Definitions and Background

Tinnitus is a surprisingly complex subject. Numerous books would be required to adequately cover the 

current body of knowledge. The present hand­book 

focuses on describing procedures for providing 

clinical services for tinnitus using the methodology 

of progressive tinnitus management (PTM).

In this opening chapter we establish common 

ground with respect to terminology and contextual 

information. Relevant definitions are provided, many 

of which are operational due to lack of consensus 

in the field. Additional background information 

includes brief descriptions of epidemiologic data, 

patient data, and conditions related to reduced tolerance (hypersensitivity) to sound.

Basic Concepts and Terminology

Tinnitus is the experience of perceiving sound that 

is not produced by a source outside of the body. The 

“phantom” auditory perception is generated somewhere in the auditory pathways or in the head or 

neck. Tinnitus often is referred to as “ringing in the 

ears.” And, in fact, the word “tinnitus” is derived 

from the Latin word tinniere, which means “to 

ring.” Patients report many different sounds—not 

just ringing—when describing the sound of their 

tinnitus, as we discuss later in this chapter.

Transient Ear Noise

It seems that almost everyone experiences “transient ear noise,” which typically is described as a 

sudden whistling sound accompanied by the perception of hearing loss (Kiang, Moxon, & Levine, 

1970). No systematic studies have been published 

to date describing the prevalence and properties 

of transient ear noise; thus, anything known about 

this phenomenon is anecdotal.

The transient auditory event is unilateral and 

seems to occur completely at random without anything precipitating the sudden onset of symptoms. 

Often the ear feels blocked during the episode. The 

symptoms generally dissipate within a period of 

about a minute. Although transient ear noise has 

been described as “brief spontaneous tinnitus” 

1
	 Progressive Tinnitus Management: Clinical Handbook for Audiologists

(Dobie, 2004b), any reference to tinnitus in this book 

does not include this auditory phenomenon.

Chronic Tinnitus

Patients often confuse transient ear noise with 

chronic tinnitus. What differentiates the two? It has 

been suggested that tinnitus is ear noise that lasts 

at least five minutes (Coles, 1984; A. C. Davis, 1995; 

Hazell, 1995). Dauman and Tyler (1992) suggested 

that the noise must last at least five minutes and

occur at least two times per week. These are reasonable criteria to define tinnitus, but superfluous 

for the typical patient who experiences tinnitus all 

or most of the time. Nonetheless, a distinction must 

be made between transient ear noise and chronic 

tinnitus, and Dauman and Tyler’s criteria are sufficient for this purpose.

Origin of Tinnitus: Somatic Versus 

Neurophysiologic

By definition, the perception of tinnitus results from 

activity in the auditory nervous system. The neural 

activity that is perceived as tinnitus can be referred 

to as a “tinnitus neural signal.” As for most sounds 

that activate the auditory system, at any point in 

time the tinnitus neural signal may or may not be 

part of the conscious experience. Whenever tinnitus is consciously perceived, the tinnitus neural 

signal is undergoing active processing by the auditory cortex (J. A. Henry, Trune, Robb, & Jastreboff, 

2007a). Although the final destination of the tinnitus neural signal always is the auditory cortex, 

the origin of tinnitus can be from either outside or 

within the auditory nervous system (referred to as 

somatic and neurophysiologic tinnitus, respectively) 

(Hazell, 1998a).

If the tinnitus has a somatic origin, it can be 

referred to as somatic tinnitus or somatosound(s). If 

the tinnitus has a neurophysiologic origin, it can 

be referred to as neurophysiologic tinnitus or sensorineural tinnitus. The word tinnitus generally refers 

to neurophysiologic tinnitus because this is the 

condition that is experienced by the great majority 

of patients.

Somatic Tinnitus (Somatosound)

Somatic tinnitus (somatosound) has an origin that 

usually is vascular, muscular, skeletal, respiratory, 

or located in the temporomandibular joint (TMJ) 

(J. A. Henry, Dennis, & Schechter, 2005). These “body 

sounds” thus have an internal acoustic source 

(Dobie, 2004b). Theoretically, the acoustic signal 

associated with any somatosound could be detected 

and characterized if the proper sensing equipment 

were available for this purpose.

