For humans, vision is the major sense. More of our brain cortex is devoted to vision than to any other sense. Yet without hearing, touch, taste, smell, and body position and movement, our experience of the world would be vastly diminished.

Like our other senses, our hearing, or audition, helps us adapt and survive. Hearing provides information and enables relationships. It lets us communicate invisibly, shooting unseen air waves across space and receiving the same from others. 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 also are acutely sensitive to sound differences. Among thousands of possible voices, we easily distinguish an unseen friend’s. Moreover, hearing is fast. Your reaction to a sudden sound is at least 10 times faster than your response when you suddenly see something “from the corner of your eye, turn your head toward it, recognize it, and respond to it” (Horowitz, 2012). A fraction of a second after such events stimulate your ear’s receptors, millions of neurons are working together to extract the essential features, compare them with past experience, and identify the sound (Freeman, 1991). For hearing as for seeing, we wonder: How do we do it?

Sound Waves: From the Environment Into the Brain

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Hit a piano key and you unleash the energy of sound waves. Moving molecules of air, each bumping into the next, create waves of compressed and expanded air, like ripples on a pond circling out from a tossed stone. Our ears detect these brief air pressure changes.

Like light waves, sound waves vary in shape. The height, or amplitude, of sound waves determines their perceived loudness. Their length, or frequency, determines the pitch (the high or low tone) we experience. Long waves have low frequency—and low pitch. Short waves have high frequency—and high pitch. Sound waves produced by a referee’s whistle are much shorter and faster than those produced by a truck horn.

We measure sounds in decibels, with zero decibels representing the lowest level detectable by human ears. Normal conversation registers at about 60 decibels. A whisper falls at about 20 decibels, and a jet plane passing 500 feet overhead registers at about 110 decibels. Prolonged exposure to any sounds above 85 decibels can produce hearing loss. Tell that to football fans of the NFL’s Kansas City Chiefs who, in 2014, broke the Guinness World Record for the noisiest stadium at 142 decibels (Liberman, 2015). Hear today, gone tomorrow.

Decoding Sound Waves

How does vibrating air morph into nerve impulses that your brain can decode as sounds?

The process begins when sound waves entering your outer ear trigger a mechanical chain reaction. Your outer ear channels the waves into your auditory canal, where they bump against your eardrum, causing this tight membrane to vibrate (FIGURE 5.26a).

In your middle ear, three tiny bones (the hammer, anvil, and stirrup) pick up the vibrations and transmit them to the cochlea, a snail-shaped tube in your inner ear.

The incoming vibrations then cause the cochlea’s membrane-covered opening (the oval window) to vibrate, sending ripples through the fluid inside the cochlea (FIGURE 5.26b). The ripples bend the hair cells lining the basilar membrane on the cochlea’s surface, much as wind bends wheat stalks in a field.

The hair cell movements in turn trigger impulses in nerve cells, whose axons combine to form the auditory nerve. The auditory nerve carries the impulses to your thalamus and then on to your auditory cortex in your brain’s temporal lobe.

From vibrating air, to tiny moving bones, to fluid waves, to electrical impulses to the brain: You hear!

Perhaps the most magical 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 these cells, which sounds like a lot until we compare that with an eye’s 130 million or so receptors. But consider a hair cell’s responsiveness. Deflect the tiny bundles of cilia on its tip by only the width of an atom, and the alert hair cell will trigger a neural response (Corey et al., 2004).

Damage to the cochlea’s hair cell receptors or their associated nerves can cause sensorineural hearing loss (or nerve deafness). Occasionally, disease damages hair cell receptors, but more often the culprits are biological changes linked with heredity and aging, or 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.

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Hair cells have been compared 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, any noise we cannot talk over (loud machinery, fans screaming at a sports event, music blasting at maximum volume) may be harmful, especially if we are exposed to it often or for a long time (Roesser, 1998). And if our ears ring after such experiences, we have been bad to our unhappy hair cells. As pain alerts us to possible bodily harm, ringing in the ears alerts us to possible hearing damage. It is hearing’s version of bleeding.

