That Sound No One Else Can Hear
Hearing a ringing, buzzing, or hissing that no one around you can hear is one of the more disorienting things the body can do to you. If it started suddenly — after a loud concert, a bout of illness, or apparently out of nowhere — the uncertainty can feel worse than the sound itself. Is something wrong? Is it permanent? Is this a sign of something serious?
This article will explain not just what triggers tinnitus, but why those triggers cause the brain to generate a phantom sound. Understanding the mechanism, many people find, takes some of the fear out of it.
What Causes Tinnitus: The Core Answer
Tinnitus is most commonly triggered by damage to the hair cells in the inner ear — from noise exposure, aging, certain medications, or other causes. This damage reduces the auditory signal reaching the brain. The brain responds by turning up its own internal amplifier, a process called central gain, which produces spontaneous neural activity perceived as sound even in silence. This is why tinnitus is ultimately a brain phenomenon, not just an ear problem. The ear may start the process, but the sound itself is generated in the brain’s auditory networks (Langguth et al. (2013); Henton & Tzounopoulos (2021)).
The Triggers: What Starts the Process
Several different events can reduce cochlear input enough to set off the chain of events described above.
Noise-induced hearing loss is the most common trigger. Loud sound — whether a single blast or years of occupational exposure — physically damages the hair cells in the cochlea. Once destroyed, these cells do not regenerate.
Age-related hearing loss (presbycusis) gradually reduces hair cell function across higher frequencies. Tinnitus is more prevalent in older adults for exactly this reason, though it can occur at any age.
Ototoxic medications can damage cochlear hair cells as a side effect. The most commonly implicated include high-dose aspirin and NSAIDs, certain aminoglycoside antibiotics, loop diuretics, and the chemotherapy drug cisplatin. If you have recently started a new medication and noticed tinnitus, tell your doctor.
Earwax (cerumen) blockage reduces the amount of sound reaching the cochlea, which can temporarily alter auditory processing. Tinnitus from this cause typically resolves when the blockage is cleared.
Head, neck, or jaw injuries can affect the auditory pathway or change the mechanical input to the inner ear. Temporomandibular joint (TMJ) problems fall into this category — the jaw joint sits very close to the ear canal and shares neural pathways with the auditory system.
Ménière’s disease, a condition involving fluid pressure changes in the inner ear, causes episodic tinnitus alongside vertigo and fluctuating hearing loss.
Pulsatile tinnitus deserves a separate mention. Unlike the continuous ringing or buzzing of neurogenic tinnitus, pulsatile tinnitus is rhythmic, often synchronised with the heartbeat, and usually has an actual internal sound source — typically a vascular cause such as turbulent blood flow near the ear. Pulsatile tinnitus warrants prompt medical evaluation to rule out treatable vascular conditions.
In all these cases, the trigger starts the process — but none of these peripheral events directly creates the sound you hear. That happens in the brain.
The trigger (ear damage, blockage, medication) starts the chain of events. The phantom sound itself is generated by the brain’s auditory networks in response to reduced cochlear input.
How the Brain Generates the Phantom Sound
To understand why reduced cochlear input causes a phantom sound, three interconnected mechanisms are worth knowing about.
Central gain: turning up a radio with no signal
Imagine a radio receiver that keeps amplifying its circuits when the broadcast signal gets weak — eventually the amplification itself produces audible static. The brain does something similar. When cochlear hair cells stop sending their normal electrical signals, auditory neurons that have lost their usual input begin firing spontaneously at higher rates. The brain treats this increased neural activity as if it were a real sound signal (Langguth et al. (2013)). A comprehensive 2021 review in Physiological Reviews confirmed that this central gain increase — the brain’s attempt to compensate for missing peripheral input — is one of the primary mechanisms initiating tinnitus (Henton & Tzounopoulos (2021)).
Tonotopic map reorganisation: the neighbourhood expands
The auditory cortex is organised like a piano keyboard: different regions process different frequencies, and adjacent frequency zones sit next to each other on the cortical surface. When hair cells tuned to a particular frequency are damaged and go quiet, the cortical region that processed that frequency loses its normal input. Over time, neighbouring neurons — those tuned to adjacent frequencies — begin to colonise the silent zone. This reorganisation of the cortical frequency map correlates with tinnitus severity (Eggermont (2015)). In plain terms: the brain’s internal map of sound gets redrawn around the damaged region, and the redrawn boundary is where the phantom tone lives.
Loss of lateral inhibition: the brake fails
Normally, inhibitory circuits — neurons that use the neurotransmitter GABA — act as a brake on spontaneous neural activity. They suppress background firing so that only genuine, meaningful signals get through. When cochlear input is lost, these GABAergic inhibitory circuits become less effective. Without adequate inhibition, large populations of auditory neurons fire synchronously, generating a coherent, organised neural signal that the brain interprets as a specific tone or noise rather than diffuse neural static (Langguth et al. (2013); Henton & Tzounopoulos (2021)).