Somatosound—Pulsatile Tinnitus

The most common type of somatosound is pulsatile

tinnitus (Lockwood, Burkard, & Salvi, 2004). Also 

referred to as venous hum or vascular noise, pulsatile tinnitus pulses in synchrony with the heartbeat 

(Sismanis, 2003). There are many potential sites 

for pulsatile tinnitus, which often can be identified by an experienced physician (Lockwood et al., 

2004; Sismanis, 1998; Wackym & Friedland, 2004). 

It is essential that these patients receive a medical 

examination as pulsatile tinnitus might indicate a 

more serious medical problem (such as intracranial 

and carotid artery abnormalities) (Hazell, 1990; 

Sismanis, 2007). The condition is treatable in some 

patients (Sismanis, 1998).

Nonpulsatile Somatosounds

Somatosounds also can be nonpulsatile, meaning that 

they have a nonvascular source (typically muscular, 

respiratory, or TMJ). Examples of nonvascular conditions that can cause somatosounds are muscular 

flutters or spasms and patulous eustachian tube.

Symptoms of Somatosounds

When evaluating a patient who complains of tinnitus, 

it is essential to determine if the symptoms suggest 

a somatic origin. If so, then the possibility exists that 

the tinnitus is amenable to medical management. 

Information about diagnosing somatic tinnitus is 

available in several publications (Hazell, 1990; Levine, 

2004; Perry & Gantz, 2000; Schwaber, 2003; Wackym & Friedland, 2004). (Please see Chapters 4 and 

5 for further information about somatosounds.)
Definitions and Background	 

Somatosounds Require Medical Evaluation

The presence of somatosounds always indicates the 

need for medical evaluation. The physician (usually an otolaryngologist or otologist) should have 

expertise in the diagnosis and treatment of somatic 

tinnitus. If the physician cannot resolve the problem with medical or surgical intervention, then the 

audiologist should provide appropriate clinical 

services, as described in later chapters.

Neurophysiologic (Sensorineural) 

Tinnitus

By far the majority of patients who complain of 

tinnitus have neurophysiologic (or sensorineural) tinnitus, that is, tinnitus that originates somewhere 

within the auditory nervous system. Although there 

is no known cure for neurophysiologic tinnitus, 

patients can learn to manage their reactions to tinnitus, thereby improving quality of life.

Origin of Neurophysiologic Tinnitus

All we can know for certain about the origin of 

a patient’s sensorineural tinnitus is that it is generated somewhere within the auditory nervous 

system. The cochlea seems a likely site because 

damage to the cochlea from noise exposure and 

other factors often results in tinnitus. However, 

some desperate patients have undergone surgical 

severing of cranial nerve VIII, which extends from 

the cochlea to the brain, although it did not stop 

their tinnitus (Fisch, 1970; House & Brackmann, 

1981; Pulec, 1984). This finding indicated that tinnitus can be generated centrally. Evidence is accumulating that supports the central generation of 

tinnitus (Møller, 2003). Cacace (2003) proposed that 

central networks of auditory system neurons may 

be involved in generating and sustaining tinnitus, 

which would explain the persistence of tinnitus following auditory nerve transection.

Understanding the pathophysiology of sensorineural tinnitus is a goal that is being pursued by 

an ever increasing number of researchers. Many 

theories have been proposed regarding tinnitus 

etiology, but are beyond the scope of this clinically oriented book. The interested reader has a 

choice of myriad publications written on this topic 

(e.g., Bauer, 2004; Eggermont & Roberts, 2004; P. 

J. Jastreboff, 1990; Kaltenbach, Zhang, & Finlayson, 2005; Kaltenbach, Zhang, & Zacharek, 2004; 

Nuttall, Meikle, & Trune, 2004; Vernon & Møller, 

1995).

