stress 1%Surgery 1%Possible TMJ syndrome 1%Barotrauma 1%

Note. TMJ = temporomandibular joint.

1210 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

nervous system (Domjan & Burkhard, 1986). A good

example is the sound of an electric fan. Unless an indi-

vidual attends to the sound, the person is not consciously

aware that the sound is present. The link between

emotion and sound may be the basis for psychological

distress in some tinnitus patients (Hallam et al., 1984;

P. J. Jastreboff, Gray, & Gold, 1996). Tinnitus is nothabituated in patients who typically seek treatment but

rather may become intrusive, annoying, or disturbing

for them and may persist as a problem even though the

underlying condition has been present for months or

even years. Once tinnitus emerges and the patient begins

to attend to it, the tinnitus becomes audible. If the pa-

tient continues to focus on the tinnitus and attaches

negative beliefs to it (e.g., ‘‘the tinnitus will get worse,’’‘‘the tinnitus will make me go deaf,’’ or ‘‘the tinnitus

means I have a terrible ear disease’’), then he/she may

suffer increasing worry, anxiety, fear, distress, despair,

and depression. In other words, just as changes in

psychological state can trigger tinnitus, psychological

reactions and negative associations can exacerbate the

condition and, in effect, amplify the perception of tin-

nitus. Effective control of these maladaptive emotionalreactions and beliefs is an important component of tin-

nitus management (Hallam et al., 1984; Hazell, 1998a;

Lindberg, Scott, Melin, & Lyttkens, 1987; Scott, Lindberg,

Lyttkens, & Melin, 1985; Sweetow, 1986, 2000).

Attributes of Tinnitus in aClinical Population

The Oregon Tinnitus Data Archive (Meikle et al.,

2004) contains a valuable description of tinnitus attri-

butes from 1,630 OTC patients. Patient data were in-

cluded in this database if the patient (a) was at least18 years of age, (b) completed a tinnitus evaluation

with at least 75% of questionnaire items having

‘‘acceptable reliability,’’ (c) was interviewed to confirm

questionnaire responses, and (d) gave informed consent.

These data, which may be generalized to only treatment-

seeking patients, suggest more than twice as many men

as women are in the archive and that 80% of all pa-

tients are over age 40. The onset of tinnitus is reportedto be ‘‘gradual’’ slightly more often than ‘‘sudden.’’ Tin-

nitus is perceived more often in the left ear or left side

of the head than in the right. More than half of patients

report that their tinnitus consists of a single sound,

whereas most of the rest can identify two or more sounds.

The great majority of patients report that their tinni-

tus sounds like ‘‘ringing’’ or a ‘‘clear tone,’’ whereas only

3% report their tinnitus to be perceived as a ‘‘hum,’’‘‘clicking,’’ ‘‘roaring,’’ or ‘‘pulse.’’ These latter sounds

are likely to be related to vascular or ear disease. Ad-

ditional findings from analyses of the archive data in-

cluded the trend for perceived tinnitus loudness to

appear higher than suggested by the patients’ matched

level (dB SL) to the tinnitus. Furthermore, about 85%

of patients reported the perceived loudness of their tin-

nitus as 5 or more on a 0–10 loudness-rating scale (10 =

very loud), whereas 70% matched their tinnitus loud-

ness to pure tones presented at 6 dB SL or less. In

contrast, only 20% of patients matched their tinnitusat 6 dB SL or less when the match was performed to

a 1000-Hz tone (i.e., a frequency outside the range

of hearing loss in most patients). These matching re-

sults support the well-known phenomenon of loudness

recruitment, which is often thought to contaminate

tinnitus-loudness measures (J. A. Henry, 1996; Tyler &

Conrad-Armes, 1983a).

Lockwood, Salvi, and Burkard (2003) reported find-

ings in a survey of more than 500 patients. The mean

length of time patients waited to seek attention was

5 years. By the time they did seek medical attention,

60% thought they had a serious medical problem and

55% thought they would go deaf—underscoring the

recognition of the patient’s misconception of the often-benign tinnitus symptom. Twenty-two percent reported

tinnitus as being equal in both ears, 34% reported uni-

lateral tinnitus, and most reported some degree of lat-

eralization. As in the Oregon database, patients reported

a wide variety of tinnitus qualities, including ‘‘ringing’’

(38%), ‘‘buzzing’’ (11%), ‘‘crickets’’ (9%), and ‘‘humming’’

(5%). Thirty-four percent of patients rated the severity

as 8 on a 1–10 subjective loudness scale (10 = very loud ).The tinnitus frequency was usually related to the pat-

tern of the hearing loss and was usually above 3000 Hz.

Sleep problems are a particular concern for many

tinnitus patients. From the sample of 1,630 Oregon

patients, more than 70% reported that their tinnitus

caused sleep disturbances (Meikle et al., 2004). Otherclinical data have revealed that the most frequently

encountered problem experienced by tinnitus patients

is sleep disturbance (Axelsson & Ringdahl, 1989; Jakes

et al., 1985; Tyler & Baker, 1983). In addition, numer-

ous studies have reported that patients with tinnitus-

related sleep problems tend to report the most severe

tinnitus (Axelsson & Ringdahl, 1989; Erlandsson,

Hallberg, & Axelsson, 1992; Folmer & Griest, 2000;Meikle, Vernon, & Johnson, 1984; Scott, Lindberg, Melin,

& Lyttkens, 1990). These data emphasize the importance

of addressing the issue of sleep with all tinnitus patients.

Perception of TinnitusThe inner ear transforms mechanical energy into

electro–chemical energy. Auditory information is trans-

mitted in the form of neural activity that travels

from the auditory nerve into the brainstem and to

higher processing centers in the thalamus and cortex.

Henry et al.: General Review of Tinnitus 1211

How does the central nervous system distinguish in-

puts generated by external events from aberrant self-

generated events? The fact that tinnitus is qualitatively

similar to externally generated sounds suggests that the

neural pathways that mediate tinnitus are the same as

those that process normal sound perception. If the cen-

tral nervous system processes aberrant neuronal firing,the result might be a perception of sound that has no

external cause (Eggermont & Sininger, 1995). Regard-

less of the causal or underlying mechanism, the end

product is the same: perception of sound in the absence

of external stimulation.

Masking of Tinnitus Versus Maskingof External Sounds

Many studies have revealed that masking of tin-

nitus does not follow the psychoacoustic rules that were

established for the masking of one sound by another

(Feldmann, 1971; Formby & Gjerdingen, 1980; Hazell,

1981; Mitchell, 1983; Mitchell, Vernon, & Creedon, 1993;

Penner, 1987; Penner & Klafter, 1992; Shailer, Tyler, &

Coles, 1981; Tyler & Conrad-Armes, 1984). All inves-tigators have agreed that the usual marked frequency

dependence seen in conventional tone-on-tone masking

is not characteristic of most attempts to mask tinnitus.

That is, unlike sounds that originate externally, the

frequency of the masker is not a reliable predictor of

tinnitus masking (Feldmann, 1971). Furthermore, in a

normal psychoacoustic masking experiment, low frequen-

cies are more effective maskers than high frequencies.Tinnitus masking usually shows no such dependence.

Normally, it is not possible to mask a broadband

or thermal noise with a tone. In tinnitus masking,

however, a tonal masker (at any frequency) can be

effective in providing relief in some patients (Feldmann,1995). Masking sounds presented to the opposite ear

are often as effective for masking tinnitus as sounds

presented ipsilaterally. In addition, simultaneous

masking (i.e., both masking and masked signals are

present) can normally be sustained for long periods of

time. In tinnitus masking, the effects are less predict-

able and often show fluctuation or adaptation in the

level of the masker needed to maintain suppression(Penner, 1983a). Furthermore, in forward masking

(where the masker precedes the signal to be masked),

the effect of the masking lasts only a few milliseconds.

In tinnitus masking, the effect of the masker can last

several minutes (Feldmann, 1995).

The conclusion from the various studies is that tin-nitus masking appears to be categorically different from

the conventional masking of one external tone by an-

other. The differences observed between the two forms

of masking suggest that the mechanism of tinnitus is

fundamentally different from normal auditory sensa-

tion. Patterns of neural activity that are responsible for

the sensation of tinnitus would seem likely to be differ-

ent from neural patterns evoked by an external sound

that gives rise to an equivalent auditory sensation. This

difference in neural activity has been partially ex-

plained by experimental observations demonstratingthat sound-on-sound masking occurs at the mechanical

stage in the cochlea (i.e., prior to transduction of the

mechanical signal to an electrochemical neural signal).

Generation of the tinnitus signal is not normally asso-

ciated with mechanical action of the cochlear partition,

and the lowest possible stage of tinnitus generation would

be the inner hair cells. This would not rule out cases of

tinnitus that are caused by some kind of mechanical ac-tion or force impinging on the cochlear partition.

‘‘Coherent’’ Versus ‘‘Incoherent’’ TinnitusThere are fundamental phenomena concerning

directional hearing and localization of sounds that

relate to the perception of tinnitus (Feldmann, 1995).

Acoustic signals presented binaurally will form asingle, centered, auditory image if the signals are

diotic (i.e., when the acoustic characteristics of the two

sounds are essentially equivalent, especially their time

pattern). The signals must be sufficiently different for

them to be perceived as two distinct stimuli.

Most tinnitus patients can lateralize their tinnitusto the right or the left ear, to both ears simultaneously,

or to some location in the head. Tinnitus that can be

heard in each ear lacks coherence and would presum-

ably originate from two sources distal to the medial

superior olive (Feldmann, 1995), which is the lowest

level of the brainstem at which binaural convergence

of auditory stimuli takes place (Gelfand, 1998). On

the basis of the premise that tinnitus is not normallyassociated with mechanical action of the cochlear

partition (Feldmann, 1988; Penner & Bilger, 1995), it

follows that tinnitus that can be heard in each ear

must originate somewhere between the synapse of

the inner hair cells and the superior olivary complex.

