China
Africa
Explore chapters and articles related to this topic
Anatomy and Physiology of Hearing
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Ananth Vijendren, Peter Valentine
Once sound is delivered into the cochlea through the stapes-oval window interface, a cochlear traveling wave is generated that traverses the BM. The arrangement of organ of Corti and basilar and tectorial membranes across the length of the cochlea gives rise to a ‘tonotopic’ relationship due to the variations in stiffness, thickness, and mass along these structures from base to apex. High-frequency sounds are best represented at the basal end and low frequencies at the apex. The movement of the BM creates relative motion between the tectorial membrane and the stereocilia of the IHCs. This allows ion channels to open and depolarise the cell, resulting in synaptic release of glutamate and firing of afferent nerve fibres.
Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Sound waves are transmitted by the pump-like effect of the stapes in the oval window, which creates shock waves that are passed to the round window where the energy dissipates. The pressure wave is transmitted through the perilymph, and leads to vibration of the basilar membrane, depending on the frequency of the sound. When the basilar membrane oscillates, the tectorial membrane has a shearing effect across the hair cells, stimulating the cochlear nerve fibers.
Nonconventional Clinical Applications of Otoacoustic Emissions: From Middle Ear Transfer to Cochlear Homeostasis to Access to Cerebrospinal Fluid Pressure
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Blandine Lourenço, Fabrice Giraudet, Thierry Mom, Paul Avan
Given this generation mechanism, it is thus easily conceivable that DPOAEs exist in the absence of cochlear amplifier, provided OHCs still contain functional mechanotransduction channels in their hair bundles. This is indeed an unusual situation in which sensorineural hearing loss is due to too weak mechanotransduction currents when OHC transduction channels open (decreased endocochlear potential, for example, or impaired coupling between tectorial membrane and hair cells).
The role of serum osmolality in Meniere’s disease with acute sensorineural hearing loss
Published in International Journal of Audiology, 2023
One possible aetiology is that cochlear hair cells were damaged by potassium intoxication after Meniere’s attack (Schuknecht 1986; Merchant, Rauch, and Nadol, 1995). Additionally, recent studies have added insight into the tectorial membrane that defective proteins otogelin and alpha-tectorin cause fragile tectorial membrane, leading to a severe perturbation of endolymph and loss of interaction between the tectorial membrane and stereocilia (Roman-Naranjo et al., 2020). Temporal bone histopathological study also demonstrated severe cochlear hydrops combined with atrophied tectorial membrane incorporated into cells of the organ of Corti in an MD donor (Schuknecht and Gulya 1983). Hence, this histopathological finding further supports that impaired interaction between the tectorial membrane and stereocilia may induce hearing deterioration.
EAS-Combined electric and acoustic stimulation
Published in Acta Oto-Laryngologica, 2021
Anandhan Dhanasingh, Ingeborg Hochmair
It is now understood that once the sound hits the OW, it creates an intracochlear vibration, and more precisely, it causes a vibration of the basilar membrane (BM) – all the way from OW to its apical end, the helicotrema. The travelling wave namely passes through different frequencies which are logarithmically distributed along the BM – from high at the OW, to lower towards the apex. Now depending on the cochlear health, inner-hair cells on stimulated pitch regions during the BM vibration (Figure 1(A)) get excited and fulfil their function as mechanoreceptor cells by transforming the mechanical force received from the BM underneath them into electric signals. This mechanical force actuates the inner-hair cells to bend against the tectorial membrane, which is covering them. The bending opens small channels in the inner-hair cells, allowing ions in the surrounding fluid (endolymph of the scala media) to rush in and convert the physical movement to an electrochemical signal which excites the auditory nerve, and which then sends the electric signals to the brainstem – and after subsequent auditory functionalities, the patient eventually perceives a relevant sound [1]. The outer-hair cells are different group that mechanically amplify low-level sound that enters the cochlea and such amplification may be powered by the movement of their hair bundles.
Integrity of the tectorial membrane is a favorable prognostic factor in atlanto-occipital dislocation
Published in British Journal of Neurosurgery, 2020
Gil Kimchi, Gahl Greenberg, Vincent C. Traynelis, Christopher D. Witiw, Nachshon Knoller, Ran Harel
The underlying instability in AOD is often attributed to rupture of the tectorial membrane and alar ligaments.2 The craniocervical junction is supported anteriorly by a ligamentous complex that comprises two distinct groups;12 the first includes the atlanto-condylar articulation, the cruciate ligament and the anterior atlanto-occipital ligament. This group provides stability chiefly to the atlanto-cranial and the atlanto-dental complexes. The second group of ligaments provides stability to the cranium-odontoid complex. It consists of the tectorial membrane, the apical ligament and the alar ligaments. Of special importance within that group is the tectorial membrane; this strong collagenous continuum of the posterior longitudinal ligament lies posteriorly to the transverse ligament and connects the dorsum of the dens to the clivus. Its primary role is to resist hyperextension, although it may also serve to limit hyperflexion as well.13 The prominent role of the tectorial membrane in craniocervical stabilization is well elucidated in a cadaver study,14 in which the authors removed the alar and transverse ligaments and applied various manipulations on the CCJ. They revealed that the tectorial membrane acts as the ‘second line of defense’ by preventing the odontoid process from translating posteriorly and consequently compressing the spinal canal.