Format

Send to

Choose Destination
See comment in PubMed Commons below
Otol Neurotol. 2008 Dec;29(8):1193-7. doi: 10.1097/MAO.0b013e31818a0906.

Generalized arteriosclerosis and changes of the cochlea in young adults.

Author information

1
Otitis Media Research Center, Department of Otolaryngology, University of Minnesota, Minneapolis, Minnesota 55455, USA.

Abstract

HYPOTHESIS:

To disclose the histopathologic findings of the cochlea in young adults with generalized arteriosclerosis.

BACKGROUND:

It is well known that arteriosclerosis begins and progresses during childhood. Although the relationship between arteriosclerosis and auditory function in elderly people was examined in many reports, the histopathologic effect of arteriosclerosis on the cochlea in young adults has not been studied.

METHODS:

This study involved quantitative analysis, including the number of spiral ganglion cells, the loss of cochlear outer hair cells, and the areas of stria vascularis and spiral ligament. It included 10 temporal bones from 6 subjects with generalized arteriosclerosis and 10 age-matched normal control temporal bones from 7 subjects.

RESULTS:

The mean number of spiral ganglion cells in the cochlea with generalized arteriosclerosis was significantly lower than that in normal controls in the basal turn. The mean loss of outer hair cells in the cochlea with generalized arteriosclerosis was significantly greater than that of normal controls in the basal and apical turns. The stria vascularis and spiral ligament were severely atrophic, with generalized arteriosclerosis in the basal turn. There was no significant difference in the thickness of the spiral modiolar artery between generalized arteriosclerosis and normal controls.

CONCLUSION:

Degeneration of the cochlea, especially in the basal turn, was already apparent in young adults with generalized arteriosclerosis.

PMID:
18833016
DOI:
10.1097/MAO.0b013e31818a0906
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center