Tinnitus: Phantom Auditory Perception, Central Gain, and the Brain That Hears a Sound That Is Not There

Abstract

Tinnitus is the perception of sound in the absence of any external acoustic source, most often a ringing or hissing that only the affected person can hear. It is a symptom rather than a disease, and in the large majority of cases it is subjective: no physical vibration reaches the ear, yet the brain generates and sustains a phantom auditory percept. The dominant modern account is central and homeostatic. When the cochlea is damaged, commonly by noise or ageing, the reduced input triggers a compensatory rise in gain, and that maladaptive plasticity produces a phantom. This article distinguishes the subjective, objective, and pulsatile forms; explains how deafferentation and central gain generate the sound; sets out how pitch, loudness, and distress are measured; and examines why the loudness of the phantom and the suffering it causes are separable and cognitively constructed.

Keywords: tinnitus, phantom auditory perception, central gain, auditory plasticity

What Tinnitus Is

*Tinnitus* is the conscious perception of sound without any corresponding external acoustic stimulus, classically described as a ringing in the ears but experienced equally as buzzing, hissing, whistling, or humming (Baguley et al., 2013). The defining feature is that the sound is heard when there is nothing outside the head to hear: no vibration is reaching the eardrum, yet a percept of sound is present. Tinnitus is therefore a *symptom*, not a disease in its own right, and it can accompany a wide range of underlying conditions, from noise-induced cochlear damage to age-related hearing loss to head injury. It is extremely common. Population surveys place the prevalence of tinnitus in adults at roughly 10 to 15 percent, with a smaller fraction reporting it as severe or disabling (Shargorodsky et al., 2010).

The decisive early reframing was to treat tinnitus not as a sound in the ear but as a *phantom auditory perception* generated by the nervous system (Jastreboff, 1990). On this view the ear is frequently the trigger but rarely the site of the percept; the ringing is manufactured and maintained centrally, in the auditory brain, which is why cutting the auditory nerve usually fails to abolish it and may make it worse. This shift, from an otological to a neurophysiological framing, is what makes tinnitus a problem for cognitive science: the phantom is a construction of the brain, subject to plasticity, attention, and emotional appraisal, rather than a faithful readout of the acoustic world. A crucial consequence, developed throughout this article, is that the *loudness* of the phantom and the *distress* it causes are separable: many people hear a constant tinnitus and are barely troubled by it, while others with an objectively similar signal are severely disabled (Baguley et al., 2013).

Key Takeaways

Tinnitus is the perception of sound with no external source; it is a symptom, not a disease, and affects roughly 10 to 15 percent of adults.
In its usual subjective form it is a phantom auditory perception generated and sustained by the brain, not a sound present in the ear.
The leading account is central: when cochlear input is reduced, the auditory brain increases gain and reorganizes, and this maladaptive plasticity produces the phantom.
The loudness of the phantom and the distress it causes are separable; distress depends on attention, emotion, and appraisal, not on loudness alone.
Tinnitus is measured by matching its pitch and loudness and, separately, by questionnaires that quantify its impact on daily life.

Figure 1

How Reduced Cochlear Input Generates a Central Phantom

Note. Damage to the cochlea reduces the input reaching central auditory structures. Rather than falling silent, the deprived pathway increases its gain and spontaneous activity to restore its accustomed output, and this elevated, reorganized activity is perceived as a sound even though nothing external is present. The phantom is generated centrally, which is why it persists when the periphery is silenced.

Forms of Tinnitus

Tinnitus is not a single entity but a family of experiences, and the first clinically important division is between *subjective* and *objective* tinnitus (Langguth et al., 2013). Subjective tinnitus, by far the more common, is a phantom perception audible only to the affected person; there is no acoustic source anywhere, and it corresponds to the central account developed here. Objective tinnitus is the rare exception that proves the rule: a genuine sound, generated inside the body by turbulent blood flow, muscle spasm, or a vascular anomaly, that can in principle be heard by an examiner and is not a phantom at all. A further common distinction is between *tonal* tinnitus, heard as a steady pitch, and *pulsatile* tinnitus, which beats in time with the pulse and points to a vascular origin that warrants investigation.

