Deciphering a Mechanism Behind Bone Conduction Hyperacusis
By Xiying Guan, Ph.D.
Bone conduction hearing is commonly used for practical purposes: Standard hearing tests measure bone conduction thresholds to assess sensorineural hearing; bone conduction hearing aids help patients with conductive and mixed hearing loss; and bone conduction earphones of various types are increasingly popular. However, the underlying mechanism of bone conduction sound transmission to the inner ear has been elusive and poorly understood because bone conduction sound transmission is complex—multiple frequency-dependent mechanisms may be involved.
An understanding of bone conduction has been further hindered due to the inability to measure bone conduction sound transmission directly in the inner ear. Also unclear is how some abnormalities can affect hearing by bone conduction. An example is bone conduction hyperacusis (hypersensitive bone conduction hearing)—an unnerving symptom experienced by patients with superior canal dehiscence (SCD), an abnormal thinness or incomplete closure of one of the bony canals in the inner ear.
Magnitude frequency responses of the scala vestibuli (PSV), scala tympani (PST), and cochlear input pressure drive (PDIFF) during bone conduction stimulation in a representative ear. Black lines are the pressures under typical conditions; red lines are the pressures after a superior canal dehiscence (a hole in one of the inner ear’s bony canals) was produced. This generally increased PSV below 1 kHz. Interestingly, the effects on PST were generally smaller.
However, recent developments now allow the experimental measurement of intracochlear sound pressures during bone conduction in fresh human cadaveric specimens, which can provide detailed information regarding inner-ear sound transmission and estimate hearing function.
For our study published in Scientific Reports in October 2020, we measured bone conduction–evoked sound pressures in two of the fluid-filled canals of the cochlea, the scala vestibuli and scala tympani. We estimated hearing at the base of the cochlea using the cochlear input pressure drive (the differential pressure across the cochlear partition that separates the canals), before and after creating an SCD.
Consistent with clinical audiograms, an SCD increased the bone conduction–driven cochlear input drive below 1 kHz. However, an SCD affected the individual canal pressures in unexpected ways: The SCD increased the scala vestibuli by 5 to 20 decibels significantly between 250 and 550 hertz, but had little effect on the scala tympani.
These findings are inconsistent with the inner-ear compression mechanism that some have used to explain bone conduction hyperacusis. We developed a new computational bone conduction model based on the inner-ear fluid-inertia mechanism, and the simulated effects of the SCD were similar to the experimental findings. This experimental-modeling study suggests that (1) inner-ear fluid inertia is an important mechanism for bone conduction hearing, and (2) the SCD facilitates the flow of sound volume velocity through the cochlear partition at low frequencies, resulting in bone conduction hyperacusis.
The intracochlear pressure measurements verified with the modeling analysis provide a new understanding of bone conduction sound transmission and the mechanism underlying SCD-induced bone conduction hyperacusis.
Xiying Guan, Ph.D., is a 2016 Emerging Research Grants scientist funded by Hyperacusis Research Ltd. He is an instructor in the department of otolaryngology–head and neck surgery, Harvard Medical School, and an investigator at the Eaton-Peabody Laboratories, Massachusetts Eye and Ear.