Ian Waterman had a perfectly ordinary life
started teaching himself how to walk using
until he caught a viral infection at age 19. For another source of feedback about his body:
reasons no one understands, the infection
his vision. Now, as long as the lights are on,
targeted a very specific set of nerves send- Ian can carefully watch his moving body to
ing information from his body to his brain. Ian judge which motor commands to send out
can still feel pain or deep pressure, as well
to keep walking. If the lights go out, howev-
as warm and cool surfaces on his skin, but
er, Ian collapses, and he has learned that in
he has no sensation of light touch below his that circumstance he just has to lie where he
neck. What's more, although Ian can still move is until the lights come on again. He has so
all of his muscles, he receives no information finely honed this ability to guide movements
about muscle activity or body position (Cole, with vision that if asked to point repeatedly
1995, 2016). You might think this deficiency to the same location in the air, he does so
wouldn't cause any problem, because you've more accurately than control participants
do. Still, it's a mental drain to have to watch
"body sense"; it's not even one of the five
and attend constantly to his body just to do
In fact, however, the loss of this infor-
mation was devastating. Ian couldn't walk
independent life, but he is always vigilant.
across a room without falling down, and he Lying in bed, he has to be very careful to
remain calm, tethering his limbs with the
other people suffering a loss like this spent covers to prevent them from flailing about.
the rest of their lives in wheelchairs. But Ian
was a young and determined person, so he Ian's house.
Every individual of every species is immersed in a sea of environmental cues that signal opportunities and hazards. Molecules in the air are sensed as odors--of food, or mates, or smoke. Vibrations traveling through air are perceived as sounds, ranging from infant cries to the roar of a predator (or a waterfall). Light reflected from surfaces is used to create a visual representation of the world. We open this chapter by considering basic principles of sensory processing, using the sense of touch to illustrate some of the major concepts. We then take a closer look at an unpleasant but crucial sense: pain. To conclude the chapter, we turn our attention to the integration of sensory inputs to guide our movement: the streamlined system that allows us to interact with our environment.
5.1Sensory Processing and the Somatosensory System
The first portion of the chapter covers the general principles that apply to all sensory systems, using touch as an example. Reading this material should allow you to: 5.1.1 Understand the concepts of labeled lines and sensory transduction. 5.1.2 Describe several different types of receptors in the skin and the stimuli they detect. 5.1.3 Relate the concepts of receptive fields and sensory adaptation. 5.1.4 Describe the neural pathway for the system reporting touch information from the body.
Because species differ in the environmental features they must sense for survival, evo-
lution has endowed each species with its own unique set of capabilities. Bats are spe-
cially equipped to detect their own ultrasonic cries, which we humans are unable to
hear. Some snakes have infrared-sensing organs in their faces that allow them to "see"
heat sources (like a warm, tasty mouse) in the dark. Some of the impressive array of
sensory modalities that animals possess are listed in TABLE 5.1.
receptor cell A specialized cell that responds to a particular energy or sub-
Receptor cells detect various forms of energy
stance in the internal or external environment and converts this energy into a change in the electrical potential across its membrane.
All animals have sensory organs containing receptor cells that sense some forms of energy--called stimuli--but not others. So in a way, receptor cells act as filters, ignoring the environmental background and converting the key stimuli into the language of
stimulus A physical event that triggers a sensory response.
the nervous system: electrical signals. Information from sensory receptors floods the brain in an unending barrage of action potentials traveling along millions of axons,
labeled lines The concept that each nerve input to the brain reports only a
and our brains must make sense of it all. What type of stimulus was that, where did it come from, how intense was it, etc. Of course, different kinds of energy--light, sound,
touch, and so on--need different sensory organs to convert them into neural activi-
ty, just as taking a photograph requires a camera,
not a microphone. There is tremendous diversity in
TABLE 5.1 Classification of Sensory Systems
sensory organs across the animal kingdom; for ex-
ample, the eye is just one type of sensory organ, yet it is found in a dazzling array of sizes, shapes, and forms, reflecting the varying survival needs of dif-
ferent animals. Likewise, the specific auditory abil-
ities of species reflect their unique ecological pres-
Although the end product of sensory receptors--action potentials--is the same for all the different sensory modalities, the brain recognizes
Photons, from light sources or reflected from surfaces
the modalities as separate and distinct because the action potentials for each sense are carried
in separate nerve tracts. This is the concept of
labeled lines: particular neurons that are, right
from the outset, labeled for distinctive sensory
Taste Vomeronasal Electroreception Magnetoreception
Substances in contact with the tongue or other taste receptors Pheromones in air or water Differences in density of electrical currents Magnetic fields for orientation
experiences. Action potentials in one line signal a sound, activity in another line signals a smell, and activity in other lines signals touch. And there are labeled lines within general sensory categories too; for example, we can distinguish different types of touch because our skin contains a variety of receptors and uses some lines to signal
Species evolve different sensory abilities in response to differing ecological pressures. Cats hear high frequencies that humans don't.