Table 1. Principal forms of tinnitus and their defining features.
Form	Source of the sound	Character
Subjective	None; a central phantom percept	Audible only to the person; the usual clinical case
Objective	A real internal sound (vascular or muscular)	Potentially audible to an examiner; rare
Tonal	Central; steady phantom pitch	A continuous ring, whistle, or hiss at a matchable pitch
Pulsatile	Often a real vascular sound	Beats with the heartbeat; warrants vascular workup

The forms differ in mechanism and in what they demand of the clinician. Subjective tonal tinnitus is the presentation that the central-gain and plasticity models were built to explain, and it is the focus of the rest of this article. Objective and pulsatile tinnitus, though uncommon, matter because they may signal a treatable structural cause and can be genuinely eliminated by addressing it. This etiological breadth is one reason estimates of how common tinnitus is vary so widely between studies: prevalence depends heavily on how the question is asked, over what time frame, and with what severity threshold, and a systematic review of the literature found that inconsistent definitions and reporting are a central obstacle to comparing figures across populations (McCormack et al., 2016).

How the Brain Generates a Phantom Sound

The central puzzle of tinnitus is that a sound is heard when no sound exists, and often when the ear that seems to host it has been damaged or even removed. The leading resolution parallels the account of hyperacusis: it is a story about *central gain* and *maladaptive plasticity* (Eggermont & Roberts, 2004). Sensory systems do not passively relay their input; they regulate their own responsiveness to keep their output within a useful range. When cochlear damage, most often from noise or ageing, reduces the input reaching the auditory brainstem, midbrain, and cortex, these central structures do not simply fall quiet. They increase their gain and their spontaneous firing to restore their accustomed activity, and they reorganize their frequency map so that neurons deprived of their normal input begin responding to neighbouring frequencies (Norena, 2011).

Demo 1 · Deafferentation generates a phantom

When the cochlea is damaged, the evoked signal reaching the auditory brain falls — but the brain raises its gain to restore its accustomed activity, and that same gain amplifies the background spontaneous firing. Drag the cochlear input loss: the evoked signal drops while spontaneous activity climbs, and once it crosses the phantom threshold a sound is heard where none exists.

Cochlear input loss: 15 dB

Input loss 15 dB → evoked signal 53, spontaneous activity 31 · no phantom yet.

A schematic homeostatic model: as cochlear input falls, compensatory gain amplifies spontaneous activity until it crosses the threshold for a phantom percept. Illustrative of the central-gain account of tinnitus, not measured neural activity; values computed locally, not stored.

This homeostatic response is adaptive in intent, because it preserves sensitivity when the input is degraded, but it carries a cost. Elevated spontaneous activity, increased neural synchrony, and a reorganized tonotopic map together constitute a signal that the rest of the auditory system reads as sound, even though nothing external produced it (Roberts et al., 2010). The perceived pitch of the tinnitus typically falls in the frequency region of greatest hearing loss, exactly where deafferentation is most severe and the map has reorganized most, which is strong evidence that the phantom is generated by the deprived, over-amplified region rather than by a lesion producing an active sound. On this account tinnitus and hyperacusis are two expressions of the same over-amplification, which is why they so often occur together.

The physiological substrate of this change is being mapped onto specific circuits and neurochemistry, and the modern synthesis frames it as maladaptive plasticity that can be triggered by peripheral insult but is maintained centrally (Shore et al., 2016). A recurring theme is a shift in the balance between excitation and inhibition: a reduction in inhibitory neurotransmission unmasks and amplifies activity in deprived neurons, raising spontaneous rates and synchrony. Critically, the trigger and the maintenance can dissociate. The cochlear damage that initiates tinnitus is peripheral, but once the central changes are established the phantom becomes self-sustaining, which is why treatments aimed only at the ear so often fail and why the durable targets are the brain's own plastic circuits.