Neurophysiologic Tinnitus Is a Phantom 

Auditory Perception

Phantom sensations such as phantom pain and 

phantom limb have characteristics that are analogous to those of tinnitus (P. J. Jastreboff, 1990, 

1995; Meikle, 1995; Møller, 2003). Tinnitus thus has 

been referred to as a phantom auditory perception 

(P. J. Jastreboff, 1990). Pain and tinnitus are similar 

with respect to their physiology, assessment, and 

treatment (Møller, 1987, 2000). These analogous 

conditions also may have similar neuropathic generating mechanisms. Because of these similarities, 

strategies of pain management can offer valuable 

clues to the management of tinnitus. In fact, the 

method of psychotherapy, cognitive-behavioral 

therapy (CBT), has been shown to be effective in 

treating chronic pain (P. H. Wilson, J. L. Henry, & 

Nicholas, 1993). The success of CBT for the treatment of pain led to the development of CBT for 

tinnitus (J. L. Henry & P. H. Wilson, 2001).

Subjective Versus Objective Tinnitus

Objective Tinnitus

By definition, objective tinnitus is tinnitus that is 

audible to the examiner (Dobie, 2004b). Objective 

tinnitus is relatively rare and always is a somatosound with an internal acoustic source (which as 

already discussed indicates an underlying condition requiring a medical evaluation by an otolaryngologist or otologist). Not all somatosounds 

are detectable by the examiner, and thus not all 

somatosounds would meet the definition of objective tinnitus. As a somatosound is an acoustically 

generated signal, the signal should be detectable 

with proper measurement techniques.
	 Progressive Tinnitus Management: Clinical Handbook for Audiologists

Subjective Tinnitus

Subjective tinnitus is perceived only by the patient. 

Any description of subjective tinnitus comes only 

from the patient, as there are no means to directly 

measure the intensity or other characteristics of the 

tinnitus. Tinnitus matching is performed to indirectly 

measure subjective tinnitus, (J. A. Henry, 2004; J. 

A. Henry, Zaugg, & Schechter, 2005a). For the 

remainder of this book, the word tinnitus generally 

refers to subjective tinnitus, that is, to neurophysiologic or sensorineural tinnitus that does not have 

an internal acoustic source. When patients have 

somatosounds, behavioral methods can be applied 

to manage reactions to these sounds if medical 

management does not resolve the symptoms.

Auditory Imagery, Auditory 

Hallucinations, and Musical Hallucinations

Auditory imagery, auditory hallucinations, and 

musical hallucinations are different forms of phantom auditory perceptions. There often is confusion 

about how these different auditory perceptions differ from tinnitus.

Auditory Imagery

Auditory imagery is a normal phenomenon that 

occurs for all people. It generally refers to the imagination of sound, such as repeating a phone number in 

one’s head, or recalling a musical passage (Kraemer, 

Macrae, Green, & Kelley, 2005; Seal, Aleman, & 

McGuire, 2004). “Auditory imaginations” can be under 

conscious control, but they also can occur outside of 

conscious control. When not under conscious control, auditory imaginations can be mildly distressing, 

as when you have a song “stuck in your head.”

Auditory Hallucinations

Auditory hallucinations have been estimated to occur 

in 10 to 15% of the general population (Nicolson, 

Mayberg, Pennell, & Nemeroff, 2006; Sommer et al., 

2008). Perhaps surprisingly, of those who experience auditory hallucinations, most do not have a 

psychotic disorder. In the nonpsychiatric population, auditory hallucinations have been described 

inconjunction with various diseases, injury, trauma, 

bereavement, sensory deprivation, religious experiences, near-death experiences, and drugs (Nicolson et al., 2006). Auditory hallucinations also may 

have nothing to do with the ability to hear, as 

people born profoundly deaf can experience them 

(du Feu & McKenna, 1999; Schonauer, Achtergarde, 

Gotthardt, & Folkerts, 1998).

Auditory hallucinations occur in 70 to 80% 

of patients with schizophrenia (Hugdahl et al., 

2008). Auditory hallucinations normally ascribed 

to psychiatric illness can be perceived as “voices, 

cries, noises, or rarely, music” (Wengel, Burke, & 

Holemon, 1989, p. 163). Musical hallucinations, 

however, are not necessarily associated with psychopathology, and tend to occur in people with 

advancing age and marked hearing loss (Sacks, 

2008). Bauman (2004) has distinguished “two basic 

types of auditory hallucinations—psychiatric auditory hallucinations and nonpsychiatric auditory 

hallucinations. People with mental illnesses often 

experience the former, while people who are hard 

of hearing often experience the latter” (pp. 17–18). 