Because cochlear damage resulting from exposure to

noise is the most common cause of tinnitus, and

because it is generally believed that tinnitus does notoriginate from the cochlear partition, it would seem

reasonable to postulate that ‘‘incoherent’’ tinnitus orig-

inates at the base of the inner hair cells (‘‘peripheral’’

origin). In contrast, tinnitus that is perceived as a

fused (coherent) image could be conjectured to originate

at some level above the superior complex (‘‘central’’

origin). It may also be true, however, that tinnitus that

is perceived as fused could simply reflect two cochleaethat are very similar in pathological state, resulting in

very similar aberrant signals.

1212 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

Theorized Mechanismsof Pathophysiology

Numerous structures within the auditory system

and neighboring anatomical regions could contribute to

the generation of tinnitus, but at present no test can

identify these regions accurately (Brix, 1995; Hazell,1995). The study of these structures in relation to

tinnitus is problematic, and, not surprisingly, a causal

relation between measurable neurophysiologic func-

tions and tinnitus generation has not yet been demon-

strated scientifically.

The study of tinnitus mechanisms is vitally impor-tant to develop effective treatments for tinnitus in all

its forms and manifestations. If pathological mecha-

nisms of tinnitus could be defined for different classi-

fications of tinnitus origin, treatment could be directed

toward addressing the cause of the disorder rather

than just the consequences. Zenner and Pfister (1999)

have proposed three broad classes of tinnitus, on the

basis of anatomical and functional divisions of theauditory system, that include conductive, sensorineu-

ral, and central tinnitus generation sites. Conductive

tinnitus would be caused by some type of vibration in

the middle ear. Sensorineural tinnitus would have nu-

merous subclasses, including tinnitus generated from

(a) outer hair cells (‘‘motor’’ tinnitus), (b) inner hair

cells (‘‘transduction’’ tinnitus), (c) the auditory nerve

(‘‘transformation’’ tinnitus), and (d) extrasensory struc-tures (vascular, muscular or other somatic sources

of ‘‘objective’’ tinnitus). Central tinnitus would involve

tinnitus originating anywhere in the central auditory

pathways. Every conceivable site of tinnitus genera-

tion is covered in this classification framework. What

remains to be learned, however, is the precise mech-

anisms of action that result in generation of the

tinnitus neural signal. These mechanisms are likelyto be multiple, even in the same individuals (Baguley,

2002; A. R. Møller, 2003).

Many theories and models have been proposed to

explain the pathophysiological basis of tinnitus (Baguley,

2002; Eggermont, 2000; Kaltenbach, 2000; A. R. Møller,2003; Vernon & Møller, 1995). The most prevalent the-

ories involve hair cells, the auditory nerve, and the cen-

tral auditory nervous system. Theories involving hair

cells include discordant hair cell function (P. J. Jastreboff,

1990), calcium imbalance (Eggermont, 2000), loss of outer

hair cell function as a trigger of tinnitus (Kaltenbach

et al., 2002), activation of cochlear NMDA (N-methyl-

D-aspartate) receptors (Guitton et al., 2003), excitatorydrift in hair cells (LePage, 1987), and enhanced gluta-

mate activity from the inner hair cells in response to

stress (Sahley & Nodar, 2001). Theories involving the

auditory nerve include synchronization of spontaneous

activity in auditory nerve fibers that is due to cross-talk

(Eggermont, 1990; Møller, 1984, 1995), deafferentation

hyperexcitability (Kiang et al., 1970), abnormal tempo-

ral pattern in auditory nerve-fiber spontaneous activity

(Eggermont, 1984), and differential activity in tonotopi-

cally adjacent fibers (Kiang et al., 1970). Theories involv-

ing the central auditory nervous system include effectsof the efferent auditory system (Hazell, 1987), increased

spontaneous activity in the dorsal cochlear nucleus

(Brozoski, Bauer, & Caspary, 2002; Kaltenbach & Afman,

2000; Kaltenbach et al., 2002; Zacharek, Kaltenbach,

Mathog, & Zhang, 2002), generation of tinnitus by broad

multimodal networks of neurons (Cacace, 2003), and cor-

tical plasticity (Lockwood et al., 1998). There are, of course,

many other theories.

Peripheral Versus Central Site ofTinnitus Generation

The most fundamental question regarding themechanism of tinnitus is its neural site of generation.

Zenner and Pfister’s (1999) classification model

described above emphasizes that tinnitus can originate

anywhere between the peripheral ear and the central

auditory pathways. Tinnitus generated in the middle

ear is relatively rare, but it does occur. Sensorineural

tinnitus is thought to be the most common form of tin-

nitus, mainly because noise exposure is so commonlyassociated with tinnitus onset, and the damage caused

by noise is cochlear. In addition, there are many other

causes of cochlear pathology. Coles (1995) referred to

the ‘‘clinical dictum’’ (p. 13) that whatever factors are

responsible for causing hearing loss are also likely to

have caused an associated tinnitus.

The earliest speculations about the site of tinnitus

generation suggested a cochlear origin. This site of

origin was posited because of the strong association

observed between tinnitus and hearing loss caused by

cochlear damage (Kiang et al., 1970). Theories that

tinnitus originated in the inner ear were further sup-

ported by observations that patients often perceived

tinnitus in the ears (P. J. Jastreboff, 1990). Becausesurgical sectioning of the auditory nerve did not al-

ways eliminate intractable tinnitus (Fisch, 1970;

J. W. House & Brackmann, 1981; Pulec, 1984), the

cochlear origin theory was not universally accepted

(Douek, 1987; Feldmann, 1995). Over time, the pre-

vailing view suggested that tinnitus was generated in

the central nervous system and was triggered by

cochlear damage (Penner & Bilger, 1995). More recently,studies have presented arguments to support both a

cochlear (Penner & Bilger, 1995; Zenner & Ernst, 1995)

and a central (Eggermont & Sininger, 1995; Lockwood

et al., 1998) locus of tinnitus origin. A. R. Møller (2003)

Henry et al.: General Review of Tinnitus 1213

took the view that pathology in the ear and auditory

nerve results in abnormal input that causes changes in

central structures. More specifically, abnormal auditory

signals activate neural plasticity within central auditory

structures, which can be expressed as tinnitus.

Tinnitus Associated WithHair Cell Damage

There are many theories that describe the under-

lying cause of tinnitus as being associated with the loss

of cochlear hair cells, some of which were listed above.The discovery of spontaneous otoacoustic emissions

(SOAEs) generated by outer hair cells led to the logical

speculation that they might prove to be an objective

correlate of some forms of tinnitus (Kemp, 1979). A

number of studies that attempted to link SOAEs with

tinnitus found that they were generally independent

events (Prieve & Fitzgerald, 2002). It does appear,

however, that some patients have tinnitus caused bySOAEs. Penner (1990), for example, observed that the

prevalence of tinnitus caused by SOAEs was 4%.

Norton, Schmidt, and Stover (1990) reported that

several studies found an association between SOAEs

and tinnitus in 6% to 12% of patients.

With the loss of hair cells or hair cell function,afferent neurons appear to trigger aberrant auditory

sensations at frequencies at or near the focus of the

lesion (P. J. Jastreboff, 1990). This ‘‘edge effect’’ theory

could explain why tinnitus is frequently associated

with hearing loss, why the frequency of tinnitus is

often related to the involved frequencies of the hearing

loss, and why tinnitus persists beyond the time

expected for normal recovery from noise exposure(Eggermont & Sininger, 1995).

Noise exposure. The histopathology associated with

noise exposure, as it is for many causes of cochlear

tinnitus, is related to hair cell damage (Coles, 1995).

However, the mechanism of tinnitus and its associa-

tion with noise exposure is unknown, but this cochleardamage somehow appears involved in the onset of

tinnitus. We know that high noise levels cause hair cell

damage that begins with the stereocilia of the outer

hair cells and progresses to loss of the hair cells

themselves (Harrison & Mount, 2001). Outer hair cells

are damaged first, followed by damage to inner hair

cells. Progressive noise damage can eventually result

in complete destruction of both inner and outer haircells in certain regions of the basilar membrane. There

can also be degeneration of associated neural elements

at each stage of damage.

The structural changes that are observable withhair cell damage are preceded by molecular damage(Wenthold, Schneider, Kim, & Dechesne, 1992). Whereas

molecular changes associated with noise damage arepotentially reversible, the subsequent structural changesare not. Wenthold et al. have suggested a hypotheticalsequence of molecular changes that correlate with dif-ferent stages of morphological changes—from initial re-sponses to hair cell death. Initial biochemical changesinvolve damage to the structural proteins that reside inthe stereocilia and on the cuticular plate. Any of thesechanges could play a role in the onset of tinnitus. Forexample, there is a group of proteins, referred to as heatshock proteins (or stress proteins), that are upregulatedin response to any condition that stresses a cell. It isthought that stress proteins bind to damaged proteins tofacilitate cellular repair and protection from further celldamage. It is thus possible that stress proteins canprotect the cochlea from damage caused by noise. Aperson who has a deficient stress protein response systemmay be at increased risk of incurring hearing loss whenexposed to noise. It would follow that such a person couldalso be at greater risk for incurring tinnitus.

It is also important to mention that calcium balance

is essential for many aspects of normal cochlear

function (Wenthold et al., 1992). Any disruption to this

calcium balance could result in tinnitus (Eggermont,

2000). Normal functioning of hair cells requires that

calcium concentrations be precisely maintained on both

sides of the hair cell membranes. It has been shown

that intense sound can increase the concentration of

cytoplasmic calcium in isolated outer hair cells, sug-

gesting that such changes in calcium concentration

may be involved in the long-term pathogenesis of noise

damage to hair cells (Fridberger & Ulfendahl, 1996).

Eggermont (2000) suggested that increased levels of

intracellular calcium, causing an increase in neuro-

transmitter release from the cells and a subsequent

increase in the spontaneous firing rates of associated

afferent fibers, may be a causal factor in tinnitus.

