Active middle ear implants (AMEI) have been used to treat hearing loss in patients for whom conventional hearing aids are unsuccessful for varied biologic or personal reasons. Several studies have discussed feedback as a potential complication of AMEI usage, though the feedback pathway is not well understood. While reverse propagation of an acoustic signal through the ossicular chain and tympanic membrane constitutes an air-conducted source of feedback, the implanted nature of the device microphone near the mastoid cortex suggests that bone conduction pathways may potentially be another significant factor. This study examines the relative contributions of potential sources of feedback during stimulation with an AMEI.
Four fresh-frozen, hemi-sectioned, human cadaver specimens were prepared with a mastoid antrostomy and atticotomy to visualize the posterior incus body. A Carina active middle ear implant actuator (Cochlear Ltd., Boulder, CO) was coupled to the incus by two means: (1) a stereotactic arm mounted independently of the specimen and (2) a fixation bracket anchored directly to the mastoid cortical bone. The actuator was driven with pure-tone frequencies in 1/4 octave steps from 500 to 6000 Hz. Acoustic sound intensity in the ear canal was measured with a probe tube microphone (Bruel & Kjær, Nærum, Denmark). Bone-conducted vibration was quantified with a single-axis laser Doppler vibrometer (Polytec Inc., Irvine, CA) from both a piece of reflective tape placed on the skin overlying the mastoid and a bone-anchored titanium screw and pedestal (Cochlear Ltd., Centennial, CO) implanted in the cortical mastoid bone.
Microphone measurements revealed ear-canal pressures of 60–89 dB SPL, peaking in the frequency range below 2 kHz. Peak LDV measurements were greatest on the mastoid bone (0.32–0.79 mm/s with mounting bracket and 0.21–0.36 mm/s with the stereotactic suspension); peak measurements on the skin ranged from 0.05 to 0.15 mm/s with the bracket and 0.03 to 0.13 mm/s with stereotactic suspension.
AMEI produce both air- and bone-conducted signals of adequate strength to be detected by the implanted device microphone, potentially resulting in reamplification. Understanding the relative contribution of these sources may play an important role in the development of targeted mitigation algorithms, as well as surgical techniques emphasizing acoustic isolation.
1Department of Otolaryngology, University of Colorado School of Medicine, Aurora, Colorado, USA;
2Cochlear Boulder LLC, Boulder, Colorado, USA; and
3Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, Colorado, USA.
RMBH was funded by NIH NIDCD T32 DC-012280.
The authors have no conflicts of interest to disclose.
Received September 27, 2017; accepted June 27, 2018.
Address for correspondence: Renee M. Banakis Hartl, MD, AuD, Department of Otolaryngology, University of Colorado School of Medicine, 12631 E. 17th Ave, MS B205, Aurora, CO 80045, USA. E-mail: Renee.BanakisHartl@ucdenver.edu