Focusing on the latter, nonpsychiatric, type, Bauman makes the following points:

n Auditory hallucinations can consist of 

music, sounds, or voices.

n “Unformed” auditory hallucinations 

sound distorted and indistinct, whereas 

“formed” auditory hallucinations sound 

clear and recognizable.

n Auditory hallucinations typically are 

experienced by hard of hearing, socially 

isolated, elderly people who also have 

tinnitus.

n People who experience auditory 

hallucinations typically don’t admit to the 

experience.

n At least 10% of hard of hearing people 

experience auditory hallucinations.

n Many people actually find auditory 

hallucinations to be pleasant. Based 

on this information, it is reasonable to 

expect some patients to report auditory 

hallucinations that are not associated with 

psychopathology.
Definitions and Background	 

If a patient who reports auditory hallucinations remains unconvinced that the sounds do not 

have an external acoustic source, then the experience may indicate presence of comorbid mental illness. In addition, the psychiatric population tends 

to experience auditory hallucinations as frequent, 

intrusive, and distressing, whereas the nonpsychiatric population may experience them as more 

positive and nonthreatening (Choong, Hunter, & 

Woodruff, 2007). One study has reported data suggesting that auditory hallucinations that occur in 

nonpsychiatric individuals suggest a general susceptibility to schizophrenia (Sommer et al., 2008).

Whenever auditory hallucinations are reported, patients should be referred to both audiology and mental health for a thorough history and 

to evaluate the auditory experiences—to determine 

if the sounds are tinnitus or auditory hallucinations 

and to determine if mental illness is involved.

Permanent Versus Temporary Tinnitus

Tinnitus can be a temporary or a permanent condition.

Permanent Tinnitus

It is, of course, impossible to determine if and when 

a person’s tinnitus becomes permanent. In general, 

the longer a person has experienced tinnitus the 

more likely it is to be permanent. A general guideline is that tinnitus of at least 12 months duration 

has a high likelihood of being a permanent condition (Dobie, 2004b). However, it also has been 

suggested that a person must have experienced 

tinnitus for at least two years before it should be 

considered permanent (Vernon, 1996).

Temporary Tinnitus

Exposure to loud noise can cause temporary threshold shift as well as temporary tinnitus (Nuttall et al., 

2004). Tinnitus induced in this fashion likely will 

resolve within a few days following the insult. 

Repeated episodes of noise exposure increase the 

likelihood that the tinnitus will become permanent.

Tinnitus also can be induced by a number of 

medications and drug interactions (DiSorga, 2001) 

(see Chapter 5). Such tinnitus usually is temporary 

(typically lasting 1 to 2 weeks postexposure), but 

can be permanent—especially with the use of aminoglycoside antibiotics or the cancer chemotherapeutic drug cisplatin (Fausti, J. A. Henry, & Frey, 

1995; Rachel, Kaltenbach, & Janisse, 2002). Aspirin 

(containing salicylate) is well known to cause temporary tinnitus, although the dosage generally has 

to be rather high to induce tinnitus (Eggermont, 

2004; Puel & Guitton, 2007). Other medications that 

can cause temporary tinnitus include NSAIDS, loop 

diuretics, and quinine. Drugs used to treat mental 

health and sleep conditions also may trigger or 

exacerbate tinnitus. Patients have reported exacerbation of tinnitus due to alcohol and caffeine.

Onset of Tinnitus

The onset of tinnitus is described as gradual for some 

and sudden for others (Axelsson & Barrenas, 1992). 

In a population study of older adults with tinnitus, 55% reported a gradual onset, 24% reported a 

sudden onset, and 21% did not know (Sindhusake, 

Golding, et al., 2003). Uncertainty about the onset 

of tinnitus can make it difficult to identify a precipitating event. Indeed, as discussed further below, 

many patients are unable to identify anything that 

was associated with the onset of their tinnitus.

Recent-Onset Tinnitus

Some patients report that they have experienced 

tinnitus for only a short period of time, usually 

measured in weeks or up to a few months. For these 

patients with recent-onset tinnitus, it first is important to rule out vestibular schwannoma or any other 

medical condition that might be causing the symptoms (which is routine practice for audiologists). If 

medical causes can be ruled out, an attempt should 

be made to determine if psychological factors such 

as stress, anxiety, depression, or lifestyle changes 

might have triggered the tinnitus onset. Patients always should be questioned about any exposure to 

loud noise. Identifying a potentially triggering event 

helps to focus the counseling most appropriately.