Measuring Tinnitus

Because subjective tinnitus is a private percept with no external correlate, measuring it means characterizing the experience itself and, separately, its impact. The psychoacoustic measures anchor the phantom to physical scales by *matching*. In pitch matching, an external tone is adjusted until it corresponds to the pitch of the tinnitus, which usually locates it in the high-frequency region of hearing loss. In loudness matching, an external sound is adjusted to the perceived loudness of the phantom, which is typically found to be only a few decibels above the person's hearing threshold, a striking result given how disabling the tinnitus may be (Langguth et al., 2013). The *minimum masking level*, the softest external noise that renders the tinnitus inaudible, adds a further psychoacoustic index.

Demo 2 · Matching the phantom

Because the phantom has no external correlate, it is pinned to physical scales by matching. Set the matched pitch against this audiogram: the tinnitus pitch typically falls in the region of greatest hearing loss. Then set the matched loudness — it is usually just a few decibels above threshold, acoustically faint next to ordinary speech, however loud the tinnitus feels.

Matched pitch: 6000 Hz

Matched loudness: 8 dB above threshold

Pitch 6000 Hz sits at 55 dB of loss · in the region of greatest loss. Matched loudness 8 dB SL — only 13% of an ordinary speech level, yet the phantom can still dominate awareness.

A fixed illustrative audiogram with a noise notch at 4–6 kHz; the matched pitch marker moves along it. The matched loudness is expressed relative to the listener’s own threshold. Illustrative, not a measured ear; values computed locally, not stored.

These psychoacoustic numbers capture the signal but not the suffering, and the two are only loosely related, which is why questionnaire measures of impact are central to assessment. Validated instruments such as the Tinnitus Handicap Inventory and the Tinnitus Functional Index quantify the emotional, attentional, and functional burden of tinnitus and yield a distress score that guides management far better than loudness matching does (Tunkel et al., 2014). The gap between a low matched loudness and a high distress score is the quantitative face of the loudness-distress dissociation: clinical guidelines therefore treat the handicap score, not the acoustic match, as the primary outcome. Standardizing these measures across studies remains difficult, and inconsistent reporting of severity is one reason the epidemiological picture has been so hard to pin down (McCormack et al., 2016).

Tinnitus and Cognition

Tinnitus belongs in cognitive psychology because whether a phantom sound becomes a source of suffering is decided not in the ear but in the systems that direct attention and assign emotional value. The clearest demonstration is the loudness-distress dissociation itself: since the matched loudness of the phantom is a poor predictor of the handicap it causes, something other than the raw signal must determine the burden. That something is the interaction of the auditory percept with limbic and attentional networks. A prominent model proposes that tinnitus becomes distressing when a failure of noise-cancellation allows the phantom into awareness and limbic-auditory interactions attach negative value to it, so that the signal captures attention and evokes an emotional reaction that further amplifies it (Rauschecker et al., 2010).

Demo 3 · Loudness is not distress

The loudness of the phantom and the suffering it causes are separable. Here the tinnitus loudness is held fixed and faint. Raise the attention-and-threat appraisal — how much the sound captures attention and is read as threatening — and watch the handicap score climb into the severe range while the loudness never moves. The distress is built by cognition, not by the signal.

Attention & threat appraisal: 30 / 100

Appraisal 30/100 → handicap score 16 (slight) · phantom loudness held at 8 dB above threshold throughout. Loudness flat, distress driven by cognition.

A schematic of the loudness-distress dissociation: the acoustic loudness is fixed and faint while the handicap score rises with attentional capture and threat appraisal. Illustrative of why treatment targets distress, not loudness; values computed locally, not stored.

