The science of sound and the mechanics of listening
One of the most elegant summaries of the processes by which sounds are produced, transmitted and then heard by the human ear was written by Aldous Huxley in his 1928 novel, “Point Counter Point”. Huxley’s prose simplifies the actual workings of the inner ear a little too much for my own (modern-day) comfort, but I consider his words as a perfect starting point for my own synopsis. Describing the events that surround a ‘pause for thought’ in a tedious conversation, Huxley wrote:
Pongileoni’s bowing and the scraping of the anonymous fiddlers had shaken the air in the great hall, had set the glass of the windows looking on to it vibrating; and this in turn had shaken the air in Lord Edward’s apartment on the further side. The shaking air rattled Lord Edwards' membrana tympani; the interlocked malleus, incus and stirrup bones were set in motion so as to agitate the membrane of the oval window and raise an infinitesimal storm in the fluid of the labyrinth. The hairy endings of the auditory nerve shuddered like weeds in a rough sea; a vast number of obscure miracles were performed in the brain, and Lord Edwards ecstatically whispered 'Bach!'
The listening process
And so the listening process begins. The malleus, incus and stirrup (or stapes) bones that Huxley mentions are amongst the smallest bones in the human body, and their strategic position between the eardrum (Huxley’s membrana tympani) and the labyrinthine inner ear does indeed permit an ‘infinitesimal storm’ in the fluid-filled cochlea (the part of the inner ear that is sensitive to sound). Well before the time that Huxley wrote this passage, however, scientists had recognised that a great deal of additional signal processing went on between the initiation of this ‘storm’ and the auditory nerve’s signalling of the sound to the brain.
Illustration of the movement of the organ of Corti in response to waves travelling along the cochlea. The inner hair cells (right) signal the wave's presence to the brain by activating the auditory nerves (the red flash along the yellow 'wire')
The significance of this additional processing was not fully recognised until the latter part of the 20th century, when we first realised that the two classes of sensory receptor that line our hearing organs had very different functions. The receptors are not quite the 'hairy endings' of the nerves that Huxley's artistic licence suggests, but his analogy does conjure up a wonderful picture in my own mind. In the late 1960's, scientists found that a group of receptors known as inner hair cells gave rise to almost 95% of the fibres that run to the brain in the auditory nerve. These, then, were the cells that actually signal the presence of a sound to the brain.
The other, roughly three times more numerous group of receptors in the ear are the outer hair cells. And while the outer hair cells are not known to signal anything at all to the brain (so far), they are absolutely essential for normal hearing. The outer hair cells perform the task of amplifying the sound-evoked movements of the fluids that fill the inner ear. In essence, they overcome the physical effects of drag in the cochlea, and permit even the faintest of sounds to initiate Huxley's 'infinitesimal storm'. Without these cells, the movements become damped, and the inner hair cells are left with too little stimulation to evoke a response. And so we lose our hearing.
Illustration of progressive loss of outer hair cells due to for example prolonged exposure to loud noise. Inner hair cells (top) can remain unaffected
Deafness Research UK estimates that as many as 8 million Britons (that's more than 12% of the population) suffer significant degrees of hearing loss. The origin of the loss in the vast majority of this population is thought to be the improper function in the inner ear. The outer hair cell are particularly vulnerable to a wide variety of insults, including exposures to loud-sounds, disease, and ototoxic drugs, as well as the “normal” processes of ageing. And once this function is lost, it seems impossible to recover.
My own research, funded in part by Deafness Research UK, is aiming to improve our understanding of exactly how the inner ear works, and what goes wrong in cases of hearing loss. Building on some startling discoveries made in the late 20th century, I am investigating the way that the motile outer hair cells amplify the sound-evoked motion of the basilar membrane (an elastic structure that can be likened to both a tuned drum skin – from the perspective of an incoming sound - and a trampoline – from the perspective of a acrobatic hair cell).
Over the last few years, I have demonstrated that while amplification is important for all sounds, it varies in both degree and in nature from one end of the coiled-up cochlea to the other. As the different regions along the length of the cochlear spiral encode different frequencies of sound, this means that different frequencies are processed in different ways: basically, the high frequency sounds that excite the most proximal, basal coils of the cochlea are amplified much more than the low frequency sounds, but the low frequency sounds are amplified much more evenly once they reach the distal, apical coils. The degree of evenness in the amplification seems to correspond (inversely) with the degree of distortion in the temporal waveforms of a sound, and it is well known that low-frequency sounds are perceptually rich in temporal information.
Another aspect of my research is revealing how the brain can modulate the amount of sound amplification that the outer hair cells produce. The modulation signals are carried by a group of nerve fibres that run outwards, from the brainstem to the cochlea, and innervate the outer hair cells almost exclusively. At present, it appears that these signals can only turn down the gain of the cochlear amplifier (that is, they only reduce the responses to sound), so this system is unlikely to offer any ways to assist people with a hearing loss, but the perceptual effects of the gain control in normal-hearing people may still be substantial.
Another little-known fact about listening is that when your ears amplify a sound, a small amount of the sound actually leaks back out into the environment: Most normal ears therefore actually produce sound, as well as receiving and detecting it. The phenomenon is known as the otoacoustic emission process, because the ear (the oto-) is acting as an emitter of sound (the acoustic emission).
Otoacoustic emissions are hugely relevant in a medical context, because they permit non-invasive assays of the sound processing that takes place in the outer, middle and inner ears combined. One of their most widespread applications is in the screening of neonatal infant’s hearing, for example; where the successful early detection of a hearing impairment can be crucial to a child’s development.
I am currently involved in an in-depth study of the processes that underlie the formation of otoacoustic emissions in the cochlea. My aim is to decipher exactly which regions of the cochlea are responsible for the emission of which frequency components in an emission, such that, in the future, audiologists will be better equipped to treat the various forms of hearing loss that correlate with abnormal pattern of otoacoustic emission.
The region of the cochlea which is responsible for a specific component in an emission is linked theoretically to the amount of time that it takes for the emission to come back out of the cochlea, and early indications from my lab suggest that the emissions take just as much time to get back out of the cochlea as a sound of the same frequency takes to reach a given region of the cochlea on its way in. I am hopeful that these studies, as well as the link between the cochlea’s mechanics and the control signals sent from the brain, will allow otoacoustic emissions to be used to probe a listener’s ears even more thoroughly in the future.
Dr Nigel Cooper is an experimental biophysicist who gained his PhD in cochlear nerve physiology at Keele University in 1989. After spells in the US and Australia as a post-doctoral researcher, he returned to the UK in 1996 to take up a Royal Society University Research Fellowship at the University of Bristol. Dr Cooper moved to Keele University in October 2002, where he became a Senior Lecturer in the School of Life Sciences.