Patients with recent-onset tinnitus are particularly susceptible to acquiring fears or concerns that 
	 Progressive Tinnitus Management: Clinical Handbook for Audiologists

the internal sound indicates the presence of a serious medical condition. These patients may be quite 

anxious about the potential ramifications of the 

auditory symptoms. It therefore is critical to provide them with only positive and reassuring information to allay any fears. They should be counseled 

that (a) their tinnitus may be a temporary condition; (b) they should protect their ears in the presence of damaging sound (or to avoid loud sounds 

entirely) to optimize the potential for spontaneous 

resolution of the tinnitus; (c) tinnitus often raises 

concerns when it is new, but most people who have 

long-term tinnitus are not particularly bothered by 

it (Dobie, 2004b; Hallam, Rachman, & Hinchcliffe, 

1984); and (d) if the tinnitus becomes bothersome 

to feel welcome to contact or return to the clinic to 

discuss ways to manage their reactions to it.

Some patients may remain unconvinced that 

the recent-onset tinnitus does not indicate a more 

serious condition, even after thorough audiologic 

and medical evaluations. These patients may need 

to be referred to a mental health clinician for assessment of comorbid psychological conditions.

Delayed-Onset Tinnitus

Delayed-onset tinnitus is thought to occur weeks, 

months, or even years following some precipitating event (e.g., exposure to loud noise, traumatic 

brain injury, treatment with ototoxic medications, 

etc.). It is not uncommon for patients to make a 

claim of delayed-onset tinnitus for litigation purposes. The possibility of such a claim being valid 

relates to the complex interaction among the presumed precursor event and more recent events that 

might have triggered the tinnitus onset. Evaluating 

a claim of delayed-onset tinnitus requires taking 

a detailed history that covers all possible circumstances that might have caused damage to the 

auditory system.

A better understanding of the mechanisms of 

tinnitus generation is needed before the existence 

of delayed onset of tinnitus can be positively confirmed or rejected (Humes, Joellenbeck, & Durch, 

2006). However, it does seem likely that noise exposure or other experiences that could have caused 

auditory damage can result in delayed-onset tinnitus, even when the tinnitus onset occurs years 

after the event.

Epidemiology of Tinnitus

Prevalence of Tinnitus

Prevalence estimates from numerous epidemiologic 

studies indicate that about 10 to 15% of all adults 

experience tinnitus (H. J. Hoffman & Reed, 2004). 

The American Tinnitus Association (ATA) estimates that 40 to 50 million Americans experience 

tinnitus as a chronic condition and that of these, 

10 to 12 million seek some form of medical help, 

and 2.5 million are “debilitated” by their tinnitus 

(S. C. Brown, 1990). Men have a higher incidence 

of tinnitus than women, likely due to occupational 

and recreational differences (H. J. Hoffman & Reed, 

2004; Meikle & Walsh, 1984).

“Causes” of Tinnitus

We often refer to “causes” of tinnitus (i.e., tinnitus 

etiology), but in fact we never know the specific 

cause of sensorineural tinnitus (J. A. Henry, Dennis, 

et al., 2005). For example, we may say that noise 

exposure “caused” a person’s tinnitus. The noise probably caused some cochlear damage, but it did not 

cause the tinnitus. Technically, instead of “causes,” 

we should use terminology that implies indirect 

causality, such as precipitating factors, events associated with tinnitus onset, tinnitus precursor events, and

tinnitus triggering events.

Auditory Pathologies Associated with Tinnitus

Numerous auditory pathologies have been associated 

with tinnitus. Sweetow (1996) has listed these with 

respect to conductive and sensorineural auditory 

pathologies (Table 1–1). It is important to realize that 

anything that can cause hearing loss also can trigger 

the onset of tinnitus (Coles, 1995; Dobie, 2004b).