This attentional and emotional entanglement sets up a self-reinforcing loop that is the target of the most effective treatments. When attention is directed toward the phantom and appraised as threatening, it becomes louder and more intrusive; the resulting distress heightens vigilance, which directs still more attention to the sound. Cognitive behavioural therapy and sound-based approaches work precisely by breaking this loop, reducing the threat value and the attentional capture rather than the signal, which is why they lower distress even when the tinnitus remains audible. Neuroimaging supports this picture, showing that tinnitus is associated not with a single auditory abnormality but with altered activity across a distributed network spanning auditory, attentional, and limbic regions (Elgoyhen et al., 2015).

The deepest current framing places tinnitus within *predictive coding*, in which perception is the brain's best inference about the causes of its input rather than a direct readout of that input. On this account the auditory system, deprived of reliable high-frequency input, fills the gap with a prediction, and tinnitus is what that prediction feels like when the precision assigned to it is abnormally high (Sedley et al., 2016). A complementary systems-level model decomposes the tinnitus percept into interacting but separable subnetworks, so that the sound itself, its loudness, its unpleasantness, and the distress it causes are generated by partly distinct circuits, which is why they can dissociate and why they may require different treatments (De Ridder et al., 2014).

Worked Example: Reading a Tinnitus Assessment

Consider an adult who reports a constant high-pitched ringing in both ears after years of occupational noise exposure. On assessment, their tinnitus pitch matches an external tone at 6000 Hz, its loudness matches an external sound just 8 dB above their hearing threshold at that frequency, and their Tinnitus Handicap Inventory score is 68 out of 100, in the severe range. Their audiogram shows a notch of hearing loss centred at 4000 to 6000 Hz. What does this pattern show?

First, the pitch match. At 6000 Hz the tinnitus sits squarely in the region of the person's hearing loss, exactly where deafferentation and tonotopic reorganization are greatest. This is the signature the central-gain model predicts: the phantom arises from the deprived, over-amplified frequency region, not from an independent source. Second, the loudness match. At only 8 dB above threshold the phantom is, in acoustic terms, very quiet, a faint sound most people would barely notice if it came from outside. Third, the handicap score. A THI of 68 places this person in the severe band, reporting substantial disruption to concentration, sleep, and mood.

The instructive point is the contradiction between the second and third numbers. An 8-dB sound is acoustically trivial, yet it is producing severe disability. The raw loudness of the phantom cannot explain the suffering, because the loudness is minimal and the suffering is major. What bridges the gap is the cognitive and emotional response: the sound has captured attention and been appraised as threatening, and it is that attentional capture and negative appraisal, not the acoustic magnitude, that the handicap score is tracking. The example makes concrete why clinicians treat the distress, and why the matched loudness, though easy to measure, is the wrong target.

Discussion

Tinnitus is a clarifying case for cognitive science because it demonstrates that the brain can generate a full-fledged perception with no external cause, and that the perception and the suffering it produces are separable phenomena. The reframing of tinnitus as a phantom auditory perception, rather than a sound in the ear, was the conceptual turn that made this visible, and it has been vindicated by the failure of peripheral treatments and by the localization of the phantom to the deprived, reorganized regions of the auditory brain (Jastreboff, 1990; Shore et al., 2016). The central-gain and maladaptive-plasticity account gives the generation of the phantom a concrete mechanism and unifies tinnitus with hyperacusis as two faces of the same over-amplification.

The account remains incomplete in instructive ways. Central gain explains why a phantom is generated but not why it is generated in some people with hearing loss and not others, nor why matched loudness predicts distress so poorly. The predictive-coding and subnetwork models address the second gap by separating the sound from the distress and casting the phantom as a high-precision prediction, but they are harder to test directly and have not yet yielded decisively better treatments (Sedley et al., 2016; De Ridder et al., 2014). A full theory will have to connect the gain of auditory neurons to the attentional and limbic systems that decide whether a faint phantom is ignored or becomes a torment, and that connection is where tinnitus stops being an auditory problem and becomes a cognitive one.

