7Extended High-Frequency Audiometry & Hidden Hearing Loss

FWhy a normal audiogram can lie

The routine pure-tone audiogram stops at 8 kHz and reports thresholds in 5–10 dB steps. A patient who hears down to 0–15 dB HL across that range is called “normal-hearing” — yet many such patients have troublesome tinnitus. The mistake is to treat a normal audiogram as a normal cochlea.

The audiogram is a coarse instrument. It samples only eight or nine frequencies, it ignores everything above 8 kHz where damage usually begins, and it measures the faintest detectable tone rather than how the ear codes everyday sound. A great deal of cochlear and neural injury can hide beneath a normal-looking tracing [2017].

For the tinnitus work-up this matters enormously. If we accept the audiogram at face value we may label the patient “idiopathic” and stop looking, when in fact there is measurable peripheral damage that both explains the tinnitus and supports the deafferentation model of central gain.

TExtended high-frequency audiometry (>8 kHz)

Extended high-frequency (EHF) audiometry tests the 9–16 kHz range (some systems reach 20 kHz) using specialised circumaural transducers. The cochlear base, which transduces these frequencies, is the first region damaged by noise, ageing and ototoxins — so EHF thresholds elevate before the standard audiogram ever moves.

In tinnitus patients with a normal conventional audiogram, EHF thresholds are frequently elevated relative to controls, and the tinnitus pitch often falls at or just above the edge of the audible region [2015]. This fits the edge-of-loss / central-gain model: tinnitus arises at the frequency border where peripheral input drops away.

EHF testing is most useful in young patients with noise or ototoxic exposure, in monitoring cisplatin or aminoglycoside therapy, and in the “normal-audiogram” tinnitus patient where it provides objective evidence of early cochlear injury to share in counselling.

CCochlear synaptopathy — the hidden lesion

Animal work showed that noise exposure causing only a temporary threshold shift can permanently destroy up to half the synapses between inner hair cells and auditory-nerve fibres, while leaving hair cells — and therefore thresholds — intact [2009]. The low-spontaneous-rate, high-threshold fibres that code suprathreshold sound are preferentially lost. This cochlear synaptopathy is the leading mechanism for “hidden hearing loss.”

Because these fibres do not set the quiet-tone threshold, the audiogram stays normal. What suffers is the coding of complex sound, especially in noise, and the reduced auditory-nerve output is a plausible trigger for the central gain that produces tinnitus [2009]. The deafferentation is real even when the audiogram is silent.

Histopathology in human temporal bones confirms substantial age-related and noise-related synapse and neuron loss that precedes hair-cell loss [2017], validating the concept beyond the animal model.

CProbing the hidden lesion in the clinic

No single clinical test is a confirmed assay for synaptopathy, but a battery moves the diagnosis forward. The most-studied measures are: word recognition in noise (disproportionately poor for the audiogram); the ABR wave-I amplitude (reduced when auditory-nerve output falls, while wave V is preserved by central gain); and the middle-ear-muscle reflex, which depends on the same vulnerable fibres [2016].

A weakened or elevated acoustic (middle-ear-muscle) reflex has emerged as a particularly promising correlate — in humans with noise exposure and tinnitus the reflex is measurably weaker than in matched controls [2017]. Combined with EHF thresholds and speech-in-noise scores, it builds a converging picture.

Individual-differences studies show these suprathreshold measures track together and separate listeners that the audiogram cannot [2015]. The practical message for the tinnitus clinician: when the audiogram is normal but the complaint is real, test above 8 kHz, test in noise, and look at wave I and the reflex before reaching for “idiopathic.”