Conservation of residual hearing during cochlear implantation has been a focused area of CI research since the first report in 1989.1 Retention of low-frequency acoustic hearing may allow fine structure processing, enhance speech understanding in noise, sound localization, and music appreciation. Hearing conservation has been made possible by advances in surgical techniques, low-trauma electrodes and the use of steroids (see ICIT Surgeons’ Blog 7/1/15; 8/1/15; 12/1/15; 1/1/16; 2/1/16; 3/1/16; 12/5/16; 3/7/17).
Although residual hearing is frequently conserved (not destroyed) during implantation, at this time there are no widely available methods to actively preserve it. Delayed loss of residual hearing after implantation is known to occur in a substantial number of patients.
Scheperle, Tejani, Omtvedt, Brown, Abbas, Hansen, Gantz, Oleson, and Ozanne2 recently described longer-term outcomes in 85 people with residual hearing who were implanted at the University of Iowa. Thirty-eight percent of subjects experienced delayed loss of residual acoustic hearing, often within the first year. No significant differences were found when comparing round window cochleostomy with bony cochleostomy or comparing four different electrode styles. These findings demonstrate excellent surgical technique and electrode design and direct our attention to reactive physiologic processes that are as yet undefined.
Of particular interest, subjects with delayed precipitous drops in acoustic threshold also had abrupt changes in electrode impedance but not necessarily in ECAP findings. The authors suggest these findings may indicate a change in the electrode environment (e.g. a fibrotic response altering cochlear micromechanics) rather than the usual explanation—loss of stimulable neural elements. Prior studies support the notion that the extent of fibrous growth is related to progressive loss of acoustic hearing.3,4
Cochlear implant surgeons perform minimally traumatic surgery to avoid damaging residual neural elements, but no methods are generally available actively to preserve those structures. In the Iowa study, 38% of subjects with initial conservation of acoustic hearing had subsequent delayed loss, usually within 12 months. Nonetheless, ECAPs were often not similarly diminished, a finding that may indicate a mechanical effect of the fibrous electrode sheath. Alternatively, it could indicate loss of cochlear hair cell function in excess of ganglion cell function. Look for further research in this domain. In the near future, drug eluting CI electrodes, neurotrophin-producing intra-cochlear cellular transplants, direct gene therapy, or other regenerative techniques may become available for actively preserving residual hearing.
1. Boggess WJ, Baker JE, Balkany TJ. Loss of residual hearing after cochlear implantation.Laryngoscope. 1989. 99:1002-5.
2. Scheperle RA, Tejani VD, Omtvedt JK, Brown CJ, Abbas PJ, Hansen MR, Gantz BJ, Oleson JJ, Ozanne MV. Delayed changes in auditory status in cochlear implant users with preserved acoustic hearing. Hear Res (2017) 350: 45-57.
3. O'Leary SJ, Monksﬁeld P, Kel G, Connolly, T, Souter MA, Chang A, Marovic P, O'Leary JS, Richardson R, Eastwood H. 2013. Relations between cochlear histopathology and hearing loss in experimental cochlear implantation. Hear Res. 298, 27-35.
4. Wilk M, Hessler R, Mugridge K, Jolly C, Fehr M, Lenarz T, Scheper V, 2016.