Predicting Atrophy of the Cochlear Stria Vascularis from the Shape of the Threshold Audiogram.

audiograms hearing loss temporal bones

Journal

The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140

Informations de publication

Date de publication:
13 Dec 2023
Historique:
received: 20 06 2023
revised: 02 10 2023
accepted: 10 10 2023
pubmed: 21 10 2023
medline: 21 10 2023
entrez: 20 10 2023
Statut: epublish

Résumé

Several lines of evidence have suggested that steeply sloping audiometric losses are caused by hair cell degeneration, while flat audiometric losses are caused by strial atrophy, but this concept has never been rigorously tested in human specimens. Here, we systematically compare audiograms and cochlear histopathology in 160 human cases from the archival collection of celloidin-embedded temporal bones at the Massachusetts Eye and Ear. The dataset included 106 cases from a prior study of normal-aging ears, and an additional 54 cases selected by combing the database for flat audiograms. Audiogram shapes were classified algorithmically into five groups according to the relation between flatness (i.e., SD of hearing levels across all frequencies) and low-frequency pure-tone average (i.e., mean at 0.25, 0.5, and 1.0 kHz). Outer and inner hair cell losses, neural degeneration, and strial atrophy were all quantified as a function of cochlear location in each case. Results showed that strial atrophy was worse in the apical than the basal half of the cochlea and was worse in females than in males. The degree of strial atrophy was uncorrelated with audiogram flatness. Apical atrophy was correlated with low-frequency thresholds and basal atrophy with high-frequency thresholds, and the former correlation was higher. However, a multivariable regression with all histopathological measures as predictors and audiometric thresholds as the outcome showed that strial atrophy was a significant predictor of threshold shift only in the low-frequency region, and, even there, the contribution of outer hair cell damage was larger.

Identifiants

pubmed: 37863653
pii: JNEUROSCI.1138-23.2023
doi: 10.1523/JNEUROSCI.1138-23.2023
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

8801-8811

Informations de copyright

Copyright © 2023 the authors.

Auteurs

Charanjeet Kaur (C)

Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, Massachusetts 02114 Charanjeet_Kaur@meei.harvard.edu.
Department of Otolaryngology-Head & Neck Surgery, Harvard Medical School, Boston, Massachusetts 02115.

Pei-Zhe Wu (PZ)

Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, Massachusetts 02114.
Department of Otolaryngology-Head & Neck Surgery, Harvard Medical School, Boston, Massachusetts 02115.

Jennifer T O'Malley (JT)

Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, Massachusetts 02114.
Otopathology Laboratory, Massachusetts Eye and Ear, Boston, Massachusetts 02114.

M Charles Liberman (MC)

Eaton-Peabody Laboratories, Massachusetts Eye and Ear, Boston, Massachusetts 02114.
Otopathology Laboratory, Massachusetts Eye and Ear, Boston, Massachusetts 02114.
Department of Otolaryngology-Head & Neck Surgery, Harvard Medical School, Boston, Massachusetts 02115.

Classifications MeSH