Biological Mechanism of Cochlear Implant Technology

Sergio Gonzalez Gonzalez

Biological Mechanism of Cochlear Implant Technology

Sergio Gonzalez Gonzalez

Published Date: 2022-01-31

Sergio Gonzalez Gonzalez^*

Department of Neurology, Parc Scientifique Agropolis. Montpellier, France .

*Corresponding Author:: Sergio Gonzalez Gonzalez
Department of Neurology, Parc Scientifique Agropolis. Montpellier, France
E-mail:aurore.marie@cilcare.com

Received date: January 01, 2022, Manuscript No. IPNBT-22-12646; Editor assigned date: January 04, 2022, PreQC No. IPNBT-22-12646; Reviewed date: January 18, 2022, QC No. IPNBT-22-12646; Revised date: January 22, 2022, Manuscript No. IPNBT-22-12646; Published date: January 31, 2022, DOI:10.36648/2573-5349.7.1.105
Citation: Gonzalez SG (2022) Biological Mechanism of Cochlear Implant Technology. J Transl Neurosc Vol:7 No:1

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Description

The World Health Organization reports that hail loss was the most common form of sensitive impairment in humans affecting 360 million persons worldwide, with a frequency of 183 million adult males and 145 million adult ladies. The most common source of hail loss is sensor neural hail loss, characterized by dysfunctions of the sensitive organ the cochlea and its associated structures. These dysfunctions may be inheritable or acquired. In the ultimate case, it can be due to environmental factors similar as chemical agents or noise exposure, or to age related anility. In cases with sensor neural hail loss, the functions of the cochlear cells and napkins are lost. Nonetheless, some audile neurons survive, and the part of the cochlear implants is to stimulate them directly by shunting the cochlea. In this case, the hail of cases with profound hail loss can be successfully rehabilitated with cochlear implants able of garbling and delivering the spectral and the temporal information of sound to the surviving audile neurons. In this review we epitomize the physiological mechanisms involved in hail loss and hair cell apoptosis, the part of cochlear implants in cochlear neuron stimulation, and the clinical advantages and disadvantages related to this cochlear device implantation [1].

Biology of Hearing Loss

The mammalian inner observance is a sensitive organ able of perceiving sound over a range of pressures and securing both infrasonic and ultrasonic frequentness in different species. In mortal hail, sound pressure swells travel down to the observance conduit and beget the vibration of the eardrum. These climates are transmitted to the cochlea via 3 small bones the malleus, the incus, and the stapes, all located in the middle observance. The movement of these bones allows the round window to move and to conduct the movement into the cochlea. The cochlea is also responsible for transducing the mechanical vibration into action eventuality that will propagate towards the part of the brain responsible for hail which allows perceiving a sound [2-4].
The cochlea is a helical structure divided along its length by a membrane, called the basilar membrane. It's large and flexible at its apex, and narrow and stiff at its base. This longitudinal stiffness grade makes the basilar membrane reply else depending on the frequency of the incoming sound. For sounds with energy in the low frequency range, climates are minimal at the apex, while for sounds with energy in the high frequency range, climate are minimal at the base. This results in a tonotopic association of the aural input along the cochlea [5]. The organ of Corte, located on the basilar membrane, houses two different subtypes of sensitive cells arranged along the conduit three rows of external hair cells and one row of inner hair cells, those are the true sensitive hair cells [6]. Each bone possesses dozens of hairs which bend back and forth with the vibration of the basilar membrane. This bending of the hair depolarizes the cell, which releases neurotransmitters onto the sensational whim-whams filaments, provoking an action implicit transmitted to the audile brain structures. Further than 90 of the sensational filaments appear at the inner hair cells. Each fiber has synaptic contact with one inner hair cell which is innervated by around 10-20 filaments. The external hair cells are innervated by only 10 of the sensational whim-whams filaments, and numerous external hair cells meet on a single fiber. These dendrites forming synaptic contact with hair cells compose the helical ganglion, a nervous structure that transmits electrical signals from the cochlea to the central nervous system. One bitsy change in one of these structures or systems can lead to Sensor Neural Hail Loss (SNHL).

Implant Technology

As mentioned ahead, in 2012, the World Health Organization reported that hail loss was the most common form of sensitive impairment in humans, affecting 360 million persons worldwide [7]. The most common source of hail loss is sensor neural hail loss, which accounts for about 90 of reported hail loss and emerges from dysfunctions of the sensitive organ the cochlea and its associated structures. These dysfunctions may be inheritable; 40 genes have been linked to beget deafness [8] or acquired. In this case, it can be due to environmental factors similar as chemical agents or noise exposure, or to age related anility [9].
It's well established that mitochondria are responsible for ATP product, and that this process induces an increase of Reactive Oxygen Species (ROS) similar as superoxide anion, hydrogen peroxide, and hydroxyl radical, playing an essential part in cell signaling [6]. Under normal conditions, ROS produced by the mitochondria are fluently metabolized by endogenous antioxidant mechanisms similar as catalase, superoxide dismutase, glutathione, and balance cell homeostasis. Still, the aging process, pharmacological treatment, or external factors, can alter this balance. This imbalance is called oxidative stress [10]. Several publications confirm that the mitochondrial ROS overproduction plays a crucial part in hail loss by cranking hair cell apoptotic pathways. More precisely, intracellular damage caused by noise, or ototoxic agents similar as aminoglycosides or cisplatin, seems to partake a final common pathway via the cytochrome translocation and capsize activation, leading to hair cell death.
In cases with SNHL, the function of the basilar membrane and the sensitive cells is lost. Nonetheless, some audile neurons survive, and the part of the Cochlear Implants (CI) is to stimulate them directly by shunting the cochlea. In this case, the hail of cases with profound hail loss secondary to ototoxic agents can be rehabilitated successfully with CI able of garbling and delivering the spectral and the temporal information of sound to the surviving audile neurons.
In patients with SNHL, the function of the basilar membrane and the sensory cells is lost. Nevertheless, some auditory neurons survive, and the role of the Cochlear Implants (CI) is to stimulate them directly by shunting the cochlea. In this case, the hearing of patients with profound hearing loss secondary to ototoxic agents can be rehabilitated successfully with CI capable of encoding and delivering the spectral and the temporal information of sound to the surviving auditory neurons.