Risk Factors

A number of studies have obtained tinnitus epidemiology data in a systematic fashion. H. J. Hoffman and Reed (2004) reviewed these studies and 

summarized the various factors that were shown 
Definitions and Background	 

to be associated with tinnitus. Their summary is 

divided between “definite” and “possible” risk factors (Table 1–2). Thus, people are “definitely” or 

“possibly” more likely to have tinnitus if these factors apply. These epidemiology data reveal factors 

that are correlated with the presence of tinnitus and 

thus are not necessarily causative agents.

The most common risk factor for the onset of 

sensorineural tinnitus is noise exposure (Axelsson 

& Barrenas, 1992; Penner & Bilger, 1995). Also, a 

direct correlation exists between degree of hearing loss and prevalence of tinnitus—the odds of 

having tinnitus increase as hearing loss increases 

(Coles, 2000). This is true regardless of the type or 

the cause of the hearing loss. Dobie (2004b) concluded that tinnitus tends to occur more frequently 

in men, the elderly, blue-collar workers, and people 

with certain health problems.

Pathophysiology of Tinnitus

Many researchers are attempting to discover the 

pathophysiologic basis of tinnitus, with the ultimate goal of finding a cure for tinnitus. Numerous theories and models have been proposed; 

currently, there is no consensus regarding tinnitus 

mechanisms. It is beyond the scope of this book 

to go into detail regarding possible mechanisms 

of tinnitus generation. The interested reader is 

advised to review numerous excellent publications 

on this topic (e.g., Baguley, 2002; Eggermont, 2000; 

Kaltenbach, 2000; Møller, 2003; Tyler, 2006; Vernon & Møller, 1995). Because everything we hear 

(including tinnitus) results from neural activity in 

the auditory nervous system, tinnitus-mechanisms 

research has focused on understanding abnormal 

neural activity that is associated with tinnitus. Most 

theories involve hair cells, the auditory nerve, and 

the central auditory nervous system (J. A. Henry, 

Dennis, et al., 2005). A few examples of proposed 

mechanisms include (there are many others):

n Hair cells: discordant function between 

inner and outer hair cells (Jastreboff, 

1990); damaged outer hair cells causing 

excessive release of neurotransmitter 

(glutamate) from inner hair cells 

Table 1–1. Auditory Pathologies AssociatedWithTinnitus

Conductive Sensorineural

Impacted cerumen

External otitis

Tympanic membrane perforations

Otitis media

External auditory meatus tumors

Cholesteatoma

Ossicular chain fixation or

discontinuity

Atresias

Otosclerosis

Carcinoma

And so forth

Endolymphatic hydrops

Perilymph fistulas

Noise damage

Vestibular schwannoma

Presbycusis

Viral diseases

Bacterial infections

Ototoxicity

Meningionoma

And so forth

Source: Sweetow (1996).

Table 1–2. Risk Factors for Tinnitus

“Definite” Risk Factors “Possible” Risk Factors

Acoustic neuroma

Age

Cardiovascular and

cerebrovascular disease

Drugs or medications

Ear infections/inflammation

Head/neck trauma and

injury

Hyper- and hypothyroidism

Loud noise exposure

Ménière’s disease

Otosclerosis

Presbycusis

Sudden deafness

Alcohol

Anxiety

Depression

Familial inheritance

Geographic region

Health status—fair/poor

Heavy weight or high body

mass index

Limited education

Low height

Low socioeconomic status

Low weight or low body

mass index

Rural residence

Smoking (cigarettes)

Source: Adapted from “Epidemiology of Tinnitus,” by H. J. Hoffman &

G.W. Reed, 2004, in Tinnitus: Theory and Management by J. B. Snow (Ed.),

(pp.16–41), Lewiston, NY: BC Decker Inc.Copyright 2004 BC Decker, Inc.

Adapted with permission.
	 Progressive Tinnitus Management: Clinical Handbook for Audiologists

producing sustained cochlear activity 

(Patuzzi, 2002).

n Auditory nerve: synchronization of 

spontaneous activity in auditory nerve 

fibers due to cross-talk (Eggermont, 

1990; Møller, 1984, 1995); cortical 

reorganization following changes in 

the auditory periphery resulting in a 

disproportionately large number of 

neurons becoming sensitive (tuned) to 

frequencies at upper and lower borders 

representing peripheral hearing loss 

(Salvi, Lockwood, & Burkard, 2000).

n Central auditory nervous system:

Increased spontaneous activity in the 

dorsal cochlear nucleus (Brozoski, Bauer, 

& Caspary, 2002; Kaltenbach & Afman, 

2000; Kaltenbach et al., 2002; Zacharek, 

Kaltenbach, Mathog, & Zhang, 2002).

