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Sensorineural Hearing Loss
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
Linnea Cheung, David M. Baguley, Andrew McCombe
Initially, excessive noise exposure causes a temporary threshold shift (TTS), resulting in a temporary HL. The high-frequency regions of the cochlea are most sensitive (between 3 and 6 kHz). Recovery of the TTS occurs over hours, days, or weeks following exposure. Expected recovery time is dependent on the loudness and duration of the noise presented. However, a permanent threshold shift (PTS) can occur at the initial insult, or it may evolve where there is continuous or repeated excessive noise exposure at levels that would only have otherwise caused a TTS. It is thought that this may be caused by metabolic factors such as excessive neurotransmitter release, changes in cochlear blood flow, and oxidative stress within the hair cells. Structural factors like depolymerisation of actin filaments in the stereocilia, swelling of the stria vascularis, and damage to afferent nerve endings and supporting cells are also thought to play a part. Synaptic connections between inner hair cells and spiral ganglion cells may also be susceptible to noise damage. Importantly, in animal studies, these synapses can be the first site of damage, even without an HL (‘hidden hearing loss’, or synaptopathy). Additionally, genetic susceptibility, smoking and cardiovascular disease, and diabetes have been implicated as risk factors.
Tinnitus
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Hearing loss in its classical meaning regards decreased hearing abilities, which can be measured for instance by pure tone audiometry. However, it is always a good idea to check for speech comprehension and the ability to hear in noise. Even if the pure tone audiometry does not indicate hearing deficiencies, the two latter tests may point at an existing hidden hearing loss. The hidden hearing loss is believed to be a result of cochlear synaptopathy, which describes damaged, malfunctioning or diminished connectivity between the inner hair cells and spiral ganglion fibers and has been a topic of many clinical and basic research investigations in the recent years (Hickox et al., 2017; Liberman et al., 2017). The topic of hidden hearing and loss of connectivity between the sensory inner hair cells and the spiral ganglion neurons is challenging the interest of the scientific and clinical community and is predicted to initiate an emergence of improved diagnostic tools.
Canine Audiology
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Kristine E. Sonstrom, Peter M. Scheifele
Hearing loss in aging dogs, or presbycusis, is indicated by histological evidence of cochlear lesions (Shimada et al., 1998; Ter Haar et al., 2008). Anatomic changes include a decrease of inner and outer hair cell counts, stria ganglion cell packing densities within the basal turn, and a smaller stria vascularis cross-sectional area in all turns. Hearing results from ABR testing indicated a progressive increase in thresholds associated with aging beginning around 8–10 years of age, mostly pronounced in the mid to high-frequency region (8–32 kHz) (Ter Haar et al., 2008). Shimada et al. (1998) identified similar findings from histological examinations in a group of 23 dogs from 3 days to 17 years old. They identified a loss of spiral ganglion cells, atrophy of the organ of Corti and stria vascularis, and thickening of the basilar membrane, most prominent at the base of the cochlea, with findings progressing with age.
Short-term overstimulation affects peripheral but not central excitability in an animal model of cochlear implantation
Published in Cochlear Implants International, 2023
Susanne Schwitzer, Moritz Gröschel, Horst Hessel, Arne Ernst, Dietmar Basta
Beside these physiological mechanisms, morphological changes could be responsible for the observed delayed responses within the auditory brainstem. Neurons in the auditory brainstem expressed c-Fos after an electrical intracochlear stimulation of two hours (Illing and Michler, 2001). c-Fos is a transcription factor for the GAP-43 gene which is responsible for the outgrowth of axonal fibers and the formation of new synapses. These processes are not very fast. This could be the explanation why the excitability in the auditory brainstem was not adapted to the changed cochlear output during the investigated time frame. Possibly this difference opens a diagnostic window to identify a present overstimulation during fitting. An increased ratio over 1 between the eCAP- and eABR-threshold is possibly an indicator of the onset of an intracochlear change in the further processing of electrical stimuli. This was found in the ‘HOS’-group after four and eight hours of stimulation and in the ‘MOS’-group after eight hours of stimulation. Possibly changes in peripheral structures and the processing of electrical stimuli were dose and time dependent. Long-term studies showed that the eABR threshold decrease or do not change over time. Furthermore, long-term electrical stimulation had a small or no effect on spiral ganglion survival (Mitchell et al., 1997; Scheper et al., 2009; Agterberg et al., 2010).
CI in single-sided deafness
Published in Acta Oto-Laryngologica, 2021
Anandhan Dhanasingh, Ingeborg Hochmair
The auditory pathway starts in the cochlea from the inner hair cells of the organ of Corti which send the signal to the spiral ganglion cell bodies (SGCB) through the peripheral neural fibres in response to the acoustic signal. The central axons of the SGCB form the cochlear nerve, and the vestibular nerve joins the cochlear nerve entering the internal auditory meatus (IAM) – commonly called as cochlear-vestibular nerve – which is a clinically relevant location, as any damage to it would normally affect both, auditory and vestibular functions. The nerve in the IAM travels a short distance of around 1cm to reach the surface of the brainstem at the ventral (anterior) cochlear nuclei (CN). Until CN, the neural fibres coming from each ear are kept separated on their own sides. The neural fibres from the ventral CN extend to the dorsal (posterior) CN, and from here most of the fibres cross the midline, travelling up in the contralateral (opposite) lateral lemniscus. At the same time, some fibres travel up in the ipsilateral (same side) lateral lemniscus. From the ventral CN, most of the neural fibres travel up to reach the contralateral superior olivary nuclei, whereas some neural fibres reach the ipsilateral superior olivary nuclei as well (Figure 1).
The role of computed tomography and magnetic resonance imaging for preoperative pediatric cochlear implantation work-up in academic institutions
Published in Cochlear Implants International, 2021
Art A. Ambrosio, Natalie Loundon, Daniel Vinocur, Peter Kruk, Hubert Ducou Le Pointe, Francois Chalard, Matthew Zapala, Daniela Carvalho
Further, additive information from CT imaging includes localizing the course of the facial nerve, independent verification of cochlear malformations, presence of chronic ear disease, as well as further evaluation of the degree of possible post-meningitic labyrinthine ossification. Further, it can characterize small IAC diameter consistent with the possible absence of the cochlear nerve in cases where a MRI is not available (Adunka et al. 2006; Choi and Kaylie, 2017; Connor and Bell, 2009; Mackeith et al., 2012; Palabiyik et al., 2017; Parry et al., 2005; Phelps and Proops, 1999; Stjernholm et al., 2001; Tamplen et al., 2016). Specifically, labyrinthine ossification visualized on CT with soft tissue fibrosis congruently demonstrated on MRI has direct implications on cochlear implant candidacy and surgical team planning with the extent of intracochlear drilling needed. This subsequently affects counseling for parents with respect to the degree of potential damage to spiral ganglion afferents, as in the case of extensive drilling required in the setting of intracochlear ossification (Arts et al., 2002).