Meniere’s disease. Tinnitus is also a symptom of

Meniere’s disease (endolymphatic hydrops), for which

the underlying pathology again appears to be hair

cell damage—possibly related to potassium toxicity

(‘‘leaky’’ potassium channels; Zenner, 1986; Zenner &

Ernst, 1995) or changes in osmolarity (Dulon, Aran, &

Schacht, 1987; Feldmann, 1995).

Perplexing observations. Not all persons with hear-

ing loss have tinnitus (Hazell, 1998a; J. L. Henry &

Wilson, 2001). Persons with profound hearing loss

(deafness) often do not complain of tinnitus, nor report

significant levels of tinnitus (Coles, 1995; Hazell,

1998a). In other words, cochlear damage does notalways result in tinnitus. It may also be the case that

cochlear damage may be slight and not significant

enough to cause substantive change in auditory sensi-

tivity. The variety of theories and the variability in the

1214 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

presentation of tinnitus and success in the treatment of

tinnitus lead to the conclusion that there are likely to be

many mechanisms, or complex combinations of mecha-

nisms (Baguley, 2002; A. R. Møller, 2000).

Theories of Central Tinnitus GenerationIn addition to the observation of tinnitus in

patients who had undergone transection of the audi-

tory nerve (Fisch, 1970; J. W. House & Brackmann,

1981; Pulec, 1984), other support for a central origin

for tinnitus has come from a study that showed

tinnitus patients with reduced amplitudes of auditory

event-related potentials (Attias, Urbach, Gold, &

Shemesh, 1993). Lockwood et al. (1998) used positronemission tomography (PET) to map brain regions that

showed activity in response to changes in tinnitus

loudness. Participants in this study had the unusual

ability to alter the loudness of their tinnitus by per-

forming oral facial movements. The interesting result

was that self-induced changes in tinnitus loudness

resulted in unilateral changes in cerebral flow, which

suggested that the spontaneous neural activity respon-sible for their tinnitus was generated centrally. Later

imaging studies produced the same general findings

(Lockwood et al., 2001; Reyes et al., 2002).

Additional support for tinnitus of central origin

has come from a series of animal studies that examined

noise-induced hyperactivity in the dorsal cochlearnucleus (DCN). Kaltenbach and Afman (2000) ob-

served that the DCN exhibits a spontaneous activity

pattern following noise exposure that is very similar to

the activity induced by a low-level tone. DCN hyper-

activity also has been induced by the chemotherapeutic

drug cisplatin (Rachel, Kaltenbach, & Janisse, 2002).

These two findings suggest that DCN hyperactivity

could be a neurophysiologic correlate of noise- andcisplatin-induced tinnitus, although both noise and the

cisplatin have their damaging effects primarily on the

outer hair cells. In fact, outer hair cell damage caused

by cisplatin has been documented in association with

DCN hyperactivity (Kaltenbach et al., 2002). Zacharek

et al. (2002) addressed the question of whether DCN

hyperactivity originates centrally or peripherally following

exposure to intense noise. They ablated noise-damagedcochleae with the result that DCN hyperactivity per-

sisted. Thus, the central hyperactivity was not de-

pendent on cochlear input, which suggested that the

hyperactivity originated centrally.

There is growing evidence that tinnitus may

originate from an anatomical location that is centralto the site of initial pathology (A. R. Møller, 2003).

Cacace (2003) reviewed the evidence and proposed a

view that networks of neurons may be involved in

generating and sustaining tinnitus. This view would

explain why tinnitus might persist following tran-

section of the auditory nerve or ablation of a damaged

cochlea. Moreover, Cacace suggested that these neural

networks might be so extensive as to involve brain

regions subserving emotions, directed attention, and

conscious perception.

Similarities With PainTinnitus has been viewed as a phantom auditory

perception, not unlike pain (Meikle, 1995; A. R. Møller,

2003). Pain and tinnitus have similar features in termsof the physiology, assessment, and management (A. R.

Møller, 1987, 2000). Tinnitus and chronic pain appear

to be mediated by neuropathic mechanisms and seem

to involve central generation in more severe cases.

Pain theories have postulated that pain is caused by

rearrangement of cortical circuits that is due to deaf-

ferentation, which can result in phantom limb sensa-

tion and associated pain (Kandel, 2000; Tonndorf,1987). Similarly, it has been theorized that tinnitus

can be caused by deafferentation of the cochlear nerve,

with subsequent reorganization of neural connections

at higher level auditory pathways (Feldmann, 1988).

Additional CommentsWhether tinnitus is generated centrally or pe-

ripherally has been the subject of considerable debate

(Feldmann, 1971; Lockwood et al., 1998). Because tin-

nitus is perceived consciously as sound, however, it

must by definition involve retrocochlear and cognitiveprocesses. Peripheral and subcortical auditory centers

are responsible for transduction, transmission, and pro-

cessing of neural information, but perception occurs

at the level of the cortex. The locus of tinnitus must

ultimately be physiologically verified, and a number of

studies are under way with this objective in mind. In

addition, psychoacoustic data concerning perceptual at-

tributes of tinnitus offer a rich source of information inproviding evidence supporting the site(s) of tinnitus

generation (Meikle, 1995; Penner & Bilger, 1995).

Assessment of the Tinnitus PatientMedical Evaluation

Although it may not be feasible in many situations,

all tinnitus patients should be referred to an otolar-

yngologist or otologist for an otologic physical exami-

nation (Perry & Gantz, 2000; Wackym & Friedland,2004). The exam enables the identification of under-

lying physical pathologies that could potentially be

treated, or even cured, medically or surgically. The

otologic exam is especially important for patients

Henry et al.: General Review of Tinnitus 1215

with pulsatile tinnitus, which often has an identifi-

able physical pathology (Sismanis, 1998; Wackym &

Friedland, 2004). The examination results in radiologic

and/or laboratory testing only if it is determined that

there is a reasonable chance that there is a correctable

cause for the tinnitus (Perry & Gantz, 2000; Wackym

& Friedland, 2004).

Audiological EvaluationBecause most tinnitus patients also have some

hearing impairment, routine audiological testing is rec-ommended for all patients who seek treatment for their

tinnitus (Henry, 2004a). Audiometric evaluation should

include pure-tone thresholds, speech-recognition thresh-

olds, word-recognition scores, and immittance measures.

When conducting audiometric testing, it is critical for

the clinician to be aware that many tinnitus patients are

also hypersensitive to sound. Thus, extreme care must

be taken when testing acoustic reflexes, which gener-ally is not advised (J. A. Henry, Jastreboff, Jastreboff,

Schechter, & Fausti, 2002). Because loudness intoler-

ance can impact testing procedures, loudness discomfort

levels (LDLs) should be determined at audiometric fre-

quencies to assess the upper limit of the auditory dy-

namic range for each patient. This information should

be used to ensure that patients are not exposed to any

sound during testing that exceeds their LDLs.

Reduced Loudness ToleranceWhen LDLs are evaluated at different audiometric

frequencies, the average of these measurements will

generally be below 100 dB HL when there is a loudness

tolerance problem (P. J. Jastreboff & Hazell, 1993).

The LDLs provide a ‘‘reasonable estimate of the prob-

lem’’ (M. M. Jastreboff & Jastreboff, 2002, p. 75), al-

though there is no consistent relation between patient’s

complaints of loudness intolerance and their LDLs

(Henry, 2004a; M. M. Jastreboff & Jastreboff, 2002).

Patients with a clinically significant problem of

reduced loudness tolerance are generally said to have

hyperacusis. Unfortunately, there is at present no

consensual definition of hyperacusis (Vernon, 2002).

Vernon and Press (1998) have defined hyperacusis as

‘‘the collapse of loudness tolerance so that almost allsounds produce loudness discomfort’’ (p. 223). This defi-

nition would not be compatible with M. M. Jastreboff

and Jastreboff ’s (2002) report that 30% of tinnitus

patients require ‘‘specific treatment for hyperacusis’’

(p. 75). A number of other clinics have reported that up

to 45% of their patients have decreased loudness tol-

erance (Coles, 1996; Gold, Frederick, & Formby, 1999;

Hazell, 1999; P. J. Jastreboff, 2000).

M. M. Jastreboff and Jastreboff (2002) have distin-

guished hyperacusis from the condition of misophonia.

They described hyperacusis as a condition of hyper-

sensitivity to sound that is restricted primarily to the

auditory pathways. Thus, when sound that is normally

well tolerated causes physical discomfort, hyperacusis

is indicated. Misophonia refers to dislike of sound and

involves primarily an emotional reaction that is

mediated by the limbic and autonomic nervous sys-tems. The reactions are context dependent, and thus

the same sound might evoke different responses in

different circumstances. If one of the emotional

responses is fear, the condition of phonophobia is indi-

cated. Phonophobia is thus a specific case of misophonia

when fear is involved. Jastreboff and Jastreboff em-

phasized that none of these conditions has any relation to

loudness recruitment, which refers to abnormally rapidgrowth in the perception of loudness (Vernon, 1976).

Because reduced loudness tolerance is so often

associated with tinnitus, it is important for the cli-

nician to be skilled in making a proper diagnosis and

providing appropriate intervention. As with tinnitus,

however, management of this condition is not stan-dardized. M. M. Jastreboff and Jastreboff (2002) have

provided a comprehensive schema for identifying

different components of the condition and treating

each accordingly. They distinguished primarily

between a physiological (hyperacusis) versus a psycho-

logical (misophonia) cause. These constitute very

different conditions and treatment should differ ac-

cordingly. Pure hyperacusis is like a pain responsewith no psychological overlay. Its treatment involves

desensitization of the auditory pathways through the

use of sound. With misophonia, however, the patient

has learned to react emotionally to certain sounds.

This is a much more complex condition to treat, espe-

cially when there is a fear component (phonophobia).

Treatment of misophonia in all its manifestations

primarily involves counseling, and some patients mayrequire the services of a psychologist.