Worldwide, 1.23 billion people are challenged by hearing loss (Global Burden of Disease, 2015). Since the early 1990s, teen hearing loss has risen by a third and now affects 1 in 5 teens (Shargorodsky et al., 2010). Teen boys more than teen girls or adults blast themselves with loud volumes for long periods (Zogby, 2006). (Does it surprise you that men’s hearing tends to be less acute than women’s?) People who spend many hours behind a power mower, above a jackhammer, or in a loud club should wear earplugs, or they risk needing a hearing aid later. “Condoms or, safer yet, abstinence,” say sex educators. “Earplugs or walk away,” say hearing educators.

Nerve deafness cannot be reversed. For now, the only way to restore hearing is a sort of bionic ear—a cochlear implant. Some 50,000 people, including some 30,000 children, receive these electronic devices each year (Hochmair, 2013). The implants translate sounds into electrical signals that, wired into the cochlea’s nerves, transmit sound information to the brain. When given to deaf kittens and human infants, cochlear implants have seemed to trigger an “awakening” of brain areas normally used in hearing (Klinke et al., 1999; Sireteanu, 1999). They can help children become skilled in oral communication (especially if they receive them as preschoolers or ideally before age 1) (Dettman et al., 2007; Schorr et al., 2005).

How Do We Locate Sounds?

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Why don’t we have one big ear—perhaps above our one nose? “All the better to hear you with,” as the wolf said to Little Red Riding Hood. Our two ears are about 6 inches apart, and they pick up two slightly different messages. Say a car to your right honks (FIGURE 5.27). Your right ear will receive a more intense sound. It will also receive the sound slightly sooner than your left ear. Because sound travels 750 miles per hour, the intensity difference and the time lag will be very small—just 0.000027 second! Lucky for us, our supersensitive sound system can detect such tiny differences (Brown & Deffenbacher, 1979; Middlebrooks & Green, 1991).

If you had to lose one sense, which would you give up? If you could have only one, which would you keep?

Although not the first sense to come to mind, touch might be a good choice for keeping. Right from the start, touch enables our development. Infant monkeys allowed to see, hear, and smell—but not touch—their mother become desperately unhappy (Suomi et al., 1976). Those separated by a screen with holes that allow touching are much less miserable. Premature babies gain weight faster and go home sooner if they are stimulated by hand massage (Field et al., 2006). As adults, we still yearn to touch—to kiss, to stroke, to snuggle.

Humorist Dave Barry was perhaps right to joke that your skin “keeps people from seeing the inside of your body, which is repulsive, and it prevents your organs from falling onto the ground.” But skin does much more. Our “sense of touch” is actually a mix of four basic and distinct skin senses: pressure, warmth, cold, and pain. Other skin sensations are variations of these four. For example, stroking side-by-side pressure spots creates a tickle. Repeated gentle stroking of a pain spot creates an itching sensation. Touching side-by-side cold and pressure spots triggers a sense of wetness (which you can experience by touching dry, cold metal).

Touch sensations involve more than feelings on our skin, however. A soft touch on the leg evokes a different cortical response when a straight man believes he was caressed by an attractive woman rather than by another man (Gazzola et al., 2012). Such responses show how quickly our thinking brain influences our sensory responses. This thought-feeling interaction also appears in the ways we experience and respond to pain.

Pain—What Is It and How Can We Control It?

Be thankful for occasional pain. Pain is your body’s way of telling you something has gone wrong. Drawing your attention to a burn, a break, or a sprain, pain orders you to change your behavior—“Stay off that ankle!” The rare people born without the ability to feel pain may experience severe injury or even death before early adulthood. Without the discomfort that makes us shift positions, their joints can fail from excess strain. Without the warnings of pain, infections can run wild and injuries multiply (Neese, 1991).

