FEATURE ARTICLE
The Design and Function of Cochlear Implants
Fusing medicine, neural science and engineering, these devices transform human speech into an electrical code that deafened ears can understand
Michael Dorman, Blake Wilson
Hear Here
In normal hearing, sound waves traveling through air reach the
tympanic membrane (ear drum) 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 oval
window, a flexible membrane in the bony shell of the cochlea.
Inside the fluid–filled cochlea, oscillations from the oval
window initiate a traveling wave along the basilar membrane
(one that divides the cochlea along its length). Another flexible
membrane, the round window, moves in a complementary way to
maintain the volume of the incompressible fluid in the cochlea.
The basilar membrane has graded mechanical properties. At the base
of the cochlea, near the oval and round windows, it is narrow and
stiff. At the other end of the cochlea, the apex, the basilar
membrane is wide and flexible. These mechanical properties give rise
to a traveling wave of displacement and to points of maximal
response according to the frequency or frequencies of the pressure
oscillations. For a wave with a single frequency, displacement
increases up to a particular point along the membrane and then drops
precipitously. High frequencies produce maxima near the base of the
cochlea, whereas low frequencies produce maxima near the apex.
Movements of the basilar membrane are sensed by a line of hair
cells, which are attached to the top of the membrane in a matrix
called the organ of Corti. Each hair cell has fine rods of protein,
called stereocilia, emerging from one end. When the basilar
membrane moves, these rods bend as if they were hinged at their
bases. The deflection initiates a chain of electrochemical events
that causes electrical spikes, or action potentials, in
cells of the spiral ganglion. These cells conduct the signal to a
relay station in the brainstem called the cochlear nucleus.
The information ascends through multiple other nuclei on its way to
the auditory cortex, the portion of the forebrain that
processes auditory information.
Within this circuit of cells, a sound's frequency is encoded by two
mechanisms. The first is a place code, which indicates the spot
along the tapered basilar membrane that moves the most. Stereocilia
on the hair cells respond to this displacement and cause action
potentials among the closest spiral–ganglion neurons. The
second mechanism is a temporal code that is produced when neurons
become synchronized, or phase–locked, to the period
of an acoustic wave. In normal hearing, neural responses can easily
match frequencies up to about 1,000 hertz. This phase–locking
ability declines progressively at higher frequencies. The perception
of frequency is probably based on some combination of place and
temporal codes, with the temporal code being effective for low
frequencies only.
Hearing is lost when hair cells become so damaged that they cannot
stimulate cells of the spiral ganglion. Without regular activity,
the portion of that ganglion cell that receives signals, the
dendrite, may atrophy and the cells may die. Fortunately, even in
the case of complete hearing loss, some spiral–ganglion cells
survive and remain connected to the appropriate
frequency–receiving areas in the cochlear nucleus. If
electrical current from the implanted electrodes can cause action
potentials among the remaining cells, then hearing can be restored.
And if multiple groups of neurons (think of these as "neural
channels") can be made to respond in low, middle and high
frequency parts of the cochlea, then perception of speech can be
restored as well.
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