It is often the case that hyperacusis leads to some

form of misophonia. That is, the experience of auditory

discomfort can lead to a psychological reactive state

involving the inappropriate use of ear protection and/

or avoidance of sound. These behaviors would con-stitute overprotection of hearing, which could exacer-

bate the condition because sound deprivation can

further reduce loudness discomfort levels (Formby &

Gold, 2002; Formby, Sherlock, & Gold, 2002). The

different components of reduced sound tolerance are

clearly not mutually exclusive; thus, the challenge for

the diagnosing clinician is to identify the relative

contribution of each. The assessment can be facil-itated by measuring LDLs, and by administering the

sound tolerance section of the TRT Initial Interview

(J. A. Henry, Schechter, et al., 2002, 2003; M. M.

Jastreboff & Jastreboff, 1999).

1216 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

Tinnitus Psychoacoustic AssessmentA tinnitus psychoacoustic assessment should also

be part of the intake evaluation. The clinical relevance

of these measures depends on the form of treatment

used because the measures have limited diagnostic

value. With masking treatment, it is always crucial to

measure or document the effects of masking stimuli on

the perception of tinnitus (J. A. Henry & Meikle, 2000;

Schechter & Henry, 2002). Therefore, minimum mask-

ing levels and trial use of sound-generating devices

must be a part of the tinnitus assessment to perform

masking. Tinnitus measures also generally are impor-

tant for individualized counseling purposes, especially

in treatments such as TRT (P. J. Jastreboff, 1995).

Psychoacoustic measures also are valuable in evaluat-

ing and verifying the patient’s subjective reports of

his/her tinnitus condition when the patent is involved

in legal action related to the tinnitus (Henry, 2004a).

Loudness and pitch. Tinnitus researchers have

attempted to unify methodology for the psychoacoustic

evaluation of tinnitus (Axelsson, Coles, Erlandsson,Meikle, & Vernon, 1993). This need was recognized as

early as 1903 (Spaulding, 1903). The advent of electro-

acoustic equipment made it technically feasible to use

pure tones to match tinnitus pitch and loudness (Jones

& Knudsen, 1928; Josephson, 1931; Wegel, 1931).

Edmund Fowler made important contributions to

tinnitus measurement in the 1930s and 1940s. He de-

scribed a method for measuring loudness recruitmentby balancing the loudness of sounds between ears,

which he termed the alternating binaural loudness

balance (ABLB; Fowler, 1936, 1937). Fowler later ap-

plied the ABLB technique as a test with patients to

balance the loudness of tinnitus in one ear with the

loudness of a tone in the contralateral ear (Fowler,

1938). The level of the comparison tone, expressed in

dB Sensation Level (SL), provided an indication ofthe tinnitus loudness as experienced by the patient.

Fowler (1940) stated that it was important to dupli-

cate, or match, the loudness and pitch of tinnitus to

contralateral tones. For pitch matching, he stressed

the importance of presenting stimuli at levels equal to

the tinnitus intensity. Fowler (1942, 1943) noted that

although patients described their tinnitus as very

loud, they usually matched the loudness to tones pre-sented at only 5–10 dB SL. Many subsequent studies

used Fowler’s same basic technique or variations of it

(Graham & Newby, 1962; Hazell et al., 1985; Kodama

& Kitahara, 1990; Penner, 1983b, 1986, 1988; Reed,

1960; Roeser & Price, 1980; Tyler, 1992; Tyler &

Conrad-Armes, 1983a, 1983b, 1984). Tinnitus loudness

matching has been observed to be a reliable measure

for most patients (J. A. Henry, Flick, Gilbert, Ellingson,& Fausti, 1999), but pitch matching yields highly var-

iable responses (J. A. Henry, Flick, Gilbert, Ellingson, &

Fausti, 2004; Penner & Bilger, 1995; Tyler & Conrad-

Armes, 1983b).

A protocol for loudness and pitch matching was

described in detail by Vernon and Meikle (1981). Theirprotocol involves three separate procedures that are

alternated systematically among threshold testing,

loudness matching, and pitch matching. The objectives

are to achieve a pitch match and a loudness match

at the pitch-match frequency. In general, the tinnitus

frequency is approached gradually by presenting suc-

cessive pairs of tones from which the patient selects

the tone that is ‘‘closest in pitch’’ to the tinnitus. Pa-tients often confuse pitch and loudness during testing;

thus, all tones used for pitch matching are presented

only at the levels previously matched to their tinnitus

loudness.

Loudness and pitch matching can be performed us-

ing a clinical audiometer as follows (J. A. Henry, 2004a).After a pure-tone audiogram has been obtained, the

examiner focuses on obtaining a pitch match and a

loudness match at the pitch-match frequency. Initial

loudness-matching tones should be presented at 10–20 dB

SL at frequencies where hearing sensitivity is essen-

tially normal and at 5–10 dB SL at frequencies where

there is hearing loss. The testing should be started at

1000 Hz. The patient is asked, ‘‘Is the pitch of yourtinnitus higher or lower than the pitch of the tone?’’

Most patients will indicate ‘‘higher,’’ and the next tone

is presented at 2000 Hz. The testing progresses in this

manner to bracket the tinnitus pitch to within an

octave. Interoctave frequencies are then tested the

same way to determine a pitch match to the closest

half octave. Patients often confuse octaves when pitch

matching (Graham & Newby, 1962; Vernon, Johnson,Schleuning, & Mitchell, 1980), so the examiner should

alternate presentation of the pitch-matched tone with

tones an octave higher and an octave lower to identify

the final pitch match. At the pitch-matched frequency,

a hearing threshold and tinnitus loudness match are

then obtained in 1-dB steps.

Matching to noise. The clinical data reported

earlier in the Attributes of Tinnitus in a Clinical

Population section reveal that the majority of tinnitus

clinic patients report that their tinnitus sounds ‘‘tonal’’

(Lockwood et al., 2003; Meikle et al., 2004). Although

most patients can match their tinnitus to a pure tone,

a closer match may be achieved when bands of noiseare varied systematically to obtain a noise match.

Limited noise matching can be done with an audio-

meter, and more precise noise-band matching can be

done with special equipment.

The noise-matching protocol performed using an

audiometer follows the pitch match. All stimuli used

Henry et al.: General Review of Tinnitus 1217

with noise matching should be presented at levels ap-

proximating the patient’s tinnitus loudness. The first

objective is to determine whether the tinnitus sounds

more like a pure tone or more like noise. Narrowband

noise, centered at the pitch-matched frequency, is pre-

sented in alternation with the pitch-matched tone, and

the patient is asked which sounds more like thetinnitus. If the tone is selected, then no further noise

matching is necessary because the tone is considered

the best match. If the noise is chosen, then it is nec-

essary to determine whether narrowband or broadband

noise sounds more like the tinnitus. Narrowband noise

is presented in alternation with white noise and the

patient again chooses the best match. A hearing thresh-

old and tinnitus loudness match are obtained in 1-dBsteps for the noise stimulus that is selected.

A more precise noise match is possible if properties

of the noise bands can be adjusted systematically to

widen or narrow the width of the band that provides

the best match. In addition, sweeping a band of noise

up and down the frequency range can add furtherprecision.

Tinnitus maskability. The minimum masking level

(MML) is the minimum level to which broadband noise

must be raised to render an individual’s tinnitus

inaudible. The MML is a common measurement made

in many tinnitus clinics and has been reported to be ameasure that correlates with treatment efficacy (P. J.

Jastreboff, Hazell, & Graham, 1994). That is, as

patients reported improvement with their tinnitus

problem, the MMLs were observed to decrease. Other-

wise, MMLs are not generally thought to contribute

any predictive information concerning treatment effi-

cacy, other than when tinnitus masking is used for

treatment. It has been reported for tinnitus maskingthat the decibel difference between the MML and the

tinnitus loudness match is generally predictive of the

effectiveness of treatment (Vernon, Griest, & Press,

1990; Vernon & Meikle, 2000). If the MML is less than

the loudness match, benefit is considered likely. If the

MML is greater than the loudness match, success is

less likely.

Clinical MML testing can be done using monaural

or binaural stimuli (J. A. Henry, 2004a). It is often dif-

ficult for patients when only monaural stimuli are pre-

sented because of difficulties determining when the

tinnitus becomes inaudible for only one side of the head.

Therefore, we recommend presenting binaural stimuli

for routine clinical testing. Broadband noise from the

audiometer is used and monaural hearing thresholds

are first obtained for the noise stimulus. The majority

of patients will be masked by noise within 10 dB SL

(Meikle et al., 2004), so it is appropriate to use 1-dB

step sizes to obtain thresholds and MMLs using

broadband noise. After obtaining thresholds, the noise

is set for binaural presentation at the threshold levels.

The noise is raised binaurally in 1-dB steps until the

patient reports that the tinnitus is inaudible. If during

testing the patient reports that the tinnitus has be-

come inaudible for one side, the noise is raised in only

the contralateral ear until the tinnitus is completely

inaudible.

Residual inhibition. Residual inhibition is the

temporary suppression or elimination of tinnitus that

is often observed following auditory stimulation (Vernon,

1982; Vernon & Meikle, 1988). Residual inhibition

was first reported by Spaulding (1903) and later by

Josephson (1931). The phenomenon was formally de-scribed by Feldmann (1971) and named ‘‘residual

inhibition’’ by Vernon and Schleuning (1978) in recog-

nition of Feldmann’s work. Residual inhibition, which

occurs with most patients who receive the appropriate

type of auditory stimulation (Meikle & Walsh, 1984;

Tyler, Babin, & Neibuhr, 1983; Vernon, 1981, 1988),

has received little investigation in terms of the specific

stimulus parameters that are responsible for activa-tion, or extension, of the effects for longer time periods.

Residual inhibition testing is performed in our

evaluation protocol immediately after MML testing

with the same broadband noise. The patient is

instructed to listen to the noise for 1 min and then to

report if there is any kind of change in the tinnitus.

