The Nonvisual Senses

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.

Hearing

THE SOUNDS OF MUSIC A violin’s short, fast waves create a high pitch. The longer, slower waves of a cello or bass create a lower pitch. Differences in the waves’ height, or amplitude, also create differing degrees of loudness. (To review the physical properties of light and sound waves, see Figure 5.10.)

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Like our other senses, our hearing, or audition, helps us adapt and survive. For those of us who communicate invisibly—by shooting unseen air waves across space and receiving back the same—hearing provides information and enables relationships. 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 know the feeling.)

Most of us, however, can hear a wide range of sounds, and the ones we hear best are those in a range similar to that of the human voice. With normal hearing, we are remarkably sensitive to faint sounds, such as a child’s whimper. (If our ears were much more sensitive, we would hear a constant hiss from the movement of air molecules.) Our distant ancestors’ survival may have depended on this keen hearing when hunting or being hunted.

We also are acutely sensitive to sound differences. Among thousands of possible voices, we easily detect a friend’s on the phone, from the moment she says “Hi.” A fraction of a second after such events stimulate the ear’s receptors, millions of neurons have worked 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

5-15 What are the characteristics of the air pressure waves that we hear as meaningful sounds?

Hit a piano key 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. 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 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.

We measure sounds in decibels, with zero decibels representing the absolute threshold for hearing. 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.

Decoding Sound Waves

5-16 How does the ear transform sound energy into neural messages?

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. In the first step, your outer ear channels the waves into the 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 (the oval window) to vibrate, creating ripples in the fluid inside the cochlea (FIGURE 5.26b). The ripples bend the hair cells lining the basilar membrane on the cochlea’s surface, like wind bending a wheat field. The hair cell movements in turn trigger impulses in nerve cells. Axons from those nerve cells combine to form the auditory nerve, which carries the neural messages to the thalamus and then on to your auditory cortex in your brain’s temporal lobe. From vibrating air to fluid waves to electrical impulses to the brain: You hear!

FIGURE 5.26 Hear here: How we transform sound waves into nerve impulses that our brain interprets (a) The outer ear funnels sound waves to the eardrum. The bones of the middle ear (hammer, anvil, and stirrup) amplify and relay the eardrum’s vibrations through the oval window into the fluid-filled cochlea. (b) As shown in this detail of the middle and inner ear, the resulting pressure changes in the cochlear fluid cause the basilar membrane to ripple, bending the hair cells on its surface. Hair cell movements trigger impulses at the base of the nerve cells, whose fibers join together to form the auditory nerve. That nerve sends neural messages to the thalamus and on to the auditory cortex.

My vote for 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 (thinking big, imagine moving the top of the Eiffel Tower half an inch), and the alert hair cell will trigger a neural response (Corey et al., 2004).

At the highest frequency you can perceive, your ears’ hair cells can switch their neural current on and off a thousand times per second! As you might expect of something so sensitive, they are, however, delicate. Blast them with hunting rifle shots or blaring iPods (as teen boys more than girls do), and the hair cells’ cilia will begin to wither or fuse together. No wonder men’s hearing tends to be less acute than women’s (Zogby, 2006).

Hearing loss that results from damage to hair cell receptors or their associated nerves is called sensorineural hearing loss (or nerve deafness). Occasionally, disease damages hair cell 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.

THAT BAYLEN MAY HEAR The crowd roared as Super Bowl–winning quarterback Drew Brees celebrated New Orleans’ 2010 victory. To protect the delicate hair cells of his son, Baylen, Brees had him wear ear muffs.

AP Photo/Mark J. Terrill

HARDWARE FOR HEARING Cochlear implants work by translating sounds into electrical signals that are transmitted to the cochlea and, via the auditory nerve, on to the brain.

Hair cells have been compared to carpet fibers. Walk around on them and they will spring back with a quick vacuuming. 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, iPods 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. People who spend many hours in a loud club, behind a power mower, or above a jackhammer 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. These electronic devices translate sounds into electrical signals that, wired into the cochlea’s nerves, transmit information about sound to the brain. By 2009, some 188,000 people worldwide had undergone surgery to have the devices implanted (NIDCD, 2011). 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 even before age 1) (Dettman et al., 2007; Schorr et al., 2005).

How Do We Locate Sounds?