Many more people live with chronic pain, which is rather like an alarm that won’t shut off. Persistent backaches, arthritis, headaches, and cancer-related pain prompt two questions: What is pain? And how might we control it?

Our feeling of pain reflects both bottom-up sensations and top-down cognition. Pain is a biopsychosocial event (Hadjistavropoulos et al., 2011). As such, pain experiences vary widely, from group to group and from person to person.

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BIOLOGICAL INFLUENCES Pain is a physical event produced by your senses. But pain differs from some of your other sensations. No one type of stimulus triggers pain, the way light triggers vision. And no specialized receptors process pain signals, the way the rods and cones in your eyes react to light rays. Instead, you have sensory receptors (nociceptors), mostly in your skin, which detect hurtful temperatures, pressure, or chemicals.

Your experience of pain also depends in part on the genes you inherited and on your physical characteristics. Women are more sensitive to pain than are men—and their senses of hearing and smell also tend to be more sensitive (Ruau et al., 2012; Wickelgren, 2009).

But pain is not merely a physical event in which injured nerves send impulses to a specific brain area—like pulling on a rope to ring a bell. With pain, as with sights and sounds, the brain sometimes gets its signals crossed. And when it does, the brain can actually create pain, as it does in phantom limb sensations following a limb amputation. Without sensory input, the brain may misinterpret other neural activity. As a dreamer may see with eyes closed, so 7 in 10 such people feel pain or movement in limbs that no longer exist (Melzack, 1992, 2005).

Phantoms may haunt other senses, too. People with hearing loss often experience the sound of silence: tinnitus, a phantom sound of ringing in the ears. Those who lose vision to glaucoma, cataracts, diabetes, or macular degeneration may experience phantom sights—nonthreatening hallucinations (Ramachandran & Blakeslee, 1998). And damage to nerves in the systems for tasting and smelling can give rise to phantom tastes or smells, such as ice water that seems sickeningly sweet or fresh air that reeks of rotten food (Goode, 1999). The point to remember: We see, hear, taste, smell, and feel pain with our brain.

PSYCHOLOGICAL INFLUENCES One powerful influence on our perception of pain is the attention we focus on it. Athletes, focused on winning, may perceive pain differently and play through it. After a tackle in the first half of a competitive game, Swedish professional soccer player Mohammed Ali Khan said he “had a bit of pain” but thought it was “just a bruise.” He played on. In the second half he was surprised to learn from an attending doctor that his leg was broken. The pain in sprain is mainly in the brain.

We also seem to edit our memories of pain. The pain we experience may not be the pain we remember. In experiments, and after medical procedures, people overlook how long a pain lasted. Their memory snapshots instead record two points: the peak moment of pain, and how much pain they felt at the end. In one experiment, people put one hand in painfully cold water for 60 seconds, and then the other hand in the same painfully cold water for 60 seconds, followed by a slightly less painful 30 seconds more (Kahneman et al., 1993). Which experience would you expect they recalled as most painful?

Curiously, when asked which trial they would prefer to repeat, most preferred the longer trial, with more net pain—but less pain at the end. Physicians have used this principle with patients undergoing colon exams—lengthening the discomfort by a minute, but lessening its intensity at the end (Kahneman, 1999). Patients experiencing this taper-down treatment later recalled the exam as less painful than did those whose pain ended abruptly. (As a painful root canal is coming to an end, if the oral surgeon asks if you’d like to go home, or to have a few more minutes of milder discomfort, there’s a case to be made for prolonging your hurt.) Endings matter.

SOCIAL-CULTURAL INFLUENCES Pain is a product of our attention, our expectations, and our culture (Gatchel et al., 2007; Reimann et al., 2010). Not surprisingly, then, our perception of pain varies with our social situation and our cultural traditions. We tend to feel more pain when others seem to be experiencing pain (Symbaluk et al., 1997). When people felt empathy for another’s pain, their own brain activity partly mirrored the activity of the actual brain in pain (Singer et al., 2004).