The noise levels established for MML are raised 10 dB

and presentation of the noise lasts 60 s. If the patient

reports a reduction in tinnitus intensity, it is helpful to

ask if there is a 10%, 25%, 50%, 75%, or 90% reduction

of the usual loudness (J. A. Henry, 2004a). The patient

continues to report one of these percentages until the

tinnitus has recovered to its usual loudness (100%).

Attempts to standardize tinnitus psychoacousticassessment. The many attempts to quantify tinnitus

using psychoacoustic techniques have had sporadic

success, and these techniques currently have limited

clinical and research application. Formal efforts over

20 years ago promoted the establishment of stan-

dardized tinnitus evaluation procedures (Evered &

Lawrenson, 1981; McFadden, 1982; Vernon & Meikle,

1981). A tinnitus assessment battery was recom-mended that included pitch and loudness matching,

tinnitus maskability, and residual inhibition. Stan-

dardized procedures for these tests have still not been

universally adopted, partially because of the need for

specialized testing equipment. Such equipment used

to be available commercially (from Danavox, Starkey,

and Norwest companies), but these instruments have

been out of production for many years. Audio benchequipment (tone generators, attenuators, amplifiers,

filters, etc.) can be adapted to perform tinnitus matching,

1218 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

but the use of bench equipment is not realistic for the

typical clinic. Most audiologists who conduct tinnitus

evaluations use their audiometers in some manner to

obtain some or all of these measurements.

Work at the VA National Center for RehabilitativeAuditory Research (NCRAR) has addressed the need

for standardization of tinnitus psychoacoustic assess-

ment (J. A. Henry et al., 1999, 2000, 2004; J. A. Henry,

Flick, Gilbert, Ellingson, & Fausti, 2001; J. A. Henry &

Meikle, 1999). The techniques described to date use

laboratory equipment. Efforts are presently under way

to develop testing instrumentation for routine clinical

application.

Methods of TreatmentIn the Theorized Mechanisms of Pathophysiology

section, we considered a number of potential mecha-

nisms that may underlie the tinnitus condition. The

present lack of knowledge concerning these mecha-

nisms, however, precludes the establishment of dif-

ferential treatment techniques to address the causerather than just the symptom. Virtually all tinnitus

treatment techniques seek ultimately to reduce the

impact of tinnitus on a person’s life. In some cases, the

tinnitus sound itself can be reduced, but there is no

systematic method for accomplishing this in patients.

Accordingly, practitioners either attempt a trial-and-

error approach to find a treatment that works for the

patient or they use a generic treatment method that isintended to work for all forms of tinnitus.

Many treatment protocols have been proposed for

tinnitus management (reviewed in Vernon, 1998).

Most patients cannot be helped by medical or surgical

treatment, and, therefore, seek other forms of pro-

fessional intervention when the tinnitus becomes in-trusive. Primary methods of tinnitus treatment are

described below.

Hearing AidsThe use of hearing aids to treat tinnitus has long

been a mainstay of tinnitus treatment provided by

audiologists (Melin, Scott, Lindberg, & Lyttkens, 1987;

Saltzman & Ersner, 1947; Surr, Montgomery, &

Mueller, 1985). Even for patients who are marginal

hearing aid candidates, high-frequency amplification

(i.e., primary gain at 3 and 4 kHz) may be readily

accepted and beneficial. The majority of audiologists do

not possess specialized tinnitus expertise, but they areaware that hearing aids may have a beneficial effect

for some patients with tinnitus.

Surr et al. (1985) reported that 62% of 200 new

hearing aid users experienced tinnitus. Use of hearing

aids resulted in ‘‘partial or total’’ tinnitus relief for half

of those with tinnitus. In a follow-up study, Surr, Kolb,

Cord, and Garrus (1999) administered the Tinnitus

Handicap Inventory (THI; Newman et al., 1996) to new

hearing aid users before and 6 weeks after the hearing

aid fitting. A statistically significant reduction in the

mean TSI scores was seen at 6 weeks. These studiesare important in showing that hearing aids can, in

some cases, provide tinnitus relief as an independent

outcome, even when treatment is for a different

purpose.

Hearing aids are an important component of

tinnitus treatment with tinnitus masking and TRT(P. J. Jastreboff & Hazell, 1998; Vernon, 1988). For

these methods, hearing aids are usually incorporated

into a combination instrument (amplification and noise

generator combined), although regular hearing aids

are also used. The primary purpose of either the com-

bination instruments or the hearing aids is to treat the

tinnitus. Improvement in hearing is considered of sec-

ondary benefit of treatment with these devices. Hear-ing aids, therefore, can be fitted either for the primary

purpose of providing tinnitus relief or to offer tinnitus

relief as a secondary benefit.

It has been estimated that up to 90% of tinnitus

patients may benefit from amplification (Johnson,

1998; Schechter, Henry, Zaugg, & Fausti, 2002). Thebenefit may be due to reduced stress associated with

hearing loss, which often accompanies tinnitus, and/or

result from amplification of ambient sounds that tend

to mask the tinnitus or make it less noticeable. There

are different philosophies concerning the use of ampli-

fication for tinnitus patients; thus, there is no clear

agreement as to when a patient would benefit from

amplification. Some clinics have reported that only20% to 30% of their patients are fitted with amplifica-

tion (Gold, Gray, Hu, & Jastreboff, 1996; P. J. Jastreboff

et al., 1996). Wedel, Wedel, and Walger (1998) reported

that their clinic dispensed amplification to 60% of their

patients.

CounselingCounseling is an important component of every

form of tinnitus treatment (Hall & Ruth, 1999; Sweetow,

1986, 2000). Some methods are based entirely on

specific psychological techniques, whereas others use

counseling to augment another modality of treatment.There are a number of common counseling points

that are appropriate for all tinnitus patients, such as

(a) avoiding high-level noise exposure, (b) making life-

style changes that would be conducive to minimizing

tinnitus intensity (e.g., reducing stress, getting ade-

quate sleep, limiting intake of alcohol, caffeine, tobacco,

etc.), (c) maintaining a constant background of sound

Henry et al.: General Review of Tinnitus 1219

(avoiding silence) to reduce the prominence of tinnitus,

and (d) staying busy with meaningful activities to

distract attention away from the tinnitus.

Psychological TreatmentsVarious psychological treatments have been used

for tinnitus. Hypnosis has been observed to provide

some limited positive effects, but studies attempting to

document these effects were methodologically flawed

(J. L. Henry & Wilson, 2001). Biofeedback was advo-

cated for tinnitus treatment in the 1970s (Grosson,

1976; J. W. House, Miller, & House, 1977), and some

studies have shown its effectiveness, but methodolog-

ical problems were again an issue (J. L. Henry &

Wilson, 2001). Progressive muscular relaxation train-

ing has been used to help patients cope with the

tension and anxiety that result from tinnitus or to

relieve stress that can exacerbate tinnitus. The liter-

ature concerning relaxation training has produced

mixed results (J. L. Henry & Wilson, 2001).

In the 1980s, psychological researchers made a

paradigm shift in their approach to tinnitus treatment,

including a decreased emphasis on relaxation training

and biofeedback and an increased focus on cognitive

aspects of tinnitus (J. L. Henry & Wilson, 2001). This

shift was due to a number of factors: (a) Relaxation and

biofeedback were ineffective for many people, (b) greater

benefit was observed using cognitive–behavioral ther-

apy (Jakes, Hallam, Rachman, & Hinchcliffe, 1986),

and (c) numerous studies had demonstrated efficacy of

cognitive–behavioral therapy for psychological prob-

lems (especially depression and anxiety; J. L. Henry &

Wilson, 2001). Another influencing factor was the

observation that tinnitus had many similarities with

pain (A. R. Møller, 1987), and numerous studies had

demonstrated the efficacy of cognitive–behavioral ther-

apy for management of chronic pain. For all of these

reasons, cognitive–behavioral therapy as applied to

pain management was modified for use with tinnitus

patients (J. L. Henry & Wilson, 2001).

Cognitive–behavioral therapy is a type of coun-

seling that identifies negative behaviors, beliefs, and

reactions and assists the patient in substituting

appropriate and positive reactions (Sweetow, 2000).Cognitive–behavioral therapy is performed most com-

monly by psychologists. The method can, however, be

administered by hearing specialists, including audiol-

ogists, because of its many similarities with aural

rehabilitation (J. L. Henry & Wilson, 2001; Sweetow,

2000). Professionals who wish to learn this method

require general training in cognitive–behavioral tech-

niques, which they must adapt to the treatment oftinnitus. A book is available that describes in detail the

methodology to administer cognitive–behavioral ther-

apy to tinnitus patients (J. L. Henry & Wilson, 2001).

Hallam et al. (1984) were instrumental in estab-

lishing many parameters that are accepted today as

key issues in the psychological management of tinni-tus. At the time their seminal paper was written, no

controlled trials had been reported that involved

counseling or psychological or psychotherapeutic tech-

niques. They systematically reviewed evidence that

supported psychological variables as factors responsi-

ble for tinnitus becoming clinically problematic. In

addition, Hallam et al. proposed a model to describe

how habituation to tinnitus occurs as normal response.They suggested that certain conditions can delay

habituation. For example, chronic stress and anxiety

(‘‘tonic arousal’’) can ‘‘lower the threshold of emotional

responsiveness in general’’ (p. 45), which could exac-

erbate the annoyance caused by tinnitus.

J. L. Henry and Wilson (2001) reviewed the studiesthat have been conducted to evaluate the efficacy of

cognitive–behavioral therapy for tinnitus distress. They

concluded that these studies offer ‘‘considerable support’’

(J. L. Henry & Wilson, 2001, p. 247) for using this form

of treatment. They noted that best results are achieved

with at least eight sessions. They further noted that pure

cognitive therapy does not maximize therapeutic poten-

tial and that it should be combined with attention con-trol, imagery training, and relaxation methods.

Andersson and Lyttkens (1999) conducted a meta-

analysis of studies that have used psychological

approaches to treat tinnitus. The various forms of treat-

ment included cognitive–behavioral (n = 11), relaxationtraining (n = 4), education (n = 2), hypnosis (n = 2),

biofeedback (n = 2), and stress management (n = 3).