20 Elephants hear 0 low frequencies that humans don't.
FIGURE 5.1 Do You Hear What I Hear? (After R. R. Fay, 1988. Hearing in vertebrates: A psychophysics databook. Hill-Fay Associates. Winnetka, IL. Courtesy of Dr. Richard Fay and the Fay Foundation.)
light touch, others to signal vibration, and yet other lines to signal stretching of the skin (FIGURE 5.2). Receptor cells convert sensory signals into electrical activity The structure of a receptor cell determines the particular kind of energy or chemical to which it will respond. And although a wide variety of cellular mechanisms are used to detect different stimuli, the outcome is always the same: an electrical change in the receptor, called a receptor potential (or generator potential), that resembles the
receptor potential Also called generator potential. A local change in the resting potential of a receptor cell in response to stimuli, which may initiate an action potential.
FIGURE 5.2 Labeled Lines
Vibration Because each receptor cell sends a signal on a particular "line," the brain "knows" what sort of touch happened.
FIGURE 5.3 Receptors in Skin
Free nerve endings (pain, itch, and temperature) Merkel's disc (touch) Meissner's corpuscle (touch) Hair follicle receptor (touch)
Pacinian (or lamellated) corpuscle (vibration and pressure)
sensory transduction The process in which a receptor cell converts the energy in a stimulus into a change in the electrical potential across its membrane. Pacinian corpuscle Also called lamellated corpuscle. A skin receptor cell type that detects vibration and pressure. threshold Here, the stimulus intensity that is just adequate to trigger an action potential in a sensory cell. Meissner's corpuscle Also called tactile corpuscle. A skin receptor cell type that detects light touch, responding especially to changes in stimuli. Merkel's disc A skin receptor cell type that detects light touch, responding especially to edges and isolated points on a surface. Ruffini corpuscle A skin receptor cell type that detects stretching of the skin.
excitatory postsynaptic potentials we discussed in Chapter 3. Converting the signal in this way--from environmental stimuli into action potentials that our brain can understand--is called sensory transduction. Our skin contains a rich array of receptors that transduce different forms of energy to provide our sense of touch. But touch is not just touch. Careful studies of skin sensations reveal qualitatively different sensory experiences: pressure, vibration, tickle, "pins and needles," and more-complex dimensions, such as smoothness or wetness-- all recorded by the receptors in the skin (FIGURE 5.3), then transmitted along separate axons to the brain. A skin receptor that provides a clear example of the process of sensory transduction is the Pacinian corpuscle (or lamellated corpuscle) (A. Zimmerman et al., 2014), a tiny onion-like structure embedded in the innermost layer of the skin that selectively responds to vibration and pressure. Acting as a filter, the corpuscle allows only vibrations of more than about 200 cycles per second to stimulate the sensory nerve ending inside it; this type of stimulation is what's created when we feel a texture against our skin (see Figure 5.3). By stretching the membrane of the sensory nerve ending, stimuli cause mechanically gated sodium channels to pop open, creating a graded receptor potential (FIGURE 5.4). The amplitude (size) of this receptor potential is directly proportional to the strength of the stimulus that was received. If the receptor potential exceeds threshold, action potentials are generated that travel via sensory nerves to the spinal cord. Other dimensions of the sense of touch are mediated by their own unique sensory receptors. In contrast to the texture sensitivity of Pacinian corpuscles, Meissner's corpuscles (also known as tactile corpuscles) and Merkel's discs mediate most of our ability to perceive the forms of objects we touch. While Merkel's discs are especially responsive to edges and to isolated points on a surface, the more numerous Meissner's corpuscles seem to respond to changes in stimuli, allowing them to detect localized movement between the skin and a surface (Heidenreich et al., 2011). Ruffini corpuscles, which are only sparsely distributed in the skin (Pare et al., 2003), detect stretching of patches of the skin when we move fingers or limbs (Johansson and Flanagan, Watson/Breedlove The Mind's Machine Foundations of Brain and Behavior 4e
The Sensorimotor System 147 Membrane stretched, excited section Na+
Pacinian corpuscle Each corpuscle surrounds an afferent nerve ending.
Vibration applied to the corpuscle stretches part of the neuronal membrane, opening the ion channels and permitting the entry of Na+, which initiates an action potential.
(B) As stimulus intensity increases, so does the neuron's response...
Response to moderate stimulus Response to strong stimulus
...until it reaches threshold, triggering an action potential, which makes us aware of the stimulus.
FIGURE 5.4 The Structure and Function of the Pacinian Corpuscle
2009). Finally, pain, itch, heat, and cold stimuli are detected by free nerve endings in the skin (see Figure 5.3), which we'll return to a little later in the chapter. All of these sensory receptors are found in their highest concentrations in regions of the skin where our sense of touch is finest (fingertips, tongue, and lips).