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CONTROLLING PAIN If pain is where body meets mind—if pain is both a physical and a psychological event—then it should be treatable both physically and psychologically. Depending on the symptoms, pain control therapies may include drugs, surgery, acupuncture, electrical stimulation, massage, exercise, hypnosis, relaxation training, and thought distraction.

We have some built-in pain controls, too. Our brain releases a natural painkiller—endorphins—in response to severe pain or even vigorous exercise. The release of these neurotransmitters has a soothing effect so that the pain we experience may be greatly reduced. People who carry a gene that boosts the normal supply of endorphins are less bothered by pain, and their brain is less responsive to it (Zubieta et al., 2003). Others, who carry a gene that disrupts the neural pain circuit, may be unable to experience pain (Cox et al., 2006). Such discoveries point the way toward future pain medications that mimic these genetic effects.

Even placebos can help, by dampening the central nervous system’s attention and responses to painful experiences—mimicking painkilling drugs (Eippert et al., 2009; Wager & Atlas, 2013). After being injected in the jaw with a stinging saltwater solution, men in one experiment received a placebo. They had been told it would relieve pain, and it did—they immediately felt better. “Nothing” worked. Their belief in the fake painkiller triggered their brain to respond by dispensing endorphins, indicated by activity in an area that releases the natural painkillers (Scott et al., 2007; Zubieta et al., 2005).

When endorphins combine with distraction, amazing things can happen. Have you ever had a health care professional suggest that you focus on a pleasant image (“Think of a warm, comfortable environment”) or perform some task (“Count backward by 3s”)? These are effective ways to activate brain pathways that decrease pain and increase tolerance (Edwards et al., 2009). For burn victims receiving painful wound care, an even more effective distraction is escaping into a computer-generated 3-D world. Functional MRI (fMRI) scans reveal that playing in virtual reality reduces the brain’s pain-related activity (Hoffman, 2004).

Better yet, research suggests, maximize pain relief by combining a placebo with distraction (Buhle et al., 2012), and amplify their effects with hypnosis. Imagine you are about to be hypnotized. The hypnotist invites you to sit back, fix your gaze on a spot high on the wall, and relax. You hear a quiet, low voice suggest, “Your eyes are growing tired . . . Your eyelids are becoming heavy . . . now heavier and heavier . . . They are beginning to close . . . You are becoming more deeply relaxed . . . Your breathing is now deep and regular . . . Your muscles are becoming more and more relaxed. Your whole body is beginning to feel like lead.” After a few minutes of this hypnotic induction, you may experience hypnosis.

Hypnotists have no magical mind-control power; they merely focus people on certain images or behaviors. To some extent, we are all open to suggestion. But highly hypnotizable people—such as the 20 percent who can carry out a suggestion not to react to an open bottle of smelly ammonia—are especially suggestible and imaginative (Barnier & McConkey, 2004; Silva & Kirsch, 1992).

Can hypnosis relieve pain? Yes. Hypnosis inhibits pain-related brain activity. In surgical experiments, hypnotized patients have required less medication, recovered sooner, and left the hospital earlier than unhypnotized control patients (Askay & Patterson, 2007; Hammond, 2008; Spiegel, 2007). Nearly 10 percent of us can become so deeply hypnotized that even major surgery can be performed without anesthesia. Half of us can gain at least some relief from hypnosis. The surgical use of hypnosis has flourished in Europe, where one Belgian medical team has performed more than 5000 surgeries with a combination of hypnosis, local anesthesia, and a mild sedative (Song, 2006). Hypnosis has also lessened some forms of chronic pain (Adachi et al., 2014).

But how does hypnosis work? Psychologists have proposed two explanations.

So, is hypnosis to be explained as normal social influence or a special dissociative state? As the debate continues, stay tuned for further research.

