Comments on: “Auditory Frequency Selectivity and the Cochlear Nerve” (E.F. Evans)

Author(s):  
J. Schwartzkopff
1992 ◽  
Vol 336 (1278) ◽  
pp. 295-306 ◽  

The past 30 years has seen a remarkable development in our understanding of how the auditory system - particularly the peripheral system - processes complex sounds. Perhaps the most significant has been our understanding of the mechanisms underlying auditory frequency selectivity and their importance for normal and impaired auditory processing. Physiologically vulnerable cochlear filtering can account for many aspects of our normal and impaired psychophysical frequency selectivity with important consequences for the perception of complex sounds. For normal hearing, remarkable mechanisms in the organ of Corti, involving enhancement of mechanical tuning (in mammals probably by feedback of electro-mechanically generated energy from the hair cells), produce exquisite tuning, reflected in the tuning properties of cochlear nerve fibres. Recent comparisons of physiological (cochlear nerve) and psychophysical frequency selectivity in the same species indicate that the ear’s overall frequency selectivity can be accounted for by this cochlear filtering, at least in band width terms. Because this cochlear filtering is physiologically vulnerable, it deteriorates in deleterious conditions of the cochlea - hypoxia, disease, drugs, noise overexposure, mechanical disturbance - and is reflected in impaired psychophysical frequency selectivity. This is a fundamental feature of sensorineural hearing loss of cochlear origin, and is of diagnostic value. This cochlear filtering, particularly as reflected in the temporal patterns of cochlear fibres to complex sounds, is remarkably robust over a wide range of stimulus levels. Furthermore, cochlear filtering properties are a prime determinant of the ‘place’ and ‘time’ coding of frequency at the cochlear nerve level, both of which appear to be involved in pitch perception. The problem of how the place and time coding of complex sounds is effected over the ear’s remarkably wide dynamic range is briefly addressed. In the auditory brainstem, particularly the dorsal cochlear nucleus, are inhibitory mechanisms responsible for enhancing the spectral and temporal contrasts in complex sounds. These mechanisms are now being dissected neuropharmacologically. At the cortical level, mechanisms are evident that are capable of abstracting biologically relevant features of complex sounds. Fundamental studies of how the auditory system encodes and processes complex sounds are vital to promising recent applications in the diagnosis and rehabilitation of the hearing impaired.


2012 ◽  
Vol 73 (S 02) ◽  
Author(s):  
A. Kasbekar ◽  
Y. Tam ◽  
R. Carlyon ◽  
J. Deeks ◽  
N. Donnelly ◽  
...  

2021 ◽  
pp. 1-8
Author(s):  
Mustafa Avcu ◽  
Mehmet Metin ◽  
Raşit Kılıç ◽  
Muhammed Alpaslan

Background: In this study, optic coherence tomography (OCT) examination was performed to check whether there was any interaction between ophthalmic axonal structures in unilateral tinnitus patients, and the relationship between optic nerve thickness and cochlear nerve thickness was evaluated. Objective: The aim of the study was to evaluate the relatioship between hearing loss, tinnitus, and nerve thicknesses. Study Design: Prospective study. Setting: Tertiary referral university hospital. Patients: The study included 88 patients with unilateral tinnitus, for which no organic cause could be found in physical examination, psychiatric evaluation, or with imaging methods. Study groups were formed of the tinnitus side and control groups were formed of the healthy side as follows: Group 1 (Non-tinnitus side normal hearing values – n = 30), Group 2 (non-tinnitus side minimal hearing loss – n = 27), Group 3 (non-tinnitus side moderate hearing loss – n = 31), Group 4 (tinnitus side normal hearing values – n = 25), Group 5 (tinnitus side minimal hearing loss – n = 25), and Group 6 (tinnitus side moderate hearing loss – n = 38). Intervention: Retinal nerve fiber layer (RNFL) thickness was evaluated with OCT, and the cochlear nerve cross-sectional area was evaluated with MRI. Main Outcome Measures: RNFL measurements were taken with OCT from the subfoveal area (RNFL-SF) and 1.5 mm temporal to the fovea (RNFL-T µm) and nasal (RNFL-N µm) sectors. On MRI, 3 measurements were taken along the nerve from the cerebellopontine angle as far as the internal auditory canal, and the mean value of these 3 measurements was calculated. Results: When the groups were evaluated in respect of cochlear nerve thickness, a significant difference was seen between Group 1 and both the groups with hearing loss and the tinnitus groups. In the subgroup analysis, a statistically significant difference was determined between Group 1 and Groups 3, 4, 5, and 6 (p = 0.013, p = 0.003, p < 0.001, and p < 0.001, respectively). When the groups were evaluated in respect of the RNFL-SF (µm), RNFL-T (µm), and RNFL-N (µm) values, the differences were determined to be statistically significant (p < 0.001 for all). In the correlation analysis, a negative correlation was determined between hearing loss and cochlear nerve diameter (r: −0.184, p = 0.014), and RNFL-N (r: −0.272, p < 0.001) and between tinnitus and cochlear nerve diameter (r: −0.536, p < 0.001), and RNFL-T (r: −0.222, p < 0.009). Conclusion: The study results clearly showed a relationship between cochlear nerve fiber thickness and hearing loss and the severity of tinnitus in cases with unilateral tinnitus and that there could be neurodegenerative factors in the disease etiology. A similar relationship seen with the RNFL supports the study hypothesis.


2021 ◽  
pp. 014556132199683
Author(s):  
Wenqi Liang ◽  
Line Wang ◽  
Xinyu Song ◽  
Fenqi Gao ◽  
Pan Liu ◽  
...  

The bony cochlear nerve canal transmits the cochlear nerve as it passes from the fundus of the internal auditory canal to the cochlea. Stenosis of the cochlear nerve canal, defined as a diameter less than 1.0 mm in transverse diameter, is associated with inner ear anomalies and severe to profound congenital hearing loss. We describe an 11-month-old infant with nonsyndromic congenital sensorineural hearing loss with cochlear nerve canal stenosis. Next-generation sequencing revealed heterozygous mutations in MYH9 and MYH14, encoding for the inner ear proteins myosin heavy chain IIA and IIC. The patient’s hearing was rehabilitated with bilateral cochlear implantation.


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