These 24 groups had been included in 18 published

studies. Criteria for studies to be included in this meta-

analysis included the following: written in English,

published in a scientific journal, and reported infor-

mation, including description of procedures, number of

participants, self-reported outcome measures, andinterpretable statistics. Outcome measures were clas-

sified into four groups: loudness, annoyance, negative

experiences (including depression and anxiety), and

sleep difficulties. Of these four, effects of treatment

were greatest on tinnitus annoyance. Effects on neg-

ative experiences were weaker than for annoyance.

Effects on sleep were weak. There was an immediate

effect on tinnitus loudness that was generally notsustained at follow-up evaluations.

Dobie (1999), in his review of randomized clinical

trials, offered a contrasting opinion regarding the vari-

ous treatments that he evaluated, including cognitive–

behavioral therapy. He concluded that, ‘‘No treatment

can yet be considered well established in terms of

1220 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

providing replicable long-term reduction of tinnitus

impact, in excess of placebo effects’’ (p. 1202). This re-

view was restricted to Medline-indexed articles and,

thus, did not include many other clinical studies pub-

lished in other journals, conference proceedings, and book

chapters. The standard, however, for research-based

evidence is for studies to be published in peer-reviewedjournals, and such studies were generally covered in

Dobie’s review.

Many studies have been conducted to evaluate

outcomes of various forms of psychological treatment,

especially cognitive–behavioral therapy. It would

appear that the evidence favors cognitive–behavioralover the other forms. It also appears that there have

been more controlled studies evaluating cognitive–

behavioral therapy than any other type of tinnitus

treatment. These types of studies are critical to make

informed decisions regarding evidence-based treat-

ment. However, some observations are relevant in

the spirit of leading toward more definitive outcome

research. It is well known that a certain number ofpatients will show improvement regardless of the type

of treatment they receive, provided there is the per-

ception on the part of the patient that expert treatment

is being provided (Isenberg, 1998). Roberts, Kewman,

Mercier, and Hovell (1993) concluded that, when both

patient and clinician believe strongly that a treatment

is efficacious, improvement occurs up to two thirds of

the time regardless of the treatment’s efficacy.

Because the nonspecific effects of therapy can be

powerful, studies of psychological forms of tinnitus

treatment must be interpreted with this consideration

in mind. In the meta-analysis conducted by Andersson

and Lyttkens (1999), most of the studies did not prop-

erly control for patient expectation effects. One possibleexception was a study in which patients were ran-

domized to receive intervention that involved either

education alone or education combined with cognitive–

behavioral therapy (J. L. Henry & Wilson, 1996). The

cognitive–behavioral group, after 6 weekly sessions,

showed improvements on some outcome scales that

were statistically greater than for the education group.

Measurement of outcomes at 12 months posttreatmentindicated, however, that the benefits of therapy had

dissipated.

Tinnitus is an auditory condition that can be thecause of numerous psychological problems. On the otherhand, some tinnitus patients have preexisting psycho-logical problems that can cause exaggerated reactions totinnitus. Psychologists are clearly well qualified toaddress these issues, even if they do not have anyparticular tinnitus expertise. Thus, psychological in-tervention in general can be helpful to many tinnituspatients.

Pharmacological ApproachesMany medications have been proposed to relieve

tinnitus. Antianxiety drugs, antipsychotics, sedatives,

antidepressants, antihistamines, anticonvulsants, and

even anesthetics have been reported to relieve tinnitus

for some people (Perry & Gantz, 2000). Some of the

medications that have been associated with tinnitus

treatment are discussed below.

Lidocaine. Lidocaine is a local anesthetic used fre-

quently by dentists. Intravenous (IV) administration of

lidocaine has been shown to abolish tinnitus in about 50%

of cases and to reduce it in many others (den Hartigh

et al., 1993; Hulshof & Vermeij, 1984; Israel, Connelly,

McTigue, Brummett, & Brown, 1982; Melding, Goodey,

& Thorne, 1978). IV administration of lidocaine is not

a practical treatment for tinnitus (because of its shorthalf-life and serious side effects), but its effectiveness

proved that tinnitus can be abolished temporarily in

some patients by a drug (Coles, 1998).

The effectiveness of lidocaine led to a search for an

oral analogue that provides the same effect on tinnitus

but without the side effects (Coles, 1998). The twomain groups of drugs that have been studied are the

antiarrythmic (e.g., tocainide) and anticonvulsant (e.g.,

carbamazapine) drugs. The antiarrythmic oral drugs

are closely related to lidocaine, but seven randomized

clinical trials failed to show replicable benefit against

tinnitus (Dobie, 1999). Carbamazapine (Tegretol;

Novartis Pharmaceuticals Corp.) failed to show benefit

in four randomized clinical trials.

Benzodiazepines. The benzodiazepines are a class of

drugs having anxiolytic, hypnotic, and anticonvulsant

properties (Dobie, 1999). Benzodiazepines that have been

studied for tinnitus relief include diazepam (Valium;

Hoffman-La Roche Inc.) and alprazolam (Xanax; PfizerInc.). Most controlled studies have shown no conclusive

benefit of any of these drugs (Lockwood et al., 2003).

Johnson, Brummett, and Schleuning (1993) demonstrated

that Xanax reduced tinnitus loudness in a controlled

study, but changes in life impact were not measured.

There are risks of dependence on the benzodiazepines

and more controlled studies are needed (Dobie, 1999).

Antidepressant drugs. Tricyclic antidepressants

and serotonin-specific reuptake inhibitors (SSRIs) are

the primary drugs that are used for treating major

depression (Dobie, 1999; Julien, 1995). These drugs,

such as the tricyclic amitriptyline (Elavil; Astra Zeneca)

and the SSRI fluoxetine (Prozac; Eli Lilly), also have

been used to treat tinnitus (Brummett, 1989; Dobie,Sakai, Sullivan, Katon, & Russo, 1993; J. W. House,

1989). Placebo-controlled studies have shown that the

antidepressants are effective at reducing depression,

but it is not clear whether they actually reduce the

Henry et al.: General Review of Tinnitus 1221

perception of tinnitus (Dobie & Sullivan, 1998). Tinni-

tus patients with sleep problems and/or major depres-

sion should be considered for antidepressant therapy

(Dobie, 1999).

Additional medications. A great many drugs have

been evaluated for their potential effectiveness in pro-

viding tinnitus relief. In addition to the drugs and classes

of drugs mentioned above, additional drugs that have

been studied include Cylandelate (vasodilator), Amylo-

barbitone (barbiturate), Baclofen (gamma-amino butyric

acid [GABA] agonist and muscle relaxant), Misoprostol(prostaglandin analog), Betahistine (histamine-like

drug), and Cinnarizine (antihistamine). Dobie (1999)

reviewed the randomized clinical trials that were con-

ducted to evaluate these different drugs. He determined

that none of them offered any definitive advantage over

placebo.

Psychiatric treatment. In the Psychological Treat-

ments section, we pointed out that psychological

intervention in general can be helpful to many tinnitus

patients, even if the psychologist is not a tinnitus

specialist. Similarly, many psychological and mood dis-

orders that are associated with tinnitus are treatable

through the use of medications by a psychiatrist.

Tinnitus MaskingEar-level masking devices produce broadband sound

that can reduce and, in some cases, eliminate the per-

ception of tinnitus (referred to, respectively, as partial

and complete masking; J. A. Henry, Schechter, Nagler,

& Fausti, 2002; Schechter & Henry, 2002; Vernon,1988). Tones and narrowband noise also can be used as

effective masking stimuli. Masking devices in combi-

nation with amplification have been recommended for

about 60% of the patients treated in a major tinnitus

clinic (Vernon & Meikle, 2000), and hearing aids alone

are sometimes sufficient to provide masking relief.

In addition to ear-level devices, augmentative

sound is often recommended for sleeping or relaxing

through the use of various styles of tabletop instru-

ments (e.g., sound effects generated by water foun-

tains, radios, CDs, etc.; J. A. Henry, Schechter, et al.,

2002; Schechter & Henry, 2002). An additional strat-

egy is the use of masking noise for some patients who

can reduce their tinnitus loudness through prolonga-tion of residual inhibition (Vernon & Meikle, 2000).

The efficacy of tinnitus masking is difficult to assess

when reviewing the literature. Some studies report only

outcomes of treatment for those patients who purchase

and use ear-level devices. These studies ignore those

patients who do not purchase and use devices, includingthose who (a) do not receive a recommendation for trial

use of devices; (b) receive a recommendation, but do not

purchase devices; and (c) purchase, but return their

devices. Furthermore, most of the studies that have

reported outcomes of treatment with tinnitus masking

are retrospective analyses of clinical data. Not surpris-

ingly, results have been generally positive. Controlled

studies (Erlandsson, Ringdahl, Hutchins, & Carlsson,

1987; Stephens & Corcoran, 1985) have not duplicatedthe effectiveness reported in the retrospective studies.

For example, Stephens and Corcoran (1985) found no

difference in benefit between patients treated by a

masker and those treated by counseling. However, our

controlled clinical trial indicated tinnitus masking is

an effective method for treating chronic tinnitus (J. A.

Henry, 2004a; J. A. Henry, Schechter, et al., 2004).

Tinnitus Retraining Therapy (TRT)TRT combines low-level, steady background sound

with a structured program of directive counseling

(J. A. Henry, Schechter, et al., 2002; P. J. Jastreboff,

et al., 1996). A patient’s emotional reactions to tinni-

tus is thought to be caused by beliefs, threats, and fearsthat are inappropriately ascribed to the tinnitus. The

counseling addresses these inappropriate reactions and

emotions as the necessary first step to achieve tinnitus

habituation (i.e., the gradual reduction or elimination of

the annoyance and the conscious perception of tinnitus

that is the primary goal of treatment with TRT). The

other component of TRT for achieving habituation is

sound therapy, which is the use of continuous back-ground sound throughout the day. A primary purpose

of the sound is to reduce the contrast between the low-

level acoustic background and the tinnitus. Sound

therapy is accomplished best using ear-level sound gen-

erators for patients who do not require amplification

(P. J. Jastreboff & Jastreboff, 2001). Hearing aids or

combination devices (amplification in a combination

unit with a sound generator) are used with TRT whenhearing loss is a problem. Open-ear fittings are recom-

mended to facilitate maximal entry of low-frequency

environmental sound into the ear canal (P. J. Jastreboff

& Jastreboff, 2000). If an open-ear configuration is not

available, then the largest possible vent should be used.

