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Restoration: Nanotechnology in Tissue Replacement and Prosthetics
Published in Harry F. Tibbals, Medical Nanotechnology and Nanomedicine, 2017
Behind the hair cells is a layer of neurons, the spiral ganglion, which contains four or five times more cells than the sensory cell layers. The network of auditory neurons in the spiral ganglion lies close to the interior or modiolar wall of the cochlear duct. The spiral ganglion neurons control the selection and organization or stimuli that are sent to the auditory cortex in the brain.
Music perception and training for pediatric cochlear implant users
Published in Expert Review of Medical Devices, 2020
CIs are auditory prostheses originally designed to restore speech sounds to people with severe-to-profound sensorineural hearing loss [7]. Unlike hearing aids, CIs do not rely on a functional middle or inner ear to amplify sound. Instead, CIs use an array of 12 to 22 electrodes located in the scala tympani to directly stimulate the organ of Corti or surviving spiral ganglion cells of the distal cochlear nerve [8,9] (Figure 1). These devices have helped support auditory perception and language development [10], so much so that about a third of postlingually deafened CI users achieve maximum performance on sentence recognition tasks in quiet [11] and deafened children who have been implanted at an early age are typically found in mainstream schooling systems with their age-matched counterparts [12]. As a result of the cost savings and performance benefits associated with implantation, the Food and Drug Administration (FDA) criteria for pediatric cochlear implantation has been recently expanded to infants as young as 9 months of age and for single-sided-deafened children aged 5 years or older. Yet, it has been estimated that less than 10% of adults in the United States and other developed countries who meet the current criteria for cochlear implants actually undergo implantation, highlighting its underusage in the present times [13,14].
Hearing loss, lead (Pb) exposure, and noise: a sound approach to ototoxicity exploration
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Krystin Carlson, Richard L. Neitzel
Takahashi, Okamoto, and Saito (1984) found a significant increase in latency of N1 and a significant increase in P1-N1 amplitude after the sixth day of treatment. A significantly longer latency of N1 action potential was observed by Yamamura et al. (1984). Output voltage lowered under 20 dB in the highest Pb treatment group of Yamamura et al. (1987). Whole nerve action potentials were elevated to 25 dB (the authors did not specify baseline or final levels) after five weeks of treatment in results from Yamamura et al. (1989). Histopathology explored by Gozdzik-Zolnierkiewicz and Moszynski (1969) showed axonal degradation and demyelination in the vestibulocochlear nerve (VIII cranial nerve), but no pathology in inner ear cells or in the spiral ganglion.
Exposure to lead, mercury, styrene, and toluene and hearing impairment: evaluation of dose-response relationships, regulations, and controls
Published in Journal of Occupational and Environmental Hygiene, 2020
The mechanism of damage to hearing varies depending on the chemical substance. An acute or chronic neurotoxic effect of exposure to aromatic solvents such as toluene and styrene is central nervous system (CNS) depression (NIOSH 1987; Möller et al. 1990; Greenberg 1997) while chronic exposures affect the inner ear (Pryor et al. 1983; 1987) causing irreversible hearing impairment by poisoning cochlear hair cells and disorganizing their membranous structures (Johnson and Canlon 1994; Campo et al. 2001). Solvents may directly affect the cells of the organ of Corti forming chemically and biologically reactive intermediates including reactive oxygen species, which may trigger the death of these cells (Chen et al. 2007). While exposures to solvents such as styrene and solvent mixtures are associated with disorders in the central auditory pathway (Abbate et al. 1993; Morata et al. 1993; Greenberg 1997; Johnson et al. 2006), exposure to lead and mercury may affect both the cochlea (Rice and Gilbert 1992; Rice 1997) and the central auditory pathways (Discalzi et al. 1993; Otto and Fox 1993; Lasky, Maier, Snodgrass, Hecox, Laughlin 1995; Lasky, Maier, Snodgrass, Laughlin, Hecox 1995). Similar to aromatic solvents, the hearing-damaging effects of lead and mercury are caused by a neurotoxic mechanism (Discalzi et al. 1993; Counter and Buchanan 2002; Hwang et al. 2009). Lead exposure affects cognitive and central auditory nervous system function and peripheral nerve conduction (Araki et al. 1992). Blood lead levels are associated with adverse effects in conduction in the distal auditory nerve and are found to impair conduction in the auditory nerve and pathway in the lower brainstem (Bleecker et al. 2003). Dimethylmercury poisoning is shown to damage the auditory neural system (Musiek and Hanlon 1999) and exposure to methyl mercury chloride causes nerve conduction hypersensitivity in the brainstem (Wassick and Yonovitz 1985). Carbon monoxide and hydrogen cyanide deprive oxygen within the cochlea (Campo et al. 2013) impairing the cochlear function under extreme exposure conditions but have reversible auditory effects when exposure levels are low (Campo et al. 2009). Aminoglycosides penetrate the outer hair cells causing a reaction which generates the release of reactive oxygen species (ROS), resulting in death of cells (Rybak and Ramkumar 2007). Anti-neoplastic drugs cause loss of cochlear hair cells and cells of the spiral ganglion (Hamers et al. 2003). Exposure to nitriles is shown to cause cochlear hair cell losses and spiral ganglion cell losses in animal studies (Crofton et al. 1994; Soler-Martín et al. 2007).