Like touch, our sense of taste involves several basic sensations. Taste’s sensations were once thought to be sweet, sour, salty, and bitter, with all others stemming from a mixture of these four (McBurney & Gent, 1979). Then, as researchers searched for specialized fibers for those four taste sensations, they discovered a fifth sensation—the savory, meaty taste of umami. You may have experienced umami as the flavor enhancer monosodium glutamate (MSG), often used in Chinese or Thai food.

Tastes give us pleasure, but they also help us survive. Pleasant tastes attracted our ancestors to foods rich in energy or protein (see TABLE 5.2). Unpleasant tastes warned them away from new foods that might be toxic. The taste preferences of today’s 2- to 6-year-olds reflect this inherited biological wisdom. At this age, children are typically fussy eaters and often turn away from new meat dishes or bitter-tasting vegetables, such as spinach and brussels sprouts (Cooke et al., 2003). But learning—another tool in our early ancestors’ survival kit—comes to the aid of frustrated parents across the globe. When given repeated small tastes of disliked new foods, children usually learn to accept them (Wardle et al., 2003). We come to like what we eat. German babies who were bottle-fed vanilla-flavored milk became adults with a striking preference for vanilla flavoring (Haller et al., 1999).

Taste is a chemical sense. Look into a mirror and you’ll see little bumps on the top and sides of your tongue. Each bump contains 200 or more taste buds. Each taste bud contains a pore that catches food chemicals. In each taste bud pore, 50 to 100 taste receptor cells project antenna-like hairs that sense food molecules. Some receptors respond mostly to sweet-tasting molecules, others to salty-, sour-, umami-, or bitter-tasting ones. Each receptor transmits its message to a matching partner cell in your brain (Barretto et al., 2015).

It doesn’t take much to trigger receptor responses. If a stream of water is pumped across your tongue, the addition of a concentrated salty or sweet taste for only one-tenth of a second will get your attention (Kelling & Halpern, 1983). When a friend asks for “just a taste” of your soft drink, you can squeeze off the straw after a mere instant.

Taste receptors reproduce themselves every week or two, so if hot food burns your tongue, it hardly matters. However, as you grow older, it may matter more, because the number of taste buds in your mouth will decrease, as will your taste sensitivity (Cowart, 1981). (No wonder adults enjoy strong-tasting foods that children resist.) Smoking and alcohol can speed up the loss of taste buds.

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There’s more to taste than meets the tongue. Our expectations also influence what we taste. When told a sausage roll was “vegetarian,” people in one experiment judged it inferior to its identical partner labeled “meat” (Allen et al., 2008). In another experiment, hearing that a wine cost $90 rather than its real $10 price made it taste better and triggered more activity in a brain area that responds to pleasant experiences (Plassman et al., 2008).

Inhale, exhale. Between birth’s first inhale and death’s last exhale, about 500 million breaths of life-sustaining air will bathe your nostrils in a stream of scent-laden molecules. The resulting experience of smell (olfaction) is strikingly intimate. With every breath, we inhale something of whatever or whoever it is we smell.

Smell, like taste, is a chemical sense. We smell something when molecules of a substance carried in the air reach a tiny cluster of receptor cells at the top of each nasal cavity. These 20 million olfactory receptors, waving like sea anemones on a reef, respond selectively—to the aroma of a cake baking, to a wisp of smoke, to a friend’s fragrance. Bypassing the brain’s sensory control center, the thalamus, they instantly alert the brain.

Odor molecules come in many shapes and sizes—so many, in fact, that it takes hundreds of different receptors, designed by a large family of genes, to recognize these molecules (Miller, 2004). We do not have one distinct receptor for each detectable odor. Instead, receptors on the surface of nasal cavity neurons work in different combinations to send messages to the brain, activating different patterns in the olfactory cortex (Buck & Axel, 1991). As the English alphabet’s 26 letters can combine to form many words, so olfactory receptors can produce different patterns to identify an estimated 1 trillion different odors (Bushdid et al., 2014). These combinations of olfactory receptors, activating different neuron patterns, allow us to detect the difference between fresh-brewed and hours-old coffee (Zou & Buck, 2006).