Treatment with TRT usually requires 1 to 2 years to

achieve the desired result.

A number of clinics have reported results of treat-

ment with TRT, both prospectively and retrospectively

(reviewed in J. A. Henry, Schechter, et al., 2002). These

studies report success rates between 70% and 85%.

Although these results may appear impressive, there

are as yet no properly controlled clinical studies of TRTefficacy reported in the peer-reviewed literature. A

prospective, controlled clinical study was recently com-

pleted at the Portland VA Medical Center. The study

1222 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

compared the relative efficacies of TRT and the tinnitus-

masking approach. Results of that study have thus far

been only briefly summarized (Henry, 2004b; Henry,

Schechter, et al., 2004). However, the results of this con-

trolled trial were comparable with previous clinical re-

ports of TRT efficacy.

Although TRT has become a relatively well-known

method of treating tinnitus, it has not been immune to

censure. Of note, the Development and Evaluation

Service of the Wessex Institute (Wessex Institute for

Health Research and Development, 1998) concluded that

there is no evidence substantiating the effectiveness of

TRT. Critics of TRT have reported a number of methodo-logical shortcomings that include lack of standardized

assessment measures (J. L. Henry & Wilson, 2001;

Lockwood et al., 2003). Wilson, Henry, Andersson,

Hallam, and Lindberg (1998) were critical of the directive

counseling protocol, stating that an education approach

to counseling patients is ‘‘nothing new’’ (p. 276) and that

this type of approach was recommended many times

prior to 1990. An additional criticism is that the onlyway to receive formal TRT training is to attend expen-

sive instructional courses conducted by a few specialists

who have pioneered and promoted the successes of the

treatment.

Electrical StimulationElectrical stimulation for suppression of tinnitus

has been researched for many years (Dauman, 2000).

Hatton, Erulkar, and Rosenberg (1960) reported unex-

pected tinnitus suppression in patients when perfor-

ming routine galvanic stimulation tests for vestibular

function. They tested this finding in a group of 33

tinnitus patients by applying direct current (DC) to

various locations on the head. In 45% of these patients,the tinnitus intensity was decreased in response to the

DC treatment. Chouard, Meyer, and Maridat (1981) used

transcutaneous electrical neural stimulation (TENS),

similar to the TENS portable unit used for treating

intractable pain. In a study of 53 participants, 47%

reported some relief. None of these patients reported

complete suppression, and tinnitus returned after a

period of days or weeks.

Commercial electrical tinnitus-suppression devices

were developed but are no longer available. Morgon,

Dubreuil, Disant, and Chanal (1984) used the Tinitop

(Audiologie-Recherche-Applications; which produces a

pulsed electrical sine wave) along with a 144-Hz acoustic

stimulus to treat 50 patients who complained of ‘‘intense,continuous tinnitus.’’ Treatments were administered

during six 45-min sessions repeated every 10 days.

Twenty-seven (54%) of these patients reported complete

or partial, although temporary, relief. A number of stud-

ies were conducted with another tinnitus-suppression

device, the Audimax Theraband (Audimax Corp.). This

wearable device uses a headband to hold electrodes,

which deliver low-level alternating current (AC), against

each mastoid. The best controlled of the Theraband stud-

ies showed some limited therapeutic benefit (Dobie,

Hoberg, & Rees, 1986). Other studies also indicatedsome limited effectiveness, although placebo effects could

have influenced the results (Dauman, 2000).

The many studies that have used electricity to

stimulate the auditory system for tinnitus relief

indicate that this is a promising area of investigation

(Dauman, 2000; Rubinstein & Tyler, 2004). However,the underlying mechanisms and most effective param-

eters of the stimuli have yet to be determined. The

general conclusion is that DC is the most effective type

of current, but DC causes tissue damage (Aran, 1983;

Dobie et al., 1986; Hazell, Meerton, & Ryan, 1989;

Staller, 1998). AC does not cause tissue damage, but is

only effective for a limited number of patients. Elec-

trical stimulation, therefore, is still considered anexperimental treatment and has not been demon-

strated as useful for common clinical practice.

Cochlear implants. Cochlear implants were reported

early on to produce tinnitus suppression in nearly 80%

of implanted patients (W. F. House, 1976). This benefit

may arise from masking by ambient sounds that arenewly perceived (Vernon, 2000) or from electrical stim-

ulation of the auditory nerve (Dauman, 2000). Other

studies have demonstrated that cochlear implants can

provide tinnitus relief in 53% to 83% of patients (Berliner,

Cunningham, House, & House, 1987; Hazell et al., 1989;

McKerrow, Schreiner, Snyder, Merzenich, & Toner, 1991).

Cochlear implants are a viable tinnitus treatment option

for individuals who are profoundly deaf with severeintractable tinnitus.

TMJ TreatmentTinnitus can be a symptom of a TMJ dysfunction.

In such cases, dental treatment or bite realignment

can help relieve TMJ pain and associated tinnitus

(Morgan, 1996). This management strategy would be

expected to be successful only in a very small percent-

age of appropriately selected tinnitus patients.

Complementary and AlternativeTreatments

A variety of nutritional supplements have been

advocated to treat tinnitus, including minerals such as

magnesium or zinc, herbal preparations such as ginkgo

biloba, homeopathic remedies, and B vitamins (Seidman

& Babu, 2003). Other complementary and alternative

Henry et al.: General Review of Tinnitus 1223

treatments include acupuncture (Park, White, & Ernst,

2000), ear-canal magnets (Coles, Bradley, Donaldson, &

Dingle, 1991), hyperbaric oxygen therapy (Kau, Sendtner-

Gress, Ganzer, & Arnold, 1997), ultrasound (Rendell,

Carrick, Fielder, Callaghan, & Thomas, 1987), and low-

power laser (Nakashima et al., 2002). Some of these

therapies have been studied to verify anecdotal claims,but there is no convincing scientific evidence that these

remedies are effective (Dobie, 2004a). Reviews of comple-

mentary and alternative methods of tinnitus treatment

can be found in Dobie (1999, 2004a) and Seidman and

Babu (2003). We briefly discuss here some of the more

popular methods that continue to receive attention.

Ginkgo biloba. Much has been written about

ginkgo biloba as a potential remedy for tinnitus. It is

important to be aware of the literature about this herb

because numerous commercial ‘‘tinnitus products’’

contain ginkgo in combination with other herbs and

minerals. Patients often ask about these commercial

formulas, or about the use of ginkgo alone. Ernst and

Stevinson (1999) reviewed five randomized controlledtrials that assessed the efficacy of ginkgo for treating

tinnitus. They concluded that all of these trials were

methodologically flawed, although the three best con-

trolled studies reported beneficial effects with ginkgo.

Holstein (2001) reviewed 19 clinical trials that had used

the standardized ginkgo extract EGb 761 (Tebonin).

Eight of these trials were controlled (five of them

randomized and double blinded). Holstein concludedthat these studies indicated that ginkgo is generally

effective in the treatment of tinnitus regardless of

its origin or duration. Drew and Davies (2001) con-

ducted a double-blind, randomized, placebo-controlled

study with 1,121 participants. The entire study was

conducted by mail and by telephone, and effects of

tinnitus were assessed through the use of question-

naires. The authors concluded that ginkgo providedno more benefit than placebo. Most recently, Hilton

and Stuart (2004) conducted a multiple-database

search of randomized, controlled trials of ginkgo used

for adults complaining of tinnitus. They evaluated

rigorously the methodological quality of more than

100 studies and determined that most trials were

poorly controlled. They concluded that there is no evi-

dence that ginkgo is effective for the primary com-plaint of tinnitus.

In reviewing the numerous studies of ginkgo and

tinnitus, few of these studies were properly controlled.

Moreover, methodological variances between those

studies that were well controlled prevent any definitive

conclusions. However, because there are a number ofreported positive outcomes, there may be potential for

ginkgo to be an effective treatment for some patients.

Patient factors that might be predictive of benefit need

to be identified and verified through research. It thus

seems worthwhile to conduct properly controlled trials

of ginkgo using treatment regimens that would opti-

mize the possibility of achieving successful outcomes.

Zinc. The trace element zinc, which is mentioned

often as a tinnitus treatment, is used commonly in com-mercial tinnitus formulas. Paaske, Pedersen, Kjems,

and Sam (1991) performed a placebo-controlled, random-

ized, double-blind investigation of zinc in 48 patients.

Only 1 of these patients had a reduced level of serum zinc.

Their study did not result in any beneficial effect from

zinc on tinnitus. They suggested a possible reason for this

negative finding was that their patients had serum zinc

levels in the normal range at the start of treatment. Ochiet al. (1997) reported reduced serum levels of zinc in

tinnitus patients relative to controls. The tinnitus

patients were reported to have a significant reduction

on a subjective tinnitus scale when treated with a regi-

men of zinc. Yetiser et al. (2002) did not find reduced zinc

levels in a group of 40 tinnitus patients and reported that

zinc therapy was effective only for some patients. Arda,

Tuncel, Akdogan, and Ozluoglu (2003) conducteda randomized, placebo-controlled study in 41 tinnitus

patients. Those patients who received zinc showed a

significant reduction in subjective tinnitus severity,

whereas those receiving placebo did not. The authors

reported that 31% of their patients had low zinc levels

but that tinnitus improvement was not limited to these

patients. These studies indicate that zinc is effective for

some patients, but it cannot be stated that zinc is gener-ally helpful for most patients.

