Sound Perception

Physics and Psychology of Sound

Our auditory systems are well adapted for detecting and interpreting many kinds of information. Sound waves are periodic compressions of air, water or other media. Sound waves vary in amplitude and frequency. The amplitude of a sound wave is its intensity. Loudness is a sensation related to amplitude but not identical to it. For example, a rapidly taking person sounds louder than slow music of the same physical amplitude. 

The frequency of a sound is the number of compressions per second, measured in Hz. Pitch is the related aspect of perception. Higher frequency sounds are higher in pitch. Most adult humans hear sounds ranging from about 15 Hz to somewhat less than 20,000Hz. Children hear higher frequencies than adults, because the ability to perceive high frequencies decreases with age and exposure to loud noises (Schneider, Trehub, Morrongiello, & Thorpe, 1986). 

Structures of the Ear

Anatomists distinguish the outer ear, middle ear, and the inner ear. The outer ear includes the pinna, the familiar structure of flesh and cartilage attached to each side of the head. By altering the reflections of sound waves, the pinna helps us locate the source of a sound. 

After sound waves pass through the auditory canal, they strike the tympanic membrane, or eardrum, in the middle ear. The tympanic membrane vibrates at the same frequency as the sound waves that strike it. The tympanic membrane connects to three tiny bones that transmit the vibrations to the oval window, a membrane of the inner ear.  These bones are sometimes known by their English names: hammer, anvil, and stirrup. The footplate of the stirrup connects to the oval window. The vibrations of the tympanic membrane transform into more forceful vibrations of the smaller stirrup. The net effect converts the sound waves into waves of greater pressure on the small oval window. This transformation is important because more force is required to move the viscous fluid behind the oval window than to move the eardrum, which has air on both sides. 

The inner ear contains a snail-shaped structure called the cochlea. The cochlea contains three long fluid-filled tunnels: the scala vestibule, scala media, and scala tympani. The stirrup makes the oval window vibrate at the entrance to the scala vestibule, thereby setting in motion the fluid in the cochlea. The auditory receptors, known as hair cells, lie between the basilar membrane of the cochlea on one side and the tectorial membrane on the other. Vibrations in the fluid of the cochlea displace the hair cells. A hair cell responds within microseconds to the displacements thereby opening ion channels in its membrane. 

Pitch Perception

The two main ways of coding sensory information are which cells are active and how frequently they fire. The size and stiffness of the basilar membrane determine which part of the basilar membrane with respond to various frequencies of sound with the greatest-amplitude traveling wave. Low-pitched tones cause maximal displacement closer to the apex where the membrane is larger and floppier and high-pitched tones cause maximal displacement near the stiff base of the basilar membrane.

In response to low-frequency sounds (up to about 100Hz - more than an octave below middle C in music), the basilar membrane vibrates in synchrony with the sound waves and auditory nerve neurons fire with each vibration. Soft sounds activate fewer neurons, and stronger sounds activate more. At low frequencies, the frequency of impulses identifies the pitch, and the number of firing cells identifies loudness. 

Because of the refractory period of the axon, as sounds exceed 100Hz, it becomes harder for a neuron to continue firing in synchrony with the sound waves. At medium frequencies, neurons spit into volleys, one volley firing with one vibration and another with the next. These volleys of responses are detected across many auditory nerve receptors. 

At higher frequencies, the area of the basilar membrane with the greatest displacement is used as a place code. In response to high-frequency tones, the neurons in the auditory nerve may fire on every second, third, fourth or later wave. 

The auditory nerve as a whole produces volleys of impulses for sounds up to about 4,000 per second. Most human hearing takes place below 4000Hz, beyond that, even staggered volleys of impulses can’t keep pace with the sound waves. 

Individual Differences

People vary in their sensitivity to pitch. An estimated 4% of people have amusia, impaired detection of frequency changes (Hyde & Peretz, 2004). Amusia is commonly called “tone deafness”. They have trouble detecting a change in sound frequency less than about 10%, whereas other people can detect a change of less than 1% (Loui, Alsop, & Schlaug, 2009). They have trouble recognizing tunes, can’t tell whether someone is singing off-key, and do not detect a “wrong” note in a melody. Many relatives of a person with amusia have the same condition, so it probably has a genetic basis.

Absolute pitch (or perfect pitch) is the ability to hear a note and identify it – for example, “That’s a C sharp.” Genetic predisposition may contribute but the main determinant is early and extensive music training. Not everyone with musical training develops absolute pitch, but almost everyone with absolute pitch had extensive musical training.

Individuals may experience one of two categories of hearing impairments. Diseases, infections, tumorous bone growth, or even excess ear wax can prevent the middle ear from transmitting sound waves properly to the cochlea resulting in conductive deafness. It is sometimes temporary. If it persists, it can be corrected either by surgery or by hearing aids that amplify the stimulus. 

The second category of heading impairment, nerve deafness, results from damage to the cochlea, the hair cells, or the auditory nerve. It can occur in any degree and may be confined to one part on the cochlea, in which case someone hears certain frequencies and not others. Nerve deafness can be inherited (Wang et al., 1998), or it can develop from a variety of disorders (Cremers & van Rijn, 1991; Robillard & Gerdsdorff, 1986), including: certain diseases, inadequate oxygen to the brain during birth, or exposure to loud noises. Researchers have found that exposure to loud sounds produces long-term damage to the synapses and neurons of the auditory system that doesn’t always show up on hearing tests. It might eventually lead to ringing in the ears, extreme sensitivity to noise, or other problems (Kujawa & Liberman, 2009).

References

Cremers, C. W. R. J., & van Rijn, P. M. (1991). Acquired causes of deafness in childhood.  Annals of the New York Academy of Sciences, 630, 197-202.

Hyde, K. L., & Peretz, I. (2004). Brains that are that out of tune but in time. Psychological Science, 15, 356-360.

Kujawa, S. G., & Liberman, M. C. (2009). Adding insult to injury: Cochlear nerve degeneration after “temporary” noise induced hearing loss. Journal of Neuroscience, 29, 14077-14085.

Loui, P., Alsop, D., & Schlaug, G. (2009). Tone deafness: A new disconnection syndrome? Journal of Neuroscience, 29, 10215-10220.

Robillard, T. A. J., & Gersdorff, M. C. H. (1986). Prevention of pre- and perinatal acquired hearing defects: Part I. Study of causes.  Journal of Auditory research, 26, 207-237.

Schneider, B. A., Trehub, S. E., Morrongiello, B. A., & Thorpe, L. A. (1986). Auditory sensitivity in preschool children. Journal of the Acoustical Society of America, 79, 447-452.

Wang, A., Liang, Y., Fridell, R. A., Probst, F. J., Wilcox, E. R., Touchman, J. W., et al. (1998). Associations of unconventional myosin MY015 mutations with human nonsyndromic deafness DFNB3. Science, 280, 1447-1451.