Aided by smell, a mother fur seal returning to a beach crowded with pups will find her own. Human mothers and nursing infants also quickly learn to recognize each other’s scents (McCarthy, 1986). A smell’s appeal—or lack of it—depends in part on learned associations (Herz, 2001). In the United States, people associate the smell of wintergreen with candy and gum, and they tend to like it. In Great Britain, wintergreen is often associated with medicine, and people find it less appealing.

Our sense of smell is less impressive than our senses of seeing and hearing. Looking out across a garden, we see its forms and colors in wonderful detail and hear a variety of birds singing. Yet we smell few of the garden’s scents without sticking our nose directly into the blossoms. We also have trouble recalling odors by name. But we have a remarkable capacity to recognize long-forgotten smells and their associated personal tales (Engen, 1987; Schab, 1991). The smell of the sea, the scent of a perfume, or the aroma of a favorite relative’s kitchen can bring to mind a happy time.

Our brain’s circuitry helps explain an odor’s power to evoke feelings, memories, and behaviors (FIGURE 5.28). A hotline runs between the brain area that receives information from the nose and other brain centers associated with emotions and memories. In experiments, people have become more suspicious when exposed to a fishy smell during a trust game (Lee & Schwarz, 2012). When exposed to a sweet taste, others became sweeter on their romantic partners and more helpful to others (Meier et al., 2012; Ren et al., 2015). And when riding on a train car with the citrus scent of a cleaning product, people left less trash behind (de Lange et al., 2012).

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Using only the five familiar senses we have so far considered, you could not put food in your mouth, stand up, or reach out and touch someone. Nor could you perform the “simple” act of taking one step forward. That act requires feedback from, and instructions to, some 200 muscles, and it engages brain power that exceeds the mental activity involved in reasoning. Like all your other voluntary movements, taking a step is possible because of your sense of kinesthesia, which keeps you aware of your body parts’ position and movement. You came equipped with millions of position and motion sensors in muscles, tendons, and joints all over your body. These sensors provide constant feedback to your brain. Twist your wrist one degree, and your brain receives an immediate update.

You can momentarily imagine being blind or deaf. Close your eyes, plug your ears, and experience the dark stillness. But what would it be like to live without the benefits of kinesthesia? Ian Waterman of Hampshire, England, knows. In 1972, at age 19, Waterman contracted a rare viral infection that destroyed the nerves that enabled his sense of light touch and of body position and movement. People with this condition report feeling disconnected from their body, as though it is dead, not real, not theirs (Sacks, 1985). With long practice, Waterman has learned to walk and eat—by visually focusing on his limbs and directing them accordingly. But if the lights go out, he crumples to the floor (Azar, 1998).

Vision interacts with kinesthesia for you, too. Stand with your right heel in front of your left toes. Easy. Now close your eyes and try again. Did you wobble?

A companion vestibular sense works hand in hand with kinesthesia to monitor your head’s (and thus your body’s) position and movement. Two structures in your inner ear join forces to help you maintain your balance. The first, your semicircular canals, look like a three-dimensional pretzel (FIGURE 5.26a). The second structure is the pair of vestibular sacs connecting those canals with the cochlea. These sacs contain fluid that moves when your head rotates or tilts. This movement stimulates hair-like receptors, which send messages to your cerebellum at the back of your brain, enabling you to sense your body position and maintain your balance.

If you twirl around and then come to an abrupt halt, it takes a few seconds for the fluid in your semicircular canals and for your kinesthetic receptors to return to their neutral state. The aftereffect fools your dizzy brain with the sensation that you’re still spinning. This illustrates a principle underlying perceptual illusions: Mechanisms that normally give us an accurate experience of the world can, under special conditions, fool us. Understanding how we get fooled provides clues to how our perceptual system works.