Animal studies offer a striking illustration of this mechanism. Research by Galazyuk and colleagues showed that enhancing GABAergic inhibition with a pharmacological agent completely and reversibly eliminated tinnitus-like behaviour, while removing the drug caused it to return. This is consistent with the idea that inhibitory circuit failure is a proximate cause of the phantom percept, not merely a side effect of central gain.
One of the clearest pieces of evidence that tinnitus is brain-generated rather than ear-generated comes from a clinical observation: sectioning the auditory nerve — physically cutting the connection between the cochlea and the brain — does not reliably eliminate chronic tinnitus. In some cases it makes it worse. Once the brain has reorganised around the phantom signal, the signal continues even without any peripheral input at all.
Many people find it reassuring to know that their tinnitus is a real, neurologically generated experience — not something they are imagining, not a sign that their brain is malfunctioning in a dangerous way. The same neural plasticity that creates tinnitus is also what makes the brain amenable to retraining.
Why the Limbic System Decides How Bad It Feels
Here is something counterintuitive: the measured loudness of tinnitus — how loud it registers on audiological testing — is a poor predictor of how distressed a person will be by it. Many people with objectively loud tinnitus are barely bothered by it; others with faint tinnitus are significantly affected. The difference lies not in the auditory signal itself, but in how the brain evaluates it.
The limbic system, including the amygdala and connected structures in the prefrontal cortex, assigns emotional weight to sensory signals. When tinnitus is first perceived, these structures evaluate whether the signal represents a threat. If the brain classifies the phantom sound as threatening or significant, it locks attentional and emotional resources onto it — making it harder to ignore and, perceptually, louder.
Research on the neural correlates of tinnitus distress has identified measurable changes in the ventromedial prefrontal cortex (vmPFC) and nucleus accumbens — structures that normally suppress signals that have been evaluated as non-threatening — in people with chronic, distressing tinnitus. Where these suppression systems work well, tinnitus fades into the background. Where they are less effective, the phantom signal stays foregrounded in awareness (Galazyuk et al. (2012)).
This is also why stress and fatigue reliably worsen perceived tinnitus severity. Neither stress nor tiredness changes the underlying neural signal — but both reduce the brain’s capacity to suppress unwanted input, so the same signal feels louder and more intrusive.
This limbic model has a practical implication: it explains why cognitive behavioural therapy (CBT) works for tinnitus without changing the sound at all. CBT does not reduce the phantom signal — it retrains the brain’s emotional and attentional response to it, reducing the distress that amplifies the experience.
Why Some People With Hearing Loss Get Tinnitus and Others Don’t
Central gain occurs in most people with cochlear damage — so why does tinnitus develop in some and not others? This is a question the research has not fully answered, and it is worth being honest about that.
The NICE clinical guideline notes that 20–30% of people with tinnitus have clinically normal audiometric hearing (NICE (2020)). This suggests that measurable hair cell damage is not always a prerequisite — or that standard hearing tests miss more subtle forms of cochlear dysfunction.
The most compelling current explanation focuses on the integrity of inhibitory circuits. Research by Knipper and colleagues proposes that the key differentiator is not how much central gain increases after hearing loss, but whether GABAergic inhibitory circuits remain intact enough to prevent that gain from generating a coherent phantom signal (Knipper et al. (2020)). Under this model, people whose inhibitory circuits hold up after cochlear damage do not develop tinnitus, even if their central gain has increased.
A complementary theoretical framework — predictive coding — suggests that tinnitus represents the brain making its best guess about missing sensory input, with individual differences in how the brain weighs top-down predictions against bottom-up signals helping to explain why outcomes vary so widely. Both the gain and prediction-based explanations are plausible; neither fully accounts for the observed individual variability (Schilling et al. (2023)).
Possibly genetic factors also affect inhibitory circuit resilience, but specific genetic evidence in humans remains limited. The science is honest about this gap.
If you have noticed new tinnitus — particularly if it is in one ear only, accompanies sudden hearing loss, or has a pulsatile rhythm matching your heartbeat — see a doctor promptly. These patterns can indicate causes that benefit from early assessment.
Key Takeaways
- Tinnitus is most commonly triggered by cochlear hair cell damage from noise, aging, medications, or other causes — but the peripheral trigger only starts the process.
- The sound itself is generated by the brain, through central gain amplification, tonotopic map reorganisation, and the breakdown of inhibitory (GABAergic) circuits that normally suppress spontaneous neural firing.
- Limbic and prefrontal structures determine how distressing tinnitus is — which is why identical acoustic signals cause minor background noise for some people and significant daily disruption for others.
- The fact that tinnitus is brain-generated is not a reason for despair: it is precisely why brain-targeted approaches — sound therapy, CBT, and emerging neuromodulation techniques — can make a real difference.
- If you have noticed new tinnitus, an early ENT evaluation is worthwhile; the acute phase, before central reorganisation becomes entrenched, offers the best chance of resolution or significant improvement.
Understanding what causes tinnitus is the first step toward managing it.
