The explosion of the cochlear implant industry has been hugely beneficial to individuals who may otherwise be deaf, but many hearing people do not realize that most hearing impaired people would see negative or no impact from cochlear implants. External hearing aids are the only solution for such people, and while hearing aid technology has been developing for a very long time, there are certain well-understood hearing barriers that external aids have never been able to solve.
So what is wrong with hearing aids? The short answer is that no matter how you change the sound entering the ear, a damaged inner ear will never process sound the same way a healthy one does.
The long answer requires a slightly more complex understanding of hearing. I have spent the past few months in a cochlear mechanics research lab, and while I am not a biologist, I have been briefed on the basic mechanisms enough times to feel I can faithfully explain them here.
Sounds, which we know to physically consist of waves of pressure, enter through the outer ear. The middle ear converts these incoming pressure waves to a very fine vibration in the stapes - a bone attached to the oval window of the cochlea. This vibrating bone will plunge in and out of the oval window, compressing and decompressing the fluid in the cochlea. The result is that the membranes within the cochlea vibrate in a manner controlled by the vibrating stapes.
In sum, the simplest mechanical aspects of the ear involve the transmission of variations in pressure outside one's ears to vibrations in a membrane inside one's ears. Unless one were to suffer middle ear damage, this process would go as expected. That is to say that for most hearing impaired individuals who suffer from damage within their inner ear, the problems begin after this sound transmission process.
Atop the basilar membrane in the cochlea rests the organ of corti - the main sensory organ of the ear. Thus, the sensation of sound is mostly linked to the vibration patterns of the basilar membrane. The basilar membrane coils along the whole cochlea, and it encodes sound frequency in position along the coil. That is to say that the position of the most vibration in the basilar membrane directly maps to the frequency of the incoming sound. For complex sounds containing many frequency components, multiple peaks will be seen along the basilar membrane as it vibrates.
This spatial encoding of frequency is the key to our hearing - the vibration of the basilar membrane is what triggers neurotransmitters at that region, so neural signalling at various locations allows us to hear sounds at various frequencies.
As it turns out, this spatial encoding is a purely mechanical property of the membrane. Even a dead person's ear will operate as I have described! So where is the catch? Well there are actually two catches, and they have to do with the sensory cells themselves.
These sensory cells are called hair cells, and they live in the organ of corti. They contain very small "hairs" called stereocilia, and when there are vibrations, these stereocilia push against the tectorial membrane and lean. This leaning causes the opening of ion channels, and due to the electrical potentials of regions in the cochlea, cause a current to flow through the hair cells. This current is the trigger for neural transmission.
Hair cells can die, and in humans, they can never regenerate. This is the first catch - it is clear that if the main sensory element of hearing is dead, then one would become hearing impaired. This also explains the frequency selectivity of some hearing impairments, as hair cells in certain regions of the cochlea may die while others remain in tact.
The second catch is considerably more technical, but has to do with our frequency selectivity. The current that is generated by basilar membrane vibration in a healthy region of the cochlea has a second effect - it actually further vibrates the basilar membrane in that region. This is due to the electromotility of outer hair cells, which is to say that these cells expand and contract as current passes through them. This electromotility adds a forcing to the basilar membrane in a manner that further amplifies vibration in a smaller region of the basilar membrane. This provides both an amplification in perceived sound level, and a more fine frequency resolution, and is known as the cochlear amplifier.
Human speech is very complex, and it requires fine frequency resolution to process. This electrical aspect of cochlear operation also fails in regions where hair cells have died.
The most obvious and least effective hearing aid is one which is simply an audio amplifier. If you imagine an ear in which some fraction of the hair cells have died, an audio amplifier will help to solve the base sensation problem - more living sensory cells will react to louder sounds. However, it will not help people who have fine hearing at certain frequencies but not at others, as all frequencies are being amplified equally. It also will not enhance frequency resolution at all!
A more sophisticated hearing aid contains a filter bank which can be programmed by the user, which, put simply, amplifies different frequency components by different amounts. This is a very nice solution to the amplification problem but not to the frequency resolution problem.
This problem, so far, has only been solved by cochlear implants in patients for whom implants are viable solutions. Cochlear implants use electrodes to directly electrically stimulate the correct frequency bands in the cochlea, bypassing the cochlear amplifier.
So can hearing aids be made better? It is hard to imagine how an external hearing aid may be able to replace the cochlear amplifier. This is why the community surrounding cochlear implants has instead decided to move towards making cochlear implants a more viable solution for more hearing impaired individuals. Efforts on this front look hopeful, and the field is still very young, so perhaps we will see a dramatic decrease in deafness in our lifetimes!
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