Acupuncture. Acupuncture is a method that can

be effective in controlling pain. Tinnitus and pain are

often theorized to share a common mechanism. Accord-

ingly, acupuncture has been studied for its effects on

tinnitus. Park et al. (2000) reviewed six randomized,controlled trials, of which four were blinded. Method-

ology and outcome measurements varied between

studies. Although the two unblinded studies showed

a positive result, the four blinded studies showed no

significant improvement with acupuncture.

Efficacy of Treatments for TinnitusDobie’s (1999) review of 69 randomized, clinical

trials included many drug studies as well as nondrug

treatments that included psychotherapy (cognitive–

behavioral therapy), electrical stimulation, magnetic

stimulation, ultrasound, biofeedback, acupuncture,

and hypnosis. Dobie updated his review to include

randomized, clinical trials that had been conductedbetween 1998 and 2003 (Dobie, 2002, 2004a). Although

he noted some promising treatments, he emphasized

the difficulty in performing these studies to control for

nonspecific (placebo) effects.

1224 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

Nonspecific effects that are due to patient expec-

tations could be the reason that most tinnitus treat-

ment efficacy studies have shown good success rates

(Axelsson, 1998; Dobie, 2004a; Tyler, Haskell, Preece,

& Bergan, 2001). To conduct such studies properly,

there should be rigorous design standards concern-

ing the following: qualifications for study inclusion, theuse of validated outcome measures, and randomi-

zation into treatment groups, including a no-treatment

(i.e., waiting list) group (Dobie, 2004a). It is critical to

include a nonspecific control group that addresses the

concern that a patient’s tinnitus condition might im-

prove simply as a function of the amount of profes-

sional attention received (Isenberg, 1998; Roberts

et al., 1993). This attention effect could be controlledfor by providing equal clinician attention but in a

nonspecific fashion (Streiner & Norman, 1998). A well-

controlled study, mentioned above, involved tinnitus

intervention either with education alone or with edu-

cation combined with cognitive–behavioral therapy

(J. L. Henry & Wilson, 1996). Although patients in

both groups received the same duration of interven-

tion, the cognitive–behavioral group received boththe education and the cognitive–behavioral training.

The authors noted, ‘‘The material was provided at a

slower pace in the education-only program’’ (p. 11).

Thus, the cognitive–behavioral group received greater

intensity of clinician interaction that could have

confounded the outcome measurements. This greater

intensity involved instruction regarding various cogni-

tive and behavioral modifications designed to improvecoping skills. The education-only group received purely

didactic information devoid of instruction concern-

ing potential strategies for making their tinnitus less

bothersome.

A cursory review of the tinnitus literature would

suggest that many diverse methodologies are effective inthe treatment of tinnitus (Axelsson, 1998). A closer look

at these studies reveals that very few of them were well

controlled, thus ‘‘The state of our therapeutic knowledge

is still quite primitive’’ (Dobie, 2004a, p. 270). Future

studies should be randomized, controlled trials that

adhere to rigorous experimental methods. Research that

follows the recommendations outlined by Dobie (2004a)

and Isenberg (1998) would produce outcome data thatare valid, comparable, and clinically useful.

DiscussionThis article reviews what amounts to an extensive

literature relating to tinnitus. Two dominant points

define the field: (a) There is increasing interest in thephenomenon of tinnitus, both in terms of understanding

its underlying mechanisms and in the development of

management techniques; and (b) many inconsistencies

exist regarding definitions and terminology, outcome

measures, methods of assessment, and approaches to

treatment. These two points emphasize the need for

professionals to work together to bring uniformity to

this field.

There have been numerous attempts to unify the

tinnitus profession to standardize techniques for eval-

uation and treatment (Evered & Lawrenson, 1981;

McFadden, 1982; Meikle & Griest, 2002; Vernon &

Fenwick, 1984). Clearly, however, clinicians and sci-

entists have not formed any common union to achieve

consensus regarding needed standardization. There

are several different schools of thought for tinnitus

treatment, each advocating their own brand of ther-

apy, which ultimately leaves the tinnitus patient

unable to make well-informed decisions regarding the

best course of treatment.

There are four areas that must be addressed to

achieve standardization within the field: (a) establish-

ing clinical methodology (procedures for screening,

assessment, outcome measures, and intervention), (b)

obtaining research evidence to support clinical method-

ology, (c) developing training for professionals (gradu-

ate programs, seminars, online courses, textbooks, etc.),

and (d) developing patient education (various media to

provide educational resources). Some suggestions are

mentioned briefly below to address these four areas.

Clinical MethodologyIt bears repeating that tinnitus is a clinically

significant condition for only about 20% of individuals

who experience permanent tinnitus (Davis & Refaie,

2000; P. J. Jastreboff & Hazell, 1998). It is therefore

important to be able to establish whether clinical

intervention is necessary and, if so, how much inter-

vention is required. This would require, first, an efficient

and effective method of screening to determine if the

patient is in need of clinical services. We have developed

the Tinnitus-Impact Screening Interview (TISI) for this

purpose (Henry, Schechter, et al., 2004). The TISI con-

sists of six interview questions and has worked well to

rapidly assess the potential need for services. In the pro-

cess of administering the TISI, many of the individual’s

questions are answered, which often provides sufficient

information for the individual to be satisfied that nothing

further is required.

Delivering clinical services in the most expeditious

manner would require a progressive intervention ap-

proach (Henry, Schechter, et al., 2004). That is, patients

should receive only as much treatment as necessary to

meet their need. The lowest tier of intervention would be

written information, or possibly a tinnitus educational

Henry et al.: General Review of Tinnitus 1225

video. The next tier might be some kind of structured

group educational session(s). If additional help was

still needed, a clinical assessment would be performed

along with some basic counseling. The assessment and

minimal counseling would either suffice for meeting the

patient’s need or would suggest the need for com-

prehensive, long-term intervention (the highest levelof service).

Research EvidenceThe delivery of health care services should be

based on research evidence (Darby, 1998; Feussner,

1998; Meikle & Griest, 2002). This is not generally the

case for tinnitus for which there are many treatmentsbut little supportive research. Properly controlled

clinical trials need to be conducted. These trials should

use a common set of guidelines to assess outcomes of

treatment (Dobie, 2004a; Isenberg, 1998). There is the

important need to conduct well-designed, large-scale

epidemiology studies to define the problem of tinnitus

and to identify factors that cause tinnitus to become

problematic for some people. Mechanisms of tinnitusare being studied, and these efforts are essential to

ultimately develop cures for tinnitus.

Professional TrainingBecause hearing-health specialists do not normally

receive training in the management of tinnitus, meth-

ods of training need to be developed that will work forbusy professionals. All professionals who are at the

point-of-contact for tinnitus patients should be aware

that tinnitus is a preventable and treatable problem.

They need to know that telling the patient that ‘‘nothing

can be done—learn to live with it’’ dispenses erroneous

information that can exacerbate the problem. A rudi-

mentary level of professional training would thus

involve only a brief informational sheet that wouldcontain information about tinnitus: Why it occurs, how

it affects patients, and methods of treatment. Profes-

sionals should be provided with brochures that can be

given to their tinnitus patients. These brochures should

contain basic information about tinnitus and should

list resources to obtain further information. Brochures

of this kind can now be obtained from the American

Tinnitus Association.

Professional training of clinicians to manage tin-

nitus patients is generally lacking. Various levels and

formats of training should be developed to appeal to

different levels of interest among clinicians. These

formats may range from a brief training booklet or a

short website training course to continuing educationand seminars that provide step-by-step training in-

structions. Most important, audiology students and

otolaryngologists should have training as part of their

formal educational program, which would obviate these

types of postcurricular programs for these professions.

Patient EducationAny individual who experiences tinnitus should

have readily available accurate, up-to-date, comprehen-

sive information about tinnitus. Most important, the

individual needs to know that help is available. The

American Tinnitus Association hosts a comprehensivewebsite (www.ata.org) containing information about

tinnitus and a list of clinical resources. Tinnitus suffer-

ers can greatly benefit from the information provided in

this website. What they cannot learn, however, is where

they can receive ‘‘standard treatment’’ for tinnitus.

Standard practice for tinnitus is not yet a reality, and its

development will require a professional organization of

tinnitus researchers and clinicians, with a leader-ship body that works together to establish standards

and guidelines for the field.

SummaryThis article provides an overview of the state of

knowledge in the field of tinnitus. Tinnitus may be

caused by a somatic disorder, or it may have a neuro-

physiological (sensorineural) origin. Whereas tinnitus

of somatic etiology is often correctable through surgery,

sensorineural tinnitus can generally only be managed.Fortunately, of the approximately 10% to 15% of the

population who experience tinnitus, about 80% do not

require clinical intervention. All individuals with tinni-

tus, however, want their tinnitus sound ‘‘silenced.’’

Many research studies are under way in the attempt

to achieve this goal. Ultimately, mechanisms-based

research offers the greatest hope for completely and

safely silencing tinnitus. In the meantime, numerousmethods exist for the treatment of tinnitus. Although

research evidence is scant, some of these methods can be

effective for the majority of patients when the protocols

are performed properly. Future efforts will undoubtedly

unify the field of tinnitus professionals and lead to a

consensual and evidence-based standard of practice for

the clinical management of tinnitus.

Acknowledgments

We acknowledge support from the Veterans Health

Administration and Veterans Affairs Rehabilitation Research

and Development Service (Grants C2300R, C2887-R, and

RCTR 597-0160) and support from the National Center for

Rehabilitative Auditory Research, Stephen Fausti, director.

1226 Journal of Speech, Language, and Hearing Research � Vol. 48 � 1204–1235 � October 2005

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Received May 11, 2004

Accepted January 5, 2005

DOI: 10.1044/1092-4388(2005/084)

Contact author: James A. Henry, VA Medical Center(NCRAR), P.O. Box 1034, Portland, OR 97207.E-mail: james.henry@med.va.gov

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