The diagnosis of superior canal dehiscence (SCD) is challenging and audiograms play an important role in raising clinical suspicion of SCD. The typical audiometric finding in SCD is the combination of increased air conduction (AC) thresholds and decreased bone conduction thresholds at low frequencies. However, this pattern is not always apparent in audiograms of patients with SCD, and some have hearing thresholds that are within the normal reference range despite subjective reports of hearing impairment. In this study, we used a human temporal bone model to measure the differential pressure across the cochlear partition (PDiff) before and after introduction of an SCD. PDiff estimates the cochlear input drive and provides a mechanical audiogram of the temporal bone. We measured PDiff across a wider frequency range than in previous studies and investigated whether the changes in PDiff in the temporal bone model and changes of audiometric thresholds in patients with SCD were similar, as both are thought to reflect the same physical phenomenon.
We measured PDiff across the cochlear partition in fresh human cadaveric temporal bones before and after creating an SCD. Measurements were made for a wide frequency range (20 Hz to 10 kHz), which extends down to lower frequencies than in previous studies and audiograms. PDiff = PSV- PST is calculated from pressures measured simultaneously at the base of the cochlea in scala vestibuli (PSV) and scala tympani (PST) during sound stimulation. The change in PDiff after an SCD is created quantifies the effect of SCD on hearing. We further included an important experimental control—by patching the SCD, to confirm that PDiff was reversed back to the initial state. To provide a comparison of temporal bone data to clinical data, we analyzed AC audiograms (250 Hz to 8kHz) of patients with symptomatic unilateral SCD (radiographically confirmed). To achieve this, we used the unaffected ear to estimate the baseline hearing function for each patient, and determined the influence of SCD by referencing AC hearing thresholds of the SCD-affected ear with the unaffected contralateral ear.
PDiff measured in temporal bones (n = 6) and AC thresholds in patients (n = 53) exhibited a similar pattern of SCD-related change. With decreasing frequency, SCD caused a progressive decrease in PDiff at low frequencies for all temporal bones and a progressive increase in AC thresholds at low frequencies. SCD decreases the cochlear input drive by approximately 6 dB per octave at frequencies below ~1 kHz for both PDiff and AC thresholds. Individual data varied in frequency and magnitude of this SCD effect, where some temporal-bone ears had noticeable effects only below 250 Hz.
We found that with decrease in frequency the progressive decrease in low-frequency PDiff in our temporal bone experiments mirrors the progressive elevation in AC hearing thresholds observed in patients. This hypothesis remains to be tested in the clinical setting, but our findings suggest that that measuring AC thresholds at frequencies below 250 Hz would detect a larger change, thus improving audiograms as a diagnostic tool for SCD.