Why don’t we have one big ear—perhaps above our one nose? “All the better to hear you with,” as the wolf in the fairy tale said to Red Riding Hood. The placement of our two ears allows us to hear two slightly different messages. We benefit in two ways. If a car to the right honks, the right ear receives a more intense sound, and it receives the sound slightly sooner than the left ear does. Because sound travels 750 miles per hour and our ears are only 6 inches apart, the intensity difference and the time lag are very small. Lucky for us, our supersensitive sound system can detect such tiny differences (Brown & Deffenbacher, 1979; Middlebrooks & Green, 1991) (FIGURE 5.27).

FIGURE 5.27 Why two ears are better than one Sound waves strike one ear sooner and more intensely than the other. From this information, our brain can compute the sound’s location. As you might therefore expect, people who lose all hearing in one ear often have difficulty locating sounds.

Touch

5-17 What are the four basic touch sensations, and which of them has identifiable receptors?

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 is essential to our development. Infant monkeys allowed to see, hear, and smell—but not touch—their mothers become desperately unhappy (Suomi et al., 1976). Those separated by a screen with holes that allow touching are much less miserable. As we noted in Chapter 3, premature babies gain weight faster and go home sooner if they are stimulated by hand massage. As lovers, we yearn to touch—to kiss, to stroke, to snuggle.

Humorist Dave Barry may have been right to jest 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 distinct skin senses for pressure, warmth, cold, and pain. Other skin sensations are variations of the basic 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).

Surprisingly, there is no simple relationship between what we feel at a given spot and the type of specialized nerve ending found there. Only pressure has identifiable receptors.

Touch sensations involve more than the feelings on our skin, however. A self-administered tickle activates a smaller area of the brain’s cortex than the same tickle would from something or someone else (Blakemore et al., 1998). (The brain is wise enough to be most sensitive to unexpected stimulation.)

Pain

5-18 What influences our feelings of pain, and how can we treat pain?

“PAIN IS A GIFT” So said a doctor studying 13-year-old Ashlyn Blocker. Ashlyn has a rare genetic mutation that prevents her from feeling pain. At birth she didn’t cry. As a child, she ran around for two days on a broken ankle. She has put her hands on a hot machine and burned the flesh off. And she has reached into boiling water to retrieve a dropped spoon. “Everyone in my class asks me about it, and I say, ‘I can feel pressure, but I can’t feel pain.’ Pain! I cannot feel it!”(Heckert, 2010).

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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 tells you to change your behavior immediately. “Stay off that turned ankle!” The rare people born without the ability to feel pain may experience severe injury or even die before early adulthood. Without the discomfort that makes us shift positions, their joints fail from excess strain. Without the warnings of pain, infections run wild, and injuries can multiply (Neese, 1991).

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

UNDERSTANDING PAIN Our pain experiences vary widely. As a group, women tend to be more sensitive to pain. This was confirmed in a study of disease-related pain reported in the medical records of 11,000 patients (Ruau et al., 2012). But our individual sensitivity to pain also varies.

Your experience of pain depends in part on the genes you inherited and on your physical characteristics. Your feeling of pain is a physical event. It is in part a property of your senses, of the region where you feel it. But your pain system differs from some of your other senses. There is no simple neural cord running from a sensing device on your skin to a specific area in your brain. No one type of stimulus triggers pain (as light triggers vision). The human body has no special receptors (like the retina’s rods and cones) for pain. Instead, different sensory receptors (nociceptors) in your skin detect hurtful temperatures, pressure, or chemicals. Thus, like the other touch senses, pain is in part a bottom-up property of your senses. But it is more than that. It is also a product of your attention, your expectations, and your culture (Gatchel et al., 2007; Reimann et al., 2010). Your experience of pain is also a top-down product of your brain.

DISTRACTED FROM THE PAIN After a tackle in the first half of a competitive game, BK Hacken soccer player Mohammed Ali Khan (in white) said he “had a bit of pain” but thought it was “just a bruise.” With his attention focused on the game, he played on. In the second half he was surprised to learn from an attending doctor that the leg was broken and would need two months to heal.

AP Photo/Reinhold Matay

With pain, as with sights and sounds, the brain sometimes gets its signals crossed. Consider people’s experiences of phantom limb sensations. After having a limb amputated, some 7 in 10 people feel pain or movement in limbs that no longer exist (Melzack, 1992, 1993). Some try to step off a bed onto a phantom leg or to lift a cup with a phantom hand. Even those born without a limb sometimes feel sensations in the missing part. The brain comes prepared to anticipate “that it will be getting information from a body that has limbs” (Melzack, 1998).

