The Role of Electrophonics in Electroacoustic Stimulation of the Guinea Pig Cochlea *†H. Christiaan Stronks, *Huib Versnel, *Vera F. Prijs, *‡John C. M. J. de Groot, *Wilko Grolman, and *Sjaak F. L. Klis *Department of Otorhinolaryngology and Head and Neck Surgery, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands; ÞNICTA Canberra Research Laboratory, Canberra, Australia; and þDepartment of Otorhinolaryngology and Head & Neck Surgery, Leiden University Medical Center, Leiden, The Netherlands Hypothesis: Interactions between cochlear responses to com- bined electrical and acoustic stimulation (EAS) depend on electrically evoked hair cell activity (i.e., electrophonics). Background: Although relevant for EAS strategies in cochlear implant users with residual low-frequency hearing, cochlear responses to EAS are not well characterized. Previously, we have shown that acoustically evoked compound action potentials (CAPs) can be suppressed by electrical stimulation. In the present study, we characterized the role of electrophonics in CAP sup- pression in guinea pigs, under conditions representative of clini- cally applied EAS. Methods: Electrophonics depend on the frequency spectrum of the electric pulse train, which is mainly determined by pulse width and, to a lesser extent, by pulse rate. We measured sup- pression of tone-evoked CAPs by electric pulse trains, while varying the pulse width (80 Y 400 Ks, n = 5) and the pulse rate (500 Y 4000 pps, n = 5). The role of outer hair cells (OHCs) in electrophonics was tested in animals with varying degrees of OHC loss (n = 24). Results: Suppression of acoustically evoked CAPs varied with pulse width, indicating that electrophonics were involved. Short pulse widths resulted in minimal CAP suppression at low acoustic frequencies. Pulse rate did not significantly affect CAP suppression. OHC loss had no significant effect on electrophonic activity. Conclusion: Electrophonic activity was present in cochleae with extensive basal hair cell loss, indicating that electrophonics can occur in EAS users. Our results show that short pulse widths are optimal for use in EAS stimulation strategies, on the assumption that minimal suppression is best. Key Words: Compound action potentialVElectrocochleographyVHybrid cochlear implantVOuter hair cellVResidual hearing. Otol Neurotol 34:579Y587, 2013. Recently, hybrid implants have been developed that combine a cochlear implant with a conventional hearing aid, delivering combined electrical and acoustic stimu- lation (EAS) in the same ear (1,2). EAS can be applied in people who have sufficient residual low-frequency acoustic hearing, sometimes even without the need for amplification. EAS increases speech understanding in noise and improves the esthetic quality of sound, when compared with electric hearing alone (3,4). Because of these beneficial effects of residual hearing, we assume that it should be optimally used and that effects of electrical stimulation on acoustic hearing should be minimized. Electrical stimulation in acoustically sensitive cochleae can generate auditory-nerve responses by at least 3 mechanisms: 1) direct stimulation of spiral ganglion cells (5), 2) generation of basilar membrane movements and hair cell activation in much the same way as acoustic stimuli do (6Y9), and 3) direct stimulation of inner hair cells (IHCs) (7). Generally, the second mechanism is re- ferred to as electrophonics (10Y13), although broader definitions include the third mechanism as well (14). For clarity, we refer to the second mechanism to define electrophonics. Outer hair cells (OHCs) are thought to play a role in the second mechanism by initiating basilar membrane movements because of their electromotile response (15Y18). However, other studies suggest that electrophonics can be generated in the absence of OHCs (10,11,19). Because selection criteria for cochlear im- plantation continue to expand, EAS users can have Address correspondence and reprint requests to H. Christiaan Stronks, Ph.D., NICTA Canberra Research Laboratory, Tower A, 7 London Circuit, Canberra ACT 2601, Locked Bag 8001, Canberra ACT 2601, Australia; E-mail: Christiaan.Stronks@nicta.com.au The authors declare no conflicts of interest. Conflicts of Interest and Source of Funding: This study was supported by the Heinsius-Houbolt Fund (Wassenaar, The Netherlands). Otology & Neurotology 34:579Y587 Ó 2013, Otology & Neurotology, Inc. 579 Copyright © 2013 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.