Relations between cochlear histopathology and hearing loss in experimental cochlear implantation

Abstract

This study reviews the cochlear histology from four hearing preservation cochlear implantation experiments conducted on 73 guinea pigs from our institution, and relates histopathological findings to residual hearing. All guinea pigs had normal hearing prior to surgery and underwent cochlear implantation via a cochleostomy with a silastic-platinum dummy electrode. Pure tone auditory brainstem response (ABR) thresholds from 2 to 32 kHz were recorded prior to surgery, and at one and four weeks postoperatively. The cochleae were then fixed in paraformaldehyde, decalcified, paraffin embedded, and mid-modiolar sections were prepared. The treatment groups were as follows: 1) Systemic dexamethasone, 0.2 mg/kg administered 1 h before implantation, 2) Local dexamethasone, 2% applied topically to the round window for 30 min prior to cochlear implantation, 3) Local n-acetyl cysteine, 200 μg applied topically to the round window for 30 min prior to implantation, 4) inoculation to keyhole-limpet hemocyanin (KLH) prior to implantation, and 5) untreated controls. There was a significant correlation between the extent of the tissue reaction in the cochlea and the presence of foreign body giant cells (FBGCs), new bone formation and injury to the osseous spiral lamina (OSL). The extent of the tissue response, as a percentage of the area of the scala tympani, limited the best hearing that was observed four weeks after cochlear implantation. Poorer hearing at four weeks correlated with a more extensive tissue response, lower outer hair cell (OHC) counts and OSL injury in the basal turn. Progressive hearing loss was also correlated with the extent of tissue response. Hearing at 2 kHz, which corresponds to the region of the second cochlear turn, did not correspond with loco-regional inner hair cell (IHC), OHC or SGC counts. We conclude that cochlear injury is associated with poorer hearing early after implantation. The tissue response is related to indices of cochlear inflammation and injury. An extensive tissue response limits hearing at four weeks, and correlates with progressive hearing loss. These latter effects may be due to inflammation, but would also be consistent with interference of cochlear mechanics.

Effect of Both Local and Systemically Administered Dexamethasone on Long-Term Hearing and Tissue Response in a Guinea Pig Model of Cochlear Implantation

“…We have observed this previously in animals receiving lower doses of medications where there was minimal impact upon hearing [O'Leary et al, 2013]. In this study, osteoneogenesis was commonly seen in association with endosteal trauma, but it is also known to occur in the cochlea after non-surgical damage such as meningitis, infection and autoimmune disease [Hoistad et al, 1998;Tinling et al, 2004;Durisin et al, 2010], so endosteal trauma appears not to be a prerequisite for its development.…”

Assessment of Cochlear Trauma During Cochlear Implantation Using Electrocochleography and Cone Beam Computed Tomography

“…Besides acute cochlear trauma during surgery, postoperative mechanisms seem to influence hearing preservation. Early inflammatory responses (33) or endolymphatic hydrops (34) could lead to hearing loss during the early postoperative phase, whereas tissue responses (8,35) and excitotoxicity because of electrical stimulation (36) could, among other factors, lead to delayed loss of residual hearing within months. Therefore, to further explore the correlation between trauma during surgery and postoperative hearing loss and gain more insight regarding the incidence of postoperative mechanisms, a tool to assess cochlear trauma during surgery is needed.…”

Correlation of Electrophysiological Properties and Hearing Preservation in Cochlear Implant Patients

“…However, it remains unclear whether with modern electrode designs and surgical techniques, the main reason for postoperative hearing loss is acute intracochlear trauma. Other mechanisms have been proposed, and recent publications have suggested postoperative mechanisms play a relevant role (5,6).…”