Phantoms may haunt our 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.

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.

We have some built-in pain controls. 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). These discoveries point the way toward future pain medications that mimic the genetic effects.

When endorphins combine with distraction, amazing things can happen. Sports injuries may go unnoticed until the after-game shower (thus demonstrating that the pain in sprain is mainly in the brain). During a 1989 basketball game, Ohio State University player Jay Burson broke his neck—and kept playing. Halfway through his lap of the 2012 Olympics 1600 meter relay, Manteo Mitchell broke one of his leg bones—and kept running.

Health care professionals understand the value of distractions and may divert patients’ attention with a pleasant image (“Think of a warm, comfortable environment”) or a request to 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). A well-trained nurse may chat with needle-shy patients and ask them to look away when the needle is inserted. For burn victims receiving painful wound care, an even more effective distraction is escaping into a computer-generated 3-D world, like the snow scene in FIGURE 5.28. Functional MRI (fMRI) scans reveal that playing in the virtual reality reduces the brain’s pain-related activity (Hoffman, 2004).

FIGURE 5.28 Virtual-reality pain control For burn victims undergoing painful skin repair, escaping into virtual reality (like the icy playground shown here) can be a powerful distraction. With attention focused elsewhere, pain and the brain’s response to painful stimulation decrease.

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The brain-pain connection is also clear in our memories of pain. The pain we experience may not be the pain we remember. In experiments, and after medical procedures, people tend to overlook how long a pain lasted. Their memory snapshots may instead record its peak moment and also how much pain they felt at the end. Researchers discovered this when they asked people to 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 of these experiences would you expect to recall 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. A physician 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 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.)

DISSOCIATION OR SOCIAL INFLUENCE? A hypnotized woman being tested by famous researcher Ernest Hilgard showed no pain when her arm was placed in an ice bath. But asked to press a key if some part of her felt the pain, she did so. To Hilgard (1986, 1992), this was evidence of dissociation, or divided consciousness. The social influence perspective, however, maintains that people responding this way are caught up in playing the role of “good subject.”

Courtesy Elizabeth Jecker

Because pain is in the brain, hypnosis may also bring relief.

HYPNOSIS AND PAIN RELIEF 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. In a quiet, low voice the hypnotist suggests, “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).

Has hypnosis proved useful in relieving pain? Yes. When unhypnotized people put their arms in an ice bath, they felt intense pain within 25 seconds (Druckman & Bjork, 1994; Jensen, 2008). When hypnotized people did the same after being given suggestions to feel no pain, they indeed reported feeling little pain. As some dentists know, light hypnosis can reduce fear, and thus hypersensitivity to pain.

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).

Psychologists have proposed two explanations for how hypnosis works. One theory proposes that hypnosis produces a dissociation—a split—between normal sensations and conscious awareness. Dissociation theory seeks to explain why, when no one is watching, hypnotized people may carry out posthypnotic suggestions (which are made during hypnosis but carried out after the person is no longer hypnotized) (Perugini et al., 1998). It also offers an explanation for why people hypnotized for pain relief may show brain activity in areas that receive sensory information, but not in areas that normally process pain-related information.

Those who reject the hypnosis-as-dissociation view believe that hypnosis is instead a form of normal social influence (Lynn et al., 1990; Spanos & Coe, 1992). In this view, hypnosis is a by-product of normal social and mental processes. Like actors caught up in their roles, people begin to feel and behave in ways appropriate for “good hypnotic subjects.” They may allow the hypnotist to direct their attention and fantasies away from pain.

Taste

5-19 How are our senses of taste and smell similar?

Like touch, our sense of taste involves several basic sensations. Until recently, these sensations were thought to be sweet, sour, salty, and bitter (McBurney & Gent, 1979). In recent decades, many researchers have searched for specialized fibers that might act as nerve pathways for those four taste sensations. During this search, they discovered a receptor for 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 exist for more than our pleasure. Nice tastes attracted our ancestors to protein or energy-rich foods that enabled their survival (see TABLE 5.2). Unpleasant tastes warned them away from new foods that might contain toxins and lead to food poisoning, which can be especially deadly for children. 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 another tool in our early ancestors’ survival kit was learning. Across the globe, frustrated parents have happily discovered that when children are given repeated small tastes of disliked new foods, they typically learn to accept these foods (Wardle et al., 2003).

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THE NOSE KNOWS Humans have some 20 million olfactory receptors. A bloodhound has 220 million (Herz, 2007).

