Quantitative evaluation of myelinated nerve fibres and hair cells in cochleae of humans with age-related high-tone hearing loss
Quantitative evaluation of myelinated nerve fibres and hair cells in cochleae of humans with age-related high-tone hearing loss
复制标题
DOI:
10.1016/0378-5955(95)00158-1
复制
发表时间:
1995-11-01
期刊:
影响因子:
2.8
通讯作者:
SchrottFischer, A
中科院分区:
文献类型:
--
作者:
Felder, E;SchrottFischer, A
In this study 9 human temporal bones from 8 individuals were fixed with Karnovsky solution by perilymphatic perfusion within 1-3 h after death and examined using the 'block-surface method' (Spoendlin and Brun, 1974; Spoendlin and Schrott, 1987) and the 'micro-dissection method' (Johnsson and Hawkins, 1967). The audiogram of 7 individuals showed high-tone hearing loss, typical for sensory-neural presbycusis. The inner (IHC) and outer hair cells (OHC) and the myelinated nerve fibers in the osseous spiral lamina were counted to correlate audiometric curves with hair-cell and nerve-fiber densities. The 'block-surface' method allows accurate hair-cell and myelinated nerve-fiber enumeration with maximal preservation of cochlear structures.The most significant change in the cochlea was not the expected loss of hair cells but an evident loss of nerve fibres in the spiral lamina along the entire length of the cochlea. This loss of nerve fibres was found to be age-related. Reductions up to 30-40% in comparison to normal-hearing middle-aged persons were found in cochleae from persons older than 60 years. In 2 cases only 13% of the fibres remained in some regions of the cochlea. The hair-cell counts showed a reduction of approximately 80% of the OHCs, mainly in the apical parts of the cochlea, and only little differences in the number of IHCs as compared with a group of normal-hearing middle-aged persons.We conclude that neither loss of hair cells nor primary degeneration of nerve fibres alone can fully explain the high-tone loss. Probably injuries of hair cells or neuronal elements at the cellular level can cause threshold elevation.