Objectives/Hypothesis: Speech perception scores using cochlear implants have ranged widely in all published series. The underlying determinants of success in word recognition are incompletely defined. Although it has been assumed that residual spiral ganglion cell population in the deaf ear may play a critical role, published data from temporal bone specimens from patients have not supported this hypothesis. The depth of insertion of a multichannel cochlear implant has also been suggested as a clinical variable that may be correlated with word recognition. In the current study these correlations were evaluated in 15 human subjects. Study Design: Retrospective review of temporal bone histopathology-.Methods: Temporal bones were fixed and prepared for histological study by standard techniques. Specimens were then serially sectioned and reconstructed by two-dimensional methods. The spiral ganglion cells were counted, and the depth of insertion of the cochlear implant as measured from the round window was determined. Correlation analyses were then performed between the NU6 word scores and spiral ganglion cell counts and the depth of insertion. Results: The segmental and total spiral ganglion cell counts were not significantly correlated (P > .50) with NU6 word scores for the 15 subjects. Statistically significant correlations were not achieved by separate analysis of implant types. Similarly, no significant correlation between the depth of insertion of the electrode array and postoperative NU6 word score was identified for the group. Conclusion: Although it is unlikely that the number of residual spiral ganglion cell counts is irrelevant to the determination of word recognition following cochlear implantation, there are, clearly, other clinical variables not yet identified that play an important role in determining success with cochlear implantation.
Although hearing loss is the most common presenting symptom in patients with acoustic neuroma, the pathophysiology of hearing loss associated with acoustic neuroma is unknown. Although primary dysfunction of the auditory nerve is intuitively logical, available histopathologic and clinical data suggest that although neural degeneration is common, it alone does not adequately account for hearing loss in many cases. The purpose of this study was to evaluate 11 cases of unoperated unilateral acoustic neuromas. Temporal bones were identified by means of a search mechanism provided by the National Temporal Bone, Hearing, and Balance Pathology Resource Registry and were prepared for light microscopy by standard techniques. Quantification of spiral ganglion cells, hair cells, stria vascularis, and spiral ligament was accomplished for each specimen. In addition, the maximum diameter and volume of each tumor were calculated from histopathologic sections. Increasing tumor size did predict a reduced spiral ganglion count. However, although there was a tendency for decreasing spiral ganglion cell count and for increasing tumor size to predict a higher pure tone average and lower speech discrimination score, these correlations did not reach statistical significance. In tumor ears in which the speech discrimination score was 50% or less, there was always significant degeneration of other structures of the inner ear in addition to neurons, including hair cells, the stria vascularis, and the spiral ligament. Endolymphatic hydrops and eosinophilic precipitate in the perilymphatic spaces were found in 2 of 3 such cases. It is concluded that acoustic neuromas appear to cause hearing loss, not only by causing degeneration of the auditory nerve, but also by inducing degenerative changes in the inner ear. It is hypothesized that the proteinaceous material seen histologically may represent the products of up-regulated genes in acoustic neuroma, some of which may interfere with normal cochlear function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.