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Taste is a chemical sense. Inside each little bump on the top and sides of your tongue are 200 or more taste buds. Each bud contains a pore. Projecting into each of these pores are antenna-like hairs from 50 to 100 taste receptor cells. These hairs detect information about molecules of food chemicals and carry it back to your taste receptor cells. Some receptors respond mostly to sweet-tasting molecules, others to salty-, sour-, umami-, or bitter-tasting ones. All send their messages to your brain.

It doesn’t take much to trigger those 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 an eyeblink.

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.

Expectations can influence 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). There’s more to taste than meets the tongue.

Smell

Life begins with an inhale and ends with an exhale. Between birth and death, you will daily inhale and exhale nearly 20,000 breaths of life-sustaining air, bathing your nostrils in a stream of scent-laden molecules. Our experience of smell (olfaction) is strikingly intimate. With every breath, we inhale something of whatever or whoever it is we smell.

FIGURE 5.29 Taste, smell, and memory Information from the taste buds (yellow arrow) travels to an area between the frontal and temporal lobes of the brain. It registers in an area not far from where the brain receives information from our sense of smell, which interacts with taste. The brain’s circuitry for smell (red area) also connects with areas involved in memory storage, which helps explain why a smell can trigger a memory.

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 receptor cells, 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. Instantly (bypassing the brain’s sensory control center, the thalamus), they alert the brain.

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). Our sense of smell is, however, 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 into the blossoms.

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, different combinations of receptors send messages to the brain’s olfactory cortex. As the English alphabet’s 26 letters can combine to form many words, so olfactory receptors can produce different patterns to identify the 10,000 odors we can detect (Malnic et al., 1999). These different combinations activate different neural patterns (Zou & Buck, 2006). And that is what allows us to smell the difference between fresh-brewed and hours-old coffee.

Odors can evoke memories (FIGURE 5.29). Though it’s difficult to recall odors by name, we have a remarkable capacity to recognize long-forgotten smells and their associated personal tales (Engen, 1987; Schab, 1991). Pleasant odors can call up pleasant memories (Ehrlichman & Halpern, 1988). The smell of the sea, the scent of a perfume, or an aroma of a favorite relative’s kitchen can bring to mind a happy time. It’s a link one British travel agent chain understood well. To evoke memories of relaxing on sunny, warm beaches, the company once piped the aroma of coconut sunscreen into its shops (Fracassini, 2000).

Our brain’s circuitry helps explain an odor’s power to evoke feelings, memories, and behaviors. A hotline runs between the brain area that receives information from the nose and brain centers associated with emotions and memories. Thus, when put in a foul-smelling room, people expressed harsher judgments of lying or keeping a found wallet and more negative attitudes toward gays (Inbar et al., 2011; Schnall et al., 2008). And when riding on a train car with the citrus scent of a cleaning product, people leave less rubbish behind (de Lange et al., 2012).

Body Position and Movement

5-20 How do we sense our body’s position and movement?

BODIES IN SPACE These high school competitive cheer team members can thank their vestibular sense for the information that enables their brains to monitor their bodies’ position so expertly.

© Robert Kanavel

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 moving your arm to grasp someone’s hand. That act requires a sixth sense that informs you about the current position of your arms and hands and their changing positions as you move them. Just taking one step forward requires feedback from, and instructions to, some 200 muscles. The brain power engaged in all this exceeds even the mental activity involved in reasoning. Let’s take a closer look.

You came equipped with millions of position and motion sensors. They are all over your body—in your muscles, tendons, and joints—and they are continually feeding information to your brain. Twist your wrist one degree, and these sensors provide an immediate update. This sense of your body parts’ position and movement is kinesthesia.

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 being able to sense the positions of your limbs when you wake during the night? 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 prolonged 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).

For all of us, vision interacts with kinesthesia. Stand with your right heel in front of your left toes. Easy. Now close your eyes and you will probably wobble.

Working hand in hand with kinesthesia is our vestibular sense. This companion sense monitors your head’s (and thus your body’s) position and movement. Controlling this sense of equilibrium are two structures in your inner ear. The first, your semicircular canals, look like a three-dimensional pretzel (FIGURE 5.26a). The second, connecting those canals with the cochlea, is the pair of vestibular sacs, which contain fluid that moves when your head rotates or tilts. When this movement stimulates hairlike receptors, sending messages to the cerebellum at the back of your brain, you 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.

TABLE 5.3 summarizes the sensory systems we have discussed.