Tinnitus and Hyperacusis Show Distinct Brainstem Signatures in Adults With Normal Audiograms

A new Massachusetts Eye and Ear study finds that adults who report ringing in the ears or unusual sound sensitivity, but who pass a standard hearing test, still carry measurable signs of cochlear nerve injury and show different brainstem activity depending on which symptom they experience.

For decades, audiology textbooks have framed tinnitus and hyperacusis (a heightened sensitivity to everyday sounds) as poorly understood "central" disorders that are mostly invisible to objective tests. The standard pure-tone audiogram, which checks how soft a beep you can detect at each pitch, often comes back normal in these patients. They are then told there is nothing wrong with their hearing, even though their daily life says otherwise.

A team at the Eaton-Peabody Laboratories, part of Massachusetts Eye and Ear and Harvard Medical School, has now sharpened that picture. Using a sensitive electrical recording from the inner ear and brainstem, they show that tinnitus and hyperacusis share an underlying peripheral injury (loss of cochlear nerve fibers) but produce two distinct neural fingerprints further up the auditory pathway.

Background: Why the Researchers Looked at This

Tinnitus is the perception of a sound, often described as ringing, hissing, or buzzing, that has no external source. Hyperacusis is a related but separate problem in which ordinary sounds, such as a dishwasher or a child laughing, feel painfully loud or intolerable. Both can be devastating, and both are common: large population surveys put tinnitus prevalence in adults at roughly 10 to 15 percent.

Animal research over the past 15 years has built a strong case that the trigger for many of these cases is cochlear nerve degeneration, sometimes called "hidden hearing loss." Hidden hearing loss refers to a loss of the synapses connecting the inner ear's hair cells to the auditory nerve, even when the hair cells themselves still work and the audiogram still looks normal. The brain, deprived of part of its expected input from the ear, is thought to "turn up the gain" centrally, which can produce phantom sound (tinnitus) or oversensitivity (hyperacusis). What had been less clear is whether tinnitus and hyperacusis use the same central gain mechanism, or different ones.

The new study set out to test that question directly in human listeners with clinically normal hearing.

How the Study Was Done

The researchers recruited adults whose audiograms were within 20 dB HL across the standard speech frequencies from 0.25 to 8 kHz, and whose extended high-frequency thresholds (above 8 kHz, where age-related and noise-related damage often shows up first) were also within 20 dB HL. By any conventional standard, all of these participants would be told their hearing is normal.

Each participant filled out the Hyperacusis Handicap Questionnaire, a validated scale for sound sensitivity, and was assessed for tinnitus. The team then recorded click-evoked electrocochleography (ECochG), a sensitive electrical readout from electrodes near the eardrum that can capture the earliest stages of the auditory pathway, from the cochlear hair cells through the auditory nerve and into the brainstem.

To separate the contribution of the peripheral nerve from the contribution of the brainstem, the team applied two different filters to the same recording. A high-frequency filter (470 to 3000 Hz) emphasizes the fast, peripheral auditory nerve response. A low-frequency filter (3.3 to 470 Hz) brings out the slower brainstem components that ride on top of the nerve response. Mixed-effects and sequential regression analyses were then used to ask which parts of the response were linked to tinnitus, which were linked to hyperacusis, and how much of each effect was independent.

What the Researchers Found

The high-frequency, peripheral part of the recording told a consistent story. Both participants with tinnitus and participants with elevated hyperacusis scores showed reduced peripheral amplitudes compared with their unaffected peers, despite all having normal audiograms. The pattern is consistent with cochlear nerve degeneration, the same kind of injury that animal models have linked to noise overexposure, aging, and certain ototoxic drugs.

Once the analysis moved past the auditory nerve and into the brainstem, however, the two symptoms started to look different. In the high-pass waveforms, the cochlear nucleus gain (a very early brainstem response) was selectively elevated in participants with tinnitus, regardless of how they scored on the hyperacusis questionnaire. In other words, the cochlear nucleus appeared to be amplifying the limited input it was getting, but only in people who heard phantom sound.

