The science of sound masking: what peer-reviewed research says about how external sounds interact with tinnitus

This article is a summary of peer-reviewed research on how external sounds interact with tinnitus at the neural level. Every claim is cited. Where the evidence is strong, we say so. Where it is inconclusive, conflicting, or based on small samples, we say that too.

I am not a doctor. I am not an audiologist. I am Justin, the founder of siasola. I have had tinnitus since I was 18. I read this research because I wanted to understand what was happening in my own head, and I built Siasola Tinnitus Masking Sounds because I wanted a sound customization tool with the precision control I could not find anywhere else.

This article is educational. It is not medical advice. If you have tinnitus, consult a qualified healthcare professional.

How tinnitus is generated: the central gain model

The dominant scientific model of tinnitus holds that it is generated in the brain, not in the ear. When cochlear damage reduces sensory input at certain frequencies, the central auditory system compensates by amplifying neural activity to maintain stable firing rates. This compensatory process, called "central gain," also amplifies spontaneous neural noise, producing the phantom sound perceived as tinnitus.

Norena (2011) published the foundational integrative model in Neuroscience & Biobehavioral Reviews, proposing that central hyperactivity results from a homeostatic mechanism that increases neural sensitivity when peripheral input decreases. The amplification of "neural noise" generates the phantom sound. Schaette and Kempter (2006) demonstrated this computationally: their model showed that when the healthy ratio between mean and spontaneous firing rate of the auditory nerve is decreased through outer hair cell loss, homeostatic compensation amplifies spontaneous activity.

A comprehensive review by Roberts et al. (2010) in the Journal of Neuroscience established that tinnitus is generated through deafferentation of tonotopically organised central auditory structures, leading to increased spontaneous firing rates and neural synchrony. The frequency spectrum of the tinnitus sound corresponds to the deafferented frequency range.

Hidden hearing loss

One important finding is that tinnitus can occur even with a normal audiogram. Schaette and McAlpine (2011) found that tinnitus patients with normal audiograms showed significantly reduced amplitude of auditory brainstem response wave I (primary auditory nerve) but normal wave V amplitude (centrally generated). Their computational model estimated 53 to 61% auditory nerve fibre deafferentation in affected regions, invisible on standard hearing tests. This is called "hidden hearing loss," and it suggests that the central gain mechanism is triggered by nerve damage that conventional testing does not detect.

A critical note

The central gain model is well-supported but not complete. Sedley (2019) argued that while peripheral damage clearly induces gain changes, "specific attribution of these changes to tinnitus is generally hampered by the absence of hearing-matched human control groups." Dramatic gain changes occur in response to auditory damage regardless of whether tinnitus develops. Predictive coding models may better explain why some people with hearing loss develop tinnitus and others do not.

The history of sound masking research

Sound masking as a systematic approach to tinnitus was first studied by Feldmann (1971), who categorised masking effects into types based on how auditory thresholds and tinnitus masking curves related. He identified convergence (34% of patients), congruence (32%), and distance (22%) patterns. He also observed that a substantial number of participants experienced brief suppression of tinnitus after the masking sound stopped, a phenomenon later termed "residual inhibition."

Vernon (1977) pioneered wearable masking devices (hearing aid-like devices producing noise in the ear) and described the purpose of masking as rendering tinnitus inaudible with a more acceptable sound. His work established the clinical framework for using external sound to address tinnitus perception.

Jastreboff (1990) proposed the neurophysiological model of tinnitus, which became the foundation for Tinnitus Retraining Therapy (TRT). A key principle of this model: the limbic system and autonomic nervous system are responsible for the distress associated with tinnitus, not just the auditory system. The TRT protocol, formalised by Jastreboff and Hazell (1993), combines directive counselling with low-level broadband sound therapy to promote habituation. Importantly, in TRT, sound should not completely mask the tinnitus; both the external sound and the tinnitus must be perceived simultaneously to promote habituation.

What clinical trials show about masking vs. TRT

Henry et al. (2006) conducted a controlled clinical trial comparing tinnitus masking and TRT in U.S. military veterans with clinically significant tinnitus. Both groups showed significant improvements. Tinnitus masking provided better results after 3 months, while TRT showed greater long-term benefit at 12 and 18 months. Both approaches demonstrated continued improvement over the full study period.

Cochrane reviews: what the highest-level evidence says

Cochrane systematic reviews represent the highest level of evidence synthesis. Two are directly relevant.

Hobson, Chisholm, and El Refaie (2012) analysed six randomised controlled trials with 553 participants. They found the limited data "failed to show strong evidence of the efficacy of sound therapy in tinnitus management," but emphasised that "the absence of conclusive evidence should not be interpreted as evidence of lack of effectiveness." The studies were too heterogeneous in methods, populations, and outcome measures to allow meta-analysis.

Sereda et al. (2018) reviewed eight RCTs with 590 participants. They found no evidence to support the superiority of sound therapy over waiting list control, placebo, or education, and no evidence to support the superiority of any one sound therapy option (hearing aid, sound generator, or combination device) over the others.

These reviews do not say sound masking does not work. They say the evidence base is insufficient to draw strong conclusions, largely because of methodological heterogeneity. This is an important distinction.

Residual inhibition: what happens after the sound stops

One of the most studied phenomena in tinnitus masking is residual inhibition, the temporary suppression of tinnitus perception after a masking sound is turned off.

Perez-Carpena et al. (2021) conducted a systematic review and found that sound stimuli produced complete residual inhibition in 34.5% of patients (range: 5.6 to 72%). A broader estimate from Galazyuk et al. (2019) found that approximately 78% of tinnitus subjects experience some degree of residual inhibition, with 65% experiencing substantial suppression.