Current Directions

The most active current questions concern epidemiology, mechanism, and treatment. On epidemiology, a large systematic review and meta-analysis has now placed the global prevalence of tinnitus at around 14 percent of adults, with incidence and burden rising with age, giving the field a firmer denominator against which to gauge risk factors and the reach of the condition (Jarach et al., 2022). This scale, and the recognition that a substantial minority are severely affected, has sharpened the case for treating tinnitus as a major public-health problem rather than a benign nuisance.

On treatment, the priority is evidence-based, standardized care. A multidisciplinary European guideline has synthesized the diagnostic and therapeutic literature and set out graded recommendations, giving strongest support to cognitive behavioural therapy for reducing tinnitus-related distress and cautioning against treatments that lack a solid evidence base (Cima et al., 2019). In parallel, the maladaptive-plasticity framework has motivated a search for treatments that target the central changes directly, including bimodal stimulation that pairs sound with somatosensory input to drive the auditory system back toward a normal state, an approach that follows from the mechanism rather than merely masking the symptom (Shore et al., 2016). Refining outcome measures so that trials of these approaches can be compared remains a continuing and necessary effort.

Common Misconceptions

Tinnitus is a sound coming from the ear.: In its usual subjective form there is no acoustic source; the sound is a phantom generated centrally by the auditory brain, which is why silencing or removing the ear does not abolish it (Jastreboff, 1990).
Louder tinnitus is always more disabling.: The matched loudness of the phantom is usually only a few decibels above threshold and predicts distress poorly; the burden depends on attention and appraisal, not acoustic magnitude (Rauschecker et al., 2010).
Nothing can be done about tinnitus.: While no treatment reliably erases the phantom, cognitive behavioural therapy and sound-based approaches substantially reduce the distress it causes, and clinical guidelines endorse them (Cima et al., 2019).
Tinnitus is a disease.: It is a symptom that can accompany many conditions, most often hearing loss; occasionally, as in pulsatile tinnitus, it signals a treatable structural cause and warrants investigation (Langguth et al., 2013).

Glossary

Central gain.: The homeostatic increase in the responsiveness of central auditory neurons that compensates for weakened peripheral input and, in excess, produces the phantom activity heard as tinnitus.
Deafferentation.: The loss of afferent input from the cochlea to central auditory structures; it is the trigger that prompts the compensatory gain increase underlying tinnitus.
Hyperacusis.: A reduced tolerance to ordinary sound attributed to the same central over-amplification; a frequent companion of tinnitus.
Loudness matching.: A psychoacoustic procedure in which an external sound is adjusted to the perceived loudness of the tinnitus; matched loudness is typically only a few decibels above threshold.
Loudness-distress dissociation.: The observation that the matched loudness of tinnitus predicts the distress it causes only weakly, because distress depends on attention and appraisal rather than acoustic magnitude.
Maladaptive plasticity.: Reorganization of auditory neural circuits following peripheral damage that, while homeostatic in intent, generates and sustains the tinnitus percept.
Minimum masking level.: The softest level of an external noise that renders the tinnitus inaudible; a psychoacoustic index of the phantom.
Objective tinnitus.: The rare form in which a genuine internal sound, usually vascular or muscular, is present and can in principle be heard by an examiner; not a phantom.
Phantom auditory perception.: The perception of sound generated by the nervous system in the absence of any external acoustic source; the modern framing of subjective tinnitus.
Pitch matching.: A procedure in which an external tone is adjusted to the pitch of the tinnitus, which usually falls in the frequency region of greatest hearing loss.
Predictive coding.: A framework in which perception is the brain's inference about the causes of its input; tinnitus is cast as a high-precision prediction filling the gap left by lost input.
Pulsatile tinnitus.: Tinnitus that beats in time with the heartbeat, often reflecting a real vascular sound and warranting investigation for a structural cause.
Subjective tinnitus.: The common form of tinnitus, audible only to the affected person, with no external acoustic source; a central phantom percept.
Tinnitus Handicap Inventory (THI).: A validated questionnaire that quantifies the emotional, functional, and attentional burden of tinnitus, used as a primary clinical outcome.
Tinnitus.: The perception of sound in the absence of an external acoustic source; a symptom rather than a disease, affecting roughly 10 to 15 percent of adults.
Tonotopic reorganization.: The remapping of frequency tuning in the auditory brain after hearing loss, in which deprived neurons respond to neighbouring frequencies and contribute to the phantom.