Data from Tinnitus 

Clinic Patients

Tinnitus Data Archive

The Oregon Health and Science University (OHSU) 

Tinnitus Clinic was started in 1975 (Vernon & 

Schleuning, 1978). Extensive data from thousands 

of patients have been collected, and these data have 

been used to develop the Tinnitus Data Archive 

(Meikle, Creedon, & Griest, 2004) (http://www

.tinnitusarchive.org/). The summarized data in the 

Archive were collected from 1,630 patients seeking 

clinical intervention for their tinnitus and are not 

generalizable to individuals with tinnitus who do 

not seek intervention.

Main Findings of the Tinnitus Data Archive

Some of the main findings of the Tinnitus Data 

Archive include (J. A. Henry, Dennis, et al., 2005):

n There are about 21⁄2 times more male than 

female patients.

n 80% of all patients are at least 40 years 

of age.

n Tinnitus onset is reported as “gradual” or 

“sudden” about equally.

n Left-sided tinnitus is reported more often 

than right-sided tinnitus.

n More than half of the patients describe 

their tinnitus as a single sound (most 

of the remainder identify two or more 

sounds).

n Most patients describe their tinnitus 

as “ringing” or “clear tone” (3% report 

“hum,” “clicking,” “roaring,” or “pulse”).

n 85% of patients indicated that their 

perceived tinnitus loudness was a 5 or 

more on a 0 to 10 loudness-rating scale 

(10 = “very loud”).

Factors Associated with Tinnitus Onset

When OHSU Tinnitus Clinic patients were asked to 

describe the circumstances of their tinnitus onset, 

43% indicated that no known events were associated. Most of the remainder reported that one factor was associated with their tinnitus onset (8% 

reported more than one factor).

For those patients describing factors associated with their tinnitus onset, the factors could be 

placed into one of four broad categories (Meikle 

et al., 2004): (1) noise-related; (2) head and neck 

trauma; (3) head and neck illness; and (4) other 

medical conditions.

Years “Aware of” Tinnitus

OHSU Tinnitus Clinic patients are asked how long 

they have been aware of experiencing tinnitus. 

From the Tinnitus Data Archive (Meikle et al., 2004), 

40% of patients had experienced their tinnitus 

for 2 years or less; 55% for 5 years or less; 70% for 

10 years or less; and 85% for 20 years or less.

Types of “Sounds” Patients Hear

Patients are asked to describe what their tinnitus 

sounds like from a list of sounds commonly reported 

by patients, or by describing a sound that is not on 

the list. The most common sound reported by far 
Definitions and Background	 

is “ringing.” The second most common sound is 

“hissing.” The third most common sound is “clear 

tone.” Numerous additional sounds are reported, 

including “high-tension wire,” “buzzing,” “transformer noise,” “sizzling,” “crickets,” “whistle,” “hum,” 

and “clicking.”

Intermittency of Tinnitus

From the Tinnitus Data Archive, 91% of patients 

reported that their tinnitus is a constant sound. In 5% 

of patients, tinnitus is intermittent and heard more 

than 50% of the time. In 1% of patients, tinnitus is 

intermittent and heard less than 50% of the time.

Reduced Tolerance 

(Hypersensitivity) to Sound

“Hyperacusis” often is reported concurrently with 

tinnitus, and audiologists need to know how to 

recognize hyperacusis and how to provide appropriate intervention if it is a significant condition. 

There is no consensual definition of hyperacusis 

(P. J. Jastreboff & M. M. Jastreboff, 2004; Vernon, 

2002). It has been defined as “the collapse of loudness tolerance so that almost all sounds produce 

loudness discomfort” (Vernon & Press, 1998). At 

the other extreme, clinics have reported that up to 

half of their patients experience decreased loudness tolerance (Coles, 1996; Gold, Frederick, & 

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

When evaluating the patient, the critical factor is 

to determine if loudness sensitivity is a significant 

problem in the patient’s life.