The low-pass waveforms revealed the opposite pattern for hyperacusis. A later brainstem component, and the size of that later component relative to the earlier one, was enlarged in participants with high hyperacusis scores, independent of whether they had tinnitus. That points to a different stage of central gain, further up the brainstem, that tracks how unpleasant ordinary sounds feel rather than whether the person hears a phantom tone.

Sequential regression analyses confirmed that these two effects only partially overlap. Each symptom carried information that the other did not. Tinnitus and hyperacusis, in this sample, behaved like related but distinct forms of central compensation to a shared peripheral injury.

What It Means for People with Hearing Loss

For people who have been told their hearing is fine but who are still struggling with tinnitus or sound sensitivity, this study is validating. It adds to a growing line of evidence that "normal audiogram" is not the same as "no auditory damage," and it gives clinicians an objective way to look for the kind of cochlear nerve loss that animal models have predicted for years.

It also suggests that future treatments may need to be matched to the symptom rather than to the audiogram. A therapy aimed at reducing cochlear nucleus hyperactivity might help phantom sound but do little for sound tolerance, while a therapy aimed at later brainstem stages might do the reverse. For now, sound therapy approaches that gently fill in missing input, such as soft background sound, low-level amplification of speech frequencies, and structured exposure to comfortable everyday sounds, remain the cornerstone of clinical care.

Sound Sensitivity and Phantom Sound: Why Gentle, Steady Amplification Matters

One practical implication of the new findings is that calmly returning a richer, more even sound environment to the ear may help quiet the centrally amplified gain that drives both tinnitus and hyperacusis. That is not a cure. It is the working clinical idea behind hearing aids and sound therapy in this group.

For adults whose audiograms are at or near the OTC threshold and who want a research-aligned approach to gentle, fine-grained amplification, Panda Quantum is built around the kinds of features that matter here. It is a 16-channel receiver-in-canal device with active noise reduction, so it can soften abrupt loud transients that often trouble hyperacusis listeners while still bringing back the speech-band detail the brain is missing. Its Bluetooth support lets users stream gentle background sound, podcasts, music, or guided sound therapy directly into the ears for masking, which is the most common self-management strategy for tinnitus.

Quantum also includes the Panda app-based in-ear hearing test. After delivery, the user pairs the device with the Panda app, runs a frequency-specific hearing test through the hearing aid itself, and the app automatically programs gain and frequency response to match the user's audiogram, similar to what an audiologist does at a clinical fitting. With up to 80 hours of total battery from the case, a 5-year warranty, and a 45-day return window, it is built for users who want to give an evidence-aligned, audiogram-matched approach a real trial. OTC devices are approved for mild-to-moderate hearing loss; people with severe or profound loss still benefit most from a clinical fitting.

Limitations of This Research

The study is cross-sectional, so it cannot prove that cochlear nerve degeneration causes tinnitus or hyperacusis, only that they travel together in adults with normal audiograms. Electrocochleography is a noisy measure at the single-person level, and the high-pass and low-pass filtering approach, while clever, is an inferential way to separate peripheral from central contributions rather than a direct anatomical measurement. The cohort was also restricted to adults with normal hearing, so the findings may not generalize to people with measurable audiometric loss, where central gain may already have shifted.

What to Do With This

If you experience persistent tinnitus or strong sound sensitivity despite a "normal" hearing test, you are not imagining it. Ask your audiologist or ENT about extended high-frequency testing, electrocochleography where available, and structured sound enrichment or masking therapy. The research increasingly supports the idea that subtle cochlear nerve injury is real, that tinnitus and hyperacusis can arise from related but distinct central responses to it, and that gentle, steady reintroduction of sound is one of the few tools currently available to help.

Vasilkov V, Liberman MC, Zhao Y, de Gruttola V, Polley DB, Maison SF. Brainstem Correlates of Tinnitus and Hyperacusis in Normal-Hearing Listeners: Distinct Neural Signatures Linked to Cochlear Nerve Degeneration. Ear and Hearing. 2026. Retrieved from PubMed. DOI 10.1097/AUD.0000000000001830