The neural mechanism was investigated by Galazyuk, Voytenko, and Longenecker (2017), who found that approximately 40% of spontaneously active neurons in the inferior colliculus showed suppression of firing extending roughly 40 seconds after a 30-second stimulus. Suppression duration increased proportionally with stimulus duration. These findings closely parallel the psychoacoustic properties of residual inhibition in patients.

Frequency specificity of residual inhibition

The Perez-Carpena et al. review also found that higher residual inhibition rates were achieved with pure tones and narrowband noise centred on the individual's tinnitus pitch, compared to broadband noise. Roberts et al. (2008) confirmed that residual inhibition functions overlap the tinnitus spectrum and the region of hearing loss in the audiogram: masking sounds that cover the hearing loss region are most effective at producing residual inhibition.

This is a key finding for anyone exploring sound masking: frequency matters. Broadband noise produces residual inhibition in some people, but sounds that target the tinnitus frequency region appear to produce it more consistently.

Noise colours: does the type of noise matter?

Barozzi et al. (2017) compared white, pink, and red (brown) noise in a controlled trial with 40 tinnitus patients. Both groups showed significant improvement. No significant difference between noise colours was found. Two-thirds of patients preferred white noise; the remaining patients chose brown noise. Mondelli et al. (2020) compared four noise types and also found no statistically significant differences: "the four noises were equally effective."

The evidence suggests that no single noise colour is clinically superior. Individual preference and comfort predict adherence better than any specific spectral profile.

Enriched acoustic environments: a promising approach

An animal study by Norena and Eggermont (2005) found that cats exposed to an enriched acoustic environment (spectrally matched to the expected hearing loss range) after noise trauma showed much less hearing loss and prevented cortical map reorganisation, compared to cats placed in quiet environments. This provided foundational evidence that structured sound exposure after cochlear damage can counteract the maladaptive neural plasticity associated with tinnitus.

In humans, Cuesta et al. (2022) studied 83 tinnitus patients who received personalised broadband noise filtered by individual hearing loss curves, listened to for 1 hour daily over 4 months. 96% of participants (80 of 83) achieved clinically relevant improvement (20+ point THI reduction). A follow-up study by Cuesta and Cobo (2024) with sequential stimuli (random-frequency tone sequences) found that 90% of patients achieved clinically relevant improvement, requiring only 1 hour daily for 4 months, compared to standard TRT requiring 4 to 8 hours daily over 12 to 18 months.

Customisation research: does personalisation improve outcomes?

Searchfield, Durai, and Linford (2017) published a state-of-the-art review in Frontiers in Psychology identifying five major personalisation approaches: hearing compensation, pitch-matched therapy, maskability, reaction to sound, and psychosocial factors. Their critical finding: "although many therapies mentioned customization, few could be classified as being personalized." Most approaches modify treatment using only a single patient characteristic.

Wang et al. (2020) reviewed the state of sound therapy for subjective tinnitus and concluded that customised sound therapy consistently outperformed non-customised approaches. Patients with more severe initial tinnitus demonstrated superior treatment responses. Extended interventions of 6 to 12 months demonstrated more robust outcomes compared to shorter protocols.

A randomised controlled trial by Goshtasbi et al. (2025) tested smartphone-based customised sound therapy in 92 participants and found significantly greater improvement in the treatment group (TFI scores 16.7 vs. 1.9, P < .001), with 38.3% achieving clinically meaningful reduction.

Sleep and tinnitus: what the data shows

Gallo et al. (2023) found that 72.2% of tinnitus participants self-rated their sleep quality as poor, with a strong correlation between tinnitus severity and poor sleep (r = 0.582). Pan et al. (2015) found that 47.7% of patients reported that being in a quiet place made their tinnitus perception worse.

Sound therapy during sleep has been studied: Theodoroff et al. (2017) randomised 60 participants to three groups using sound therapy during sleep for 3 months and found that tinnitus-matched and noise stimuli produced greater TFI reduction than passive bedside sound generators, supporting the concept that targeted sound during sleep may provide benefit beyond generic background noise.

What this means (and what it does not mean)

The research shows that:

1. Tinnitus is generated in the brain through compensatory neural amplification after hearing damage, including damage invisible on standard hearing tests.
2. External sounds can change tinnitus perception during exposure. This is well-documented across decades of research.
3. Residual inhibition is real. Approximately 78% of tinnitus subjects experience some temporary suppression after sound exposure, and frequency-targeted sounds produce higher rates than broadband noise.
4. No single noise colour is superior. Clinical trials find no significant differences between white, pink, and brown noise.
5. Personalised and frequency-targeted approaches show promising results, though the evidence base needs larger trials and longer follow-up periods.
6. Cochrane reviews cannot confirm strong efficacy for sound therapy alone, primarily due to methodological heterogeneity across studies.

What this does not mean: this research does not prove that any specific app, device, or protocol will change your experience of tinnitus. Every study cited here used controlled conditions that may not translate to self-directed use. Individual responses vary widely.

Why I built this tool

I built siasola Tinnitus Masking Sounds because I have tinnitus and I wanted precision control over pitch, layering, and mixing. The research on frequency-targeted masking, residual inhibition, and customisation informed the features I built: per-layer pitch controls, a 5-layer mixer, 95+ sounds, and a pitch exploration tool. The app is a sound customization tool, not a medical device. It does not claim to produce any specific outcome.

If you have tinnitus, talk to an audiologist. Read the research yourself. Make informed decisions with professional guidance.

References

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Disclaimer

This article is for educational purposes only. It is not medical advice. siasola Tinnitus Masking Sounds is a sound customization tool, not a medical device. It does not diagnose, treat, cure, or prevent any condition. If you have tinnitus, consult a qualified healthcare professional about your specific situation.