Like our other senses, our audition, or hearing, helps us adapt and survive. Hearing people share information invisibly—by shooting unseen air waves across space. Hearing loss is therefore an invisible disability. To not catch someone’s name, to not grasp what someone is asking, and to miss the hilarious joke is to be deprived of what others know, and sometimes to feel excluded. (As a person with hearing loss, I [DM] know the feeling.)

Most of us, however, can hear a wide range of sounds, and the ones we hear best are those in the range of the human voice. With normal hearing, we are remarkably sensitive to faint sounds, such as a child’s whimper. (If our ears were only slightly more sensitive, we would hear a constant hiss from the movement of air molecules.) We are also remarkably attuned to sound variations. Among thousands of possible human voices, we easily recognize an unseen friend’s, from the moment she says “Hi.” Moreover, hearing is fast. “It might take you a full second to notice something out of the corner of your eye, turn your head toward it, recognize it, and respond to it,” notes auditory neuroscientist Seth Horowitz (2012). “The same reaction to a new or sudden sound happens at least 10 times as fast.” A fraction of a second after such events stimulate the ear’s receptors, millions of neurons have simultaneously coordinated in extracting the essential features, comparing them with past experience, and identifying the stimulus (Freeman, 1991). For hearing as for our other senses, we wonder: How do we do it?

18-1 What are the characteristics of air pressure waves that we hear as sound?

Draw a bow across a violin, and you will unleash the energy of sound waves. Jostling molecules of air, each bumping into the next, create waves of compressed and expanded air, like the ripples on a pond circling out from a tossed stone. As we swim in our ocean of moving air molecules, our ears detect these brief air pressure changes.

Like light waves, sound waves vary in shape (FIGURE 18.1). The height, or amplitude, of sound waves determines their loudness. Their length, or frequency, determines the pitch we experience. Long waves have low frequency—and low pitch. Short waves have high frequency—and high pitch. Sound waves produced by a violin are much shorter and faster than those produced by a cello or a bass guitar.

227

We measure sounds in decibels, with zero decibels representing the absolute threshold for hearing. Every 10 decibels correspond to a tenfold increase in sound intensity. Thus, normal conversation (60 decibels) is 10,000 times more intense than a 20-decibel whisper. And a temporarily tolerable 100-decibel passing subway train is 10 billion times more intense than the faintest detectable sound.

18-2 How does the ear transform sound energy into neural messages?

The intricate process that transforms vibrating air into nerve impulses, which our brain decodes as sounds, begins when sound waves enter the outer ear. An elaborate mechanical chain reaction begins as the visible outer ear channels the waves through the auditory canal to the eardrum, a tight membrane, causing it to vibrate (FIGURE 18.2). In the middle ear, a piston made of three tiny bones (the hammer, anvil, and stirrup) picks up the vibrations and transmits them to the cochlea, a snail-shaped tube in the inner ear. The incoming vibrations cause the cochlea’s membrane (the oval window) to vibrate, jostling the fluid that fills the tube. This motion causes ripples in the basilar membrane, bending the hair cells lining its surface, not unlike the wind bending a wheat field. Hair cell movement triggers impulses in the adjacent nerve cells. Axons of those cells converge to form the auditory nerve, which sends neural messages (via the thalamus) to the auditory cortex in the brain’s temporal lobe. From vibrating air to moving piston to fluid waves to electrical impulses to the brain: Voila! We hear.

228

Perhaps the most intriguing part of the hearing process is the hair cells—“quivering bundles that let us hear” thanks to their “extreme sensitivity and extreme speed” (Goldberg, 2007). A cochlea has 16,000 of them, which sounds like a lot until we compare that with an eye’s 130 million or so photoreceptors. But consider their responsiveness. Deflect the tiny bundles of cilia on the tip of a hair cell by the width of an atom—the equivalent of displacing the top of the Eiffel Tower by half an inch—and the alert hair cell, thanks to a special protein at its tip, triggers a neural response (Corey et al., 2004).

