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This chapter is an update of the chapter with the same title in the first edition of this book. Parts of the update were drawn from several recent publications, including and . Author BSW is a consultant for MED EL GmbH and author MFD is a consultant for Advanced Bionics LLC. However, none of the statements in this chapter favors either of those companies or any other company.
Deafness and severe impairments in hearing were hopeless conditions until only recently. Controlled electrical stimulation of the auditory nerve changed that, and the resulting return of hearing is now widely regarded as one of the great advances in modern medicine.
The device that produces and presents the electrical stimuli is called a cochlear implant (CI). Just 40 years ago CIs provided little more than a sensation of sound and sound cadences ( ). The implants were useful for an alerting function (e.g., hearing a loud sound that might be an oncoming car) and as an adjunct to lipreading. Many experts in otology and the hearing sciences at the time were highly skeptical that implants could ever support useful speech reception with hearing alone. In the 1980s, however, implant systems with multiple channels of sound processing and multiple sites of stimulation in the cochlea were developed, and these systems supported significantly higher levels of speech reception than their single-channel and single-site predecessors. In the late 1980s and continuing to the present, new and better processing strategies, in conjunction with multielectrode implants, have produced additional large gains in performance. Indeed, a principal conclusion of the 1995 United States National Institutes of Health (NIH) Consensus Conference on Cochlear Implants in Adults and Children ( ) was that “A majority of those individuals with the latest speech processors for their implants will score above 80 percent correct on high-context sentences, even without visual cues.” This degree of functional restoration is remarkable, and far greater than that achieved to date with any other type of neural prosthesis.
More about the history of the CI is presented in Chapter 99 in this book.
The primary purpose of the present chapter is to indicate how electrical stimulation at the auditory nerve can bring a person from total or nearly total deafness to useful hearing. In addition, some possibilities for further improvements in the design and performance of CIs are mentioned. Further information about these topics is presented in several detailed reviews published during the past 10 years, including , and .
In normal hearing sound waves traveling through air reach the tympanic membrane via the ear canal, causing vibrations that move the three small bones of the middle ear. This action produces a piston-like movement of the stapes, the third bone in the chain. The “footplate” of the stapes is attached to a flexible membrane in the bony shell of the cochlea called the oval window. Inward and outward movements of this membrane induce pressure oscillations in the cochlear fluids, which in turn initiate a traveling wave of displacement along the basilar membrane (BM), a highly specialized structure that divides the cochlea along its length. This membrane has graded mechanical properties. At the base of the cochlea, near the stapes and the oval window, it is narrow and stiff. At the other end, near the apex, the membrane is wide and flexible. These properties give rise to the traveling wave and to points of maximal response according to the frequency or frequencies of the pressure oscillations in the cochlear fluids. The traveling wave propagates from the base to the apex. For an oscillation with a single frequency, the magnitude of displacements increases up to a particular point along the membrane and then drops precipitously thereafter. High frequencies produce maxima near the base of the cochlea, whereas low frequencies produce maxima near the apex.
Motion of the BM is sensed by the inner hair cells (IHCs) in the cochlea, which are attached to the top of the BM in a matrix of cells called the organ of Corti. Each hair cell has fine rods of protein, called stereocilia, emerging from one end. When the BM moves at the location of a hair cell, the rods are deflected as if hinged at their bases. Such deflections in one direction increase the release of a chemical transmitter substance at the base (other end) of the cells, and deflections in the other direction inhibit the release. The variations in the concentration of the chemical transmitter substance act at the terminal ends of auditory neurons, which are immediately adjacent to the bases of the IHCs. Increases in chemical transmitter substance increase discharge activity in the nearby neurons, whereas decrements in the substance inhibit activity. Changes in neural activity thus reflect events at the BM. These changes are transmitted to the brain via the auditory nerve, the collection of all neurons that innervate the cochlea.
The steps described above are illustrated in the top panel of Fig. 100.1 , which shows a cartoon of the main anatomical structures, including the tympanic membrane, the three bones of the middle ear, the oval window, the BM, the IHCs, and the adjacent neurons of the auditory nerve.
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