Our definitions of conditions pertaining to 

decreased loudness tolerance are consistent with 

those published by J. A. Henry, Zaugg, and Schechter (2005a), which were adapted from P. J. Jastreboff 

and Hazell (2004).

Hyperacusis

Hyperacusis is a physical condition of discomfort 

or pain caused by sound. The effect is restricted 

primarily to the auditory pathways. Thus, a condition of “pure” hyperacusis causes physical discomfort, but no emotional responses are involved. 

For a given patient with pure hyperacusis, sound 

would be uncomfortably loud at levels most people find comfortable—regardless of the type of sound. 

This means that a patient who reports that he or 

she can tolerate some sounds at louder levels than 

other sounds is probably not experiencing pure 

hyperacusis.

Misophonia

M. M. Jastreboff and P. J. Jastreboff (2002) introduced the term misophonia. The term means “dislike 

of sound,” and implies that there is an emotional 

reaction to sound. A misophonic reaction is a learned 

response. This means that a misophonic patient 

might report that a particular sound is problematic in some situations, but not in others. When 

questioned in detail, these patients often report 

reactions that would be inconsistent with pure 

hyperacusis. For example, they might report that 

certain “unpleasant” sounds become uncomfortably loud at levels below which “pleasant” sounds 

are tolerated comfortably.

Phonophobia

P. J. and M. M. Jastreboff (2000) defined use of the 

term phonophobia for clinical application. Phonophobia is a fear response caused by sound, and is 

considered a subcategory of misophonia. Misophonia can cause any kind of negative emotional 

response, but phonophobia specifically causes a 

fear reaction. A defining feature of phonophobia 

is the anticipation that sound will be uncomfortably loud. Thus, phonophobia refers to a person’s 

state of mind with respect to sounds and sound 

environments.

Loudness Recruitment

Loudness recruitment often is confused with hyperacusis (Vernon, 2002). Recruitment refers to abnormally rapid growth in the perception of loudness 

(Vernon, 1976). It usually is a phenomenon of cochlear 
10	 Progressive Tinnitus Management: Clinical Handbook for Audiologists

or sensorineural hearing loss. Recruitment generally is associated with reduced auditory thresholds 

and normal loudness discomfort levels (Figure 1–1). 

Thus, the dynamic range is compressed, but there 

is normal tolerance to louder sounds.

Treatment for Conditions of Reduced 

Sound Tolerance

In Chapter 6, we describe methodology for the 

treatment of reduced sound tolerance. The overall approach is to first determine if the condition 

is a severe problem for the patient. If so, then 

the patient should receive special treatment that 

focuses on the condition. If the condition is a mild 

or moderate problem, then the patient needs to be 

educated about the sensitizing effects of using hearing protection, and the desensitizing effects of using 

therapeutic sound (Formby & Gold, 2002). Normally, the use of sound that is advocated for tinnitus management will indirectly provide adequate 

treatment for reduced sound tolerance in mild and 

moderate cases. Consultation with a mental health 

provider might be useful if a patient fears sound 

and/or has other intense fears.

0

10

20

30

40

50

60

70

80

90

100

Frequency (kHz)

dB HL

0.25 0.5 1 2 4 8

LDLs

Thresholds

0

10

20

30

40

50

60

70

80

90

100

Frequency (kHz)

dB HL

0.25 0.5 1 2 4 8

LDLs

Thresholds

Figure 1–1. Tolerance to sound can be estimated by obtaining loudness discomfort levels (LDLs), which indicate the

threshold level at which sound becomes uncomfortably loud. A. LDLs at and above about 100 dB HL are in the normal

range. Note that the hearing sensitivity is reduced in the higher frequencies, resulting in a compressed dynamic range

at those frequencies—and loudness recruitment. However, the LDLs at 100 dB HL reflect normal tolerance to louder

sounds.B. LDLs are reduced to 70 dB HL, indicating a condition of reduced loudness tolerance. From Tinnitus Retraining

Therapy: Patient Counseling Guide (p. 168), by J. A. Henry, D. R.Trune, M. J. A. Robb, & P. J. Jastreboff, 2007, San Diego, CA:

Plural Publishing, Inc. Copyright 2007 by Plural Publishing. Reprinted with permission.

A B