Key Researchers

David M. Baguley

(1961-2022). A professor of hearing sciences at the University of Nottingham whose foundational reviews defined tinnitus and hyperacusis for a generation of clinicians and co-authored the influential Lancet seminar that set the modern clinical framing.
ORCID - Faculty page

Christopher R. Cederroth

An auditory neuroscientist at the Karolinska Institutet who leads work on the genetics and epidemiology of tinnitus and serves as editor-in-chief of a leading auditory-neuroscience journal, connecting the phantom to its heritable and population-level determinants.
ORCID - Faculty page - Google Scholar

Jos J. Eggermont

A professor emeritus at the University of Calgary whose influential review of the neuroscience of tinnitus, and whose work on cortical reorganization after hearing loss, helped establish the maladaptive-plasticity account of the phantom.
Faculty page - Google Scholar

Pawel J. Jastreboff

A professor emeritus of otolaryngology at Emory University who originated the neurophysiological model of tinnitus and the tinnitus retraining therapy that follows from it, reframing tinnitus as a phantom auditory perception generated by the brain.
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Berthold Langguth

A psychiatrist and neuroscientist at the University of Regensburg and a leader in tinnitus neuromodulation who led the widely cited Lancet Neurology review on the causes and clinical management of tinnitus.
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Dirk De Ridder

(b. 1966). A neurosurgeon and neuroscientist at the University of Otago who developed, with Vanneste, the integrative subnetwork model of auditory phantom perception, decomposing the tinnitus percept into interacting but separable circuits.
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Richard J. Salvi

An auditory neuroscientist at the University at Buffalo and director of its Center for Hearing and Deafness who advanced the central-gain account of tinnitus through studies of auditory plasticity after cochlear insult.
Faculty page

Susan E. Shore

A professor emerita at the University of Michigan whose discovery of bimodal auditory-somatosensory plasticity in the dorsal cochlear nucleus grounded a mechanism-based bimodal stimulation treatment for tinnitus.
ORCID - Faculty page - Wikipedia

Frequently Asked Questions

What is tinnitus?

Tinnitus is the perception of sound, such as ringing, buzzing, or hissing, in the absence of any external acoustic source. It is a symptom rather than a disease, and in its usual subjective form it is a phantom sound generated by the brain rather than a sound present in the ear (Baguley et al., 2013).

Is tinnitus a sound in my ears or in my brain?

In the common subjective form there is no external sound anywhere; the percept is generated centrally in the auditory brain, which is why it usually persists even when the ear is silenced or the auditory nerve is cut (Jastreboff, 1990).

What causes tinnitus?

Most often it follows a reduction in cochlear input from noise exposure or ageing. The deprived auditory brain increases its gain and reorganizes, and this maladaptive plasticity generates and sustains the phantom (Eggermont & Roberts, 2004; Shore et al., 2016).

Why does my tinnitus bother me so much when it is quiet?

Because the loudness of the phantom and the distress it causes are separable. The matched loudness is usually only a few decibels above threshold, and the burden depends on how much the sound captures attention and is appraised as threatening, not on its acoustic magnitude (Rauschecker et al., 2010).

How is tinnitus measured?

In two complementary ways: psychoacoustic matching of its pitch and loudness against external sounds, and validated questionnaires such as the Tinnitus Handicap Inventory that quantify its impact on daily life. The questionnaire score guides treatment better than the loudness match (Langguth et al., 2013; Tunkel et al., 2014).

Can tinnitus be cured?

