The ear, of course, provides one of the five senses of the human body. The outer ear, consisting of the pinna and outer ear canal, is basically the sound gathering portion of anatomy. The input impedance at the entrance to the ear canal would be important for the acoustic load of earphones but is of little consequence for the consideration of, say, implantable middle ear devices. Our sense of directionality is dependent on differential arrival times at the outer ear, and the binaural difference in loudness and arrival time at the auditory cortex of the brain is the neurophysiological basis of determining directionality of sound.
The outer ear is connected to the middle ear by the tympanic membrane through the ear canal. The middle ear consists of the tympanic membrane, ear ossicles (malleus, incus, and stapes), an attic air space dorsal to the middle ear space, the middle ear space containing the ossicles, the antrum with air-containing air cells, and the aditis ad antrum, which connects the antrum and middle ear space. As the impedance-matching portion of the auditory pathway, the middle ear converts variations in air pressure into variations in fluid pressure (perilymph in the cochlea), where the footplate of the stapes enters the cochlea or inner ear. This impedance mismatch from air to fluid mechanics is accomplished by the middle ear anatomy and mechanics, with the primary basis of middle ear impedance matching being the surface area ratio of the tympanic membrane and the footplate of the stapes. For normal sound transmission (but not excessively high frequencies) the ossicles act as a unit, a solid body, and the footplate moves as a piston. Hence, the middle ear transfer function would involve the acoustic input pressure at the tym panic membrane and the middle ear output being the same as the input pressure in the scala vestibuli of the cochlea (through the stapes footplate). Transfer function and impedance characteristics are important for middle ear hearing devices when the ossicular chain is preserved, residual hearing is unimpaired and the ability of high fidelity of amplification is provided by a MEIHD.
The inner ear is the cochlea, a fluid-filled chamber where displacement of the fluids by a traveling wave is converted into a nerve action potential by hair cells. The 30,000 hair cells act as miniature displacement transducers that respond to deformations in the perilymph (cochlear fluid). They elicit action potentials that are tonotopically arranged (in an ordered frequency array) both in the cochlea and the brain. Cochlear outer hair cells respond to the traveling wave in the cochlea, have a contractile function (actin filaments), and serve as controllable amplifiers for the inner hair cells, which send action potentials to the auditory cortex. Loss of outer hair cells results in about a 60-dB loss of hearing. The inner ear normally encodes frequencies by responding to the cochlear fluid movements where different frequencies cause maximum vibration amplitude at different points along the basilar membrane in the cochlea. The threshold for hearing is 1011 M of movement by the tympanic membrane with a dynamic range of 120 dB (sound pressure level, or SPL). Higher frequencies cause traveling waves in the basal portions of the basilar membrane, while lower frequencies affect apical regions of the membrane. This is called tonotopic organization (frequency selectivity) and the cochlear acts as a spectrum analyzer.
In reality, the "sensorineural" hearing loss that is treated by hearing aids and MEIHDs is the same pathology as is indicated for cochlear implants: loss of inner ear hair cells. In moderate to severe hearing loss, the reduction in hair cell numbers is such that sensitivity to sounds has been reduced; amplified sounds or ossicular movements recruit a greater portion of the remaining hair cells and socially adequate hearing is restored. In profound hearing loss, the hair cell population is so low that neither acoustic amplification by hearing aids nor mechanical overdrive by MEIHDs can provide adequate restoration of hearing. Direct stimulation of spiral ganglion cells by passing electrical current across these nerves effectively bypasses the hair cell transducers and initiates action potentials to the first relay in the auditory pathway to the brain, the cochlear nucleus. In yet a third form of neural hearing loss, the Vlllth cranial nerve, the statoacoustic nerve, has been damaged or diseased and the auditory pathway interrupted. This most often occurs during surgical removal of acoustic neuromas, tumors that invade the VIIIth nerve. In this instance, for patients with no VIIIth nerve, neural prostheses have been designed for provision of an auditory signal by directly stimulating the cochlear nucleus in the brain stem by electrical means. The auditory brainstem implant is the most recent of neural prostheses to be implanted for a form of neural deafness. Still, it may be appropriate to refer to all of the above forms of deafness simply as "sensory" impairments, as hearing is one of the five senses.
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