Across the world, 360 million people are challenged by hearing loss (WHO, 2012). Damage to the cochlea’s hair cell receptors or their associated nerves can cause sensorineural hearing loss (or nerve deafness). Occasionally, disease damages these receptors, but more often the culprits are biological changes linked with heredity, aging, and prolonged exposure to ear-splitting noise or music. Sensorineural hearing loss is more common than conduction hearing loss, which is caused by damage to the mechanical system that conducts sound waves to the cochlea.

The cochlea’s hair cells have been likened to carpet fibers. Walk around on them and they will spring back. But leave a heavy piece of furniture on them and they may never rebound. As a general rule, if we cannot talk over a noise, it is potentially harmful, especially if prolonged and repeated (Roesser, 1998). Such experiences are common when sound exceeds 100 decibels, as might occur when in a frenzied sports arena, playing loud music through headphones, or listening to bagpipes (FIGURE 18.3). Ringing of the ears after exposure to loud sounds indicates that we have been bad to our unhappy hair cells. One study of teen rock concert attendees found that after three hours of sound averaging 99 decibels, 54 percent reported not hearing as well, and 1 in 4 had ringing in their ears. As pain alerts us to possible bodily harm, ringing of the ears alerts us to possible hearing damage. It is hearing’s equivalent of bleeding.

The rate of teen hearing loss, now 1 in 5, has risen by a third since the early 1990s (Shargorodsky et al., 2010). Teen boys more than teen girls or adults blast themselves with loud volumes for long periods (Zogby, 2006). Males’ greater noise exposure may help explain why men’s hearing tends to be less acute than women’s. But regardless of gender, those who spend many hours in a loud nightclub, behind a power mower, or above a jackhammer should wear earplugs. “Condoms or, safer yet, abstinence,” say sex educators. “Earplugs or walk away,” say hearing educators.

229

For now, the only way to restore hearing for people with nerve deafness is a sort of bionic ear—a cochlear implant, which 50,000 people a year, including some 30,000 children, now receive (Hochmair, 2013). This electronic device translates sounds into electrical signals that, wired into the cochlea’s nerves, convey information about sound to the brain (FIGURE 18.4). Cochlear implants in deaf kittens and human infants have seemed to trigger an “awakening” of the pertinent brain area (Klinke et al., 1999; Sireteanu, 1999). These devices can help children become proficient in oral communication (especially if they receive them as preschoolers or even before age 1) (Dettman et al., 2007; Schorr et al., 2005). Cochlear implants also help restore hearing for most adults, but only if their brain learned to process sound during childhood.

18-3 How do we detect loudness, discriminate pitch, and locate sounds?

RESPONDING TO LOUD AND SOFT SOUNDS How do we detect loudness? If you guessed that it’s related to the intensity of a hair cell’s response, you’d be wrong. Rather, a soft, pure tone activates only the few hair cells attuned to its frequency. Given louder sounds, neighboring hair cells also respond. Thus, your brain interprets loudness from the number of activated hair cells.

If a hair cell loses sensitivity to soft sounds, it may still respond to loud sounds. This helps explain another surprise: Really loud sounds may seem loud to people with or without normal hearing. As a person with hearing loss, I [DM] used to wonder what really loud music must sound like to people with normal hearing. Now I realize it sounds much the same; where we differ is in our perception of soft sounds.

HEARING DIFFERENT PITCHES How do we know whether a sound is the high-frequency, high-pitched chirp of a bird or the low-frequency, low-pitched roar of a truck? Current thinking on how we discriminate pitch combines two theories.

So, here is our current thinking on how we discriminate pitch:

LOCATING SOUNDS Why don’t we have one big ear—perhaps above our one nose? “The better to hear you with,” the wolf said to Red Riding Hood. Thanks to the placement of our two ears, we enjoy stereophonic (“three-dimensional”) hearing. Two ears are better than one for at least two reasons. If a car to your right honks, your right ear will receive a more intense sound, and it will receive the sound slightly sooner than your left ear (FIGURE 18.5). Because sound travels 761 miles per hour and our ears are but 6 inches apart, the intensity difference and the time lag are extremely small. A just noticeable difference in the direction of two sound sources corresponds to a time difference of just 0.000027 second! Lucky for us, our supersensitive auditory system can detect such minute differences (Brown & Deffenbacher, 1979; Middlebrooks & Green, 1991).