No treatment reliably erases the phantom, but the distress it causes can be substantially reduced. Cognitive behavioural therapy has the strongest evidence, and sound-based approaches are widely used; guidelines endorse treating the distress rather than chasing the sound (Cima et al., 2019).

How common is tinnitus?

Roughly 10 to 15 percent of adults experience tinnitus, and a large recent meta-analysis places the global prevalence near 14 percent, with a smaller fraction reporting it as severe or disabling (Shargorodsky et al., 2010; Jarach et al., 2022).

Yes. Both are attributed to the same central over-amplification following reduced cochlear input: increased gain applied to the deprived region generates the phantom of tinnitus, while the same gain over-amplifies real sound in hyperacusis, which is why they frequently occur together (Norena, 2011).

References

Baguley, D., McFerran, D., & Hall, D. (2013). Tinnitus. The Lancet, 382(9904), 1600-1607. https://doi.org/10.1016/S0140-6736(13)60142-7

Cima, R. F. F., Mazurek, B., Haider, H., Kikidis, D., Lapira, A., Noreña, A., & Hoare, D. J. (2019). A multidisciplinary European guideline for tinnitus: Diagnostics, assessment, and treatment. HNO, 67(Suppl 1), 10-42. https://doi.org/10.1007/s00106-019-0633-7

De Ridder, D., Vanneste, S., Weisz, N., Londero, A., Schlee, W., Elgoyhen, A. B., & Langguth, B. (2014). An integrative model of auditory phantom perception: Tinnitus as a unified percept of interacting separable subnetworks. Neuroscience & Biobehavioral Reviews, 44, 16-32. https://doi.org/10.1016/j.neubiorev.2013.03.021

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Jarach, C. M., Lugo, A., Scala, M., van den Brandt, P. A., Cederroth, C. R., Odone, A., et al. (2022). Global prevalence and incidence of tinnitus: A systematic review and meta-analysis. JAMA Neurology, 79(9), 888-900. https://doi.org/10.1001/jamaneurol.2022.2189

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Noreña, A. J. (2011). An integrative model of tinnitus based on a central gain controlling neural sensitivity. Neuroscience & Biobehavioral Reviews, 35(5), 1089-1109. https://doi.org/10.1016/j.neubiorev.2010.11.003

Rauschecker, J. P., Leaver, A. M., & Mühlau, M. (2010). Tuning out the noise: Limbic-auditory interactions in tinnitus. Neuron, 66(6), 819-826. https://doi.org/10.1016/j.neuron.2010.04.032

Roberts, L. E., Eggermont, J. J., Caspary, D. M., Shore, S. E., Melcher, J. R., & Kaltenbach, J. A. (2010). Ringing ears: The neuroscience of tinnitus. The Journal of Neuroscience, 30(45), 14972-14979. https://doi.org/10.1523/JNEUROSCI.4028-10.2010

Sedley, W., Friston, K. J., Gander, P. E., Kumar, S., & Griffiths, T. D. (2016). An integrative tinnitus model based on sensory precision. Trends in Neurosciences, 39(12), 799-812. https://doi.org/10.1016/j.tins.2016.10.004

Shargorodsky, J., Curhan, G. C., & Farwell, W. R. (2010). Prevalence and characteristics of tinnitus among US adults. The American Journal of Medicine, 123(8), 711-718. https://doi.org/10.1016/j.amjmed.2010.02.015

Shore, S. E., Roberts, L. E., & Langguth, B. (2016). Maladaptive plasticity in tinnitus - triggers, mechanisms and treatment. Nature Reviews Neurology, 12(3), 150-160. https://doi.org/10.1038/nrneurol.2016.12

Tunkel, D. E., Bauer, C. A., Sun, G. H., Rosenfeld, R. M., Chandrasekhar, S. S., Cunningham, E. R., Jr., et al. (2014). Clinical practice guideline: Tinnitus. Otolaryngology-Head and Neck Surgery, 151(2 Suppl), S1-S40. https://doi.org/10.1177/0194599814545325

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