1. Discuss the relationship between the ecology of a species and its sensory capabilities. 2. What are labeled lines? What do they transmit? 3. Give a general explanation of sensory transduction. What is a receptor potential? 4. Identify and describe four sensory receptors found in the skin. Sensory information processing is selective and analytical Many people assume that the sensory systems simply capture an accurate snapshot of stimulation and transmit it to the brain--in other words, that the sensory systems providWeaatsnonu/nBcroeelodrloevdewindow on the world. But neuroscientists realize that the sensory orgTahne sMainndd'spMatahchwinaeys convey only limited--even distorted--information to the brain. Foundations of Brain and Behavior 4e A gDoraogdondeyaMl oefdsiaeGlercotuiopn and analysis takes place along sensory pathways, before the infMorMm4ae_t0io5.n04e.avier rea0c5h/e1s8/th20e20brain. So the brain ultimately receives a highly filtered representation of the external world, in which stimuli that are critical for survival are strongly emphasized at the expense of less important stimuli. This processing and filtering is seen in several aspects of sensory transduction, including stimulus coding and processing across receptive fields, as well as in adaptation and active suppression by the brain, which we discuss next. Sensory events are encoded as streams of action potentials We've already seen that the nervous system uses labeled lines to identify the type of stimulus that is encountered. But how do sensory neurons tell the brain about the intensity or location of a stimulus? Because the action potentials produced by a sensory
free nerve ending An axon that terminates in the skin and has no specialized cell associated with it. Free nerve endings detect pain or itch, or changes in temperature.
somatosensory system A set of specialized receptors and neural mechanisms responsible for body sensations such as touch and pain. receptive field The stimulus region and features that affect the activity of a cell in a sensory system. sensory adaptation The progressive loss of receptor response as stimulation is maintained. View Animation 5.3: Somatosensory Receptive Fields
neuron always have the same size and duration, the intensity of a sensory stimulus must be encoded in the number and frequency of the action potentials, the rhythm in which clusters of action potentials occur, and so on. We can respond to amazingly small differences in stimulus intensity, over a wide range of intensities. Although a single sensory receptor neuron could simply encode the intensity of a stimulus in the frequency of action potentials that the cell produces, only a very limited range of intensities could be represented this way, because neurons can fire only so fast (up to maybe 1,200 action potentials per second, and probably less in most neurons). Some sensory systems solve this problem by employing multiple sensory receptor cells, each specializing in just one part of the overall range of intensities, to cover the whole range. As the strength of a stimulus increases, additional sensory neurons sensitive to the higher intensities are "recruited"; thus, intensity of a stimulus can be represented by the number and thresholds of activated cells. The position of a stimulus, either outside or inside the body, is likewise an important piece of information. Some sensory systems--the somatosensory system ("body sensation" system), for example--reveal this information by the position of receptors on the sensory surface. Thanks to labeled lines that uniquely convey spatial information, we can directly encode which patch of skin that darn mosquito is biting, in order to know exactly where to aim the slap. Similarly, in the visual system an object's spatial location determines which receptors in the eye are stimulated. In bilateral receptor systems--the two eyes, two ears, and two nostrils--differences in stimulation of the left and right receptors are encoded, providing the brain with additional cues to the location of the stimulus (this type of processing is discussed in more detail in Chapter 6). Neurons at all levels of the visual and the touch pathways--from the surface sheet of receptors all the way up to the cerebral cortex--are arranged in an orderly, maplike manner. The map at each level is not exact, but it does reflect both spatial positions and receptor density. More cells are allocated to the spatial representation of sensitive, densely innervated sites, like the lips, than to sites that are less sensitive, such as the skin of the back. Each cell in the sensory map thus preferentially responds to a particular type of stimulus occurring in a particular place, as we'll see next. Sensory neurons respond to stimuli falling in their receptive fields The receptive field of a sensory neuron consists of a region of space in which a stimulus will alter that neuron's firing rate. To determine this receptive field, investigators record the neuron's electrical responses to a variety of stimuli to see what makes the activity of that cell change from its resting rate. For example, which patch of skin must we stimulate to change the activity of one particular touch receptor? Experiments show that these somatosensory receptive fields are shaped like doughnuts, with either an excitatory center and an inhibitory surround (FIGURE 5.5), or an inhibitory center and an excitatory surround. Such somatosensory receptive fields make it easier to detect edges on the objects we feel. Receptive fields differ in size and shape and in the quality of stimulation that activates them. For example, some neurons respond preferentially to light touch, while others fire most rapidly in response to painful stimuli, and still others respond to cooling. Experiments tracing sensory information along the pathway from the receptor cell to the brain show that neurons at every level will respond to particular stimuli, so each of these cells has its own receptive field. But as each successive neuron performs additional processing, the receptive fields change considerably, as we will see later in this chapter and in Chapter 6 and Chapter 7. RECEPTORS MAY SHOW ADAPTATION TO UNCHANGING STIMULI Sensory adaptation is the progressive decrease in a receptor's response to sustained stimulation (FIGURE 5.6). This process allows us to ignore unimportant events. By not noticing the touch of our clothes on our skin, the buzz of overhead lights, and other stimuli that are unchanging, our sensory systems avoid overload and can remain vigilant for
Action potentials are recorded from individual somatosensory neurons of the cortex while different locations of the skin are touched.
Neuron A responds to touch on a speci c region of the forelimb.
Neuron B, only a few centimeters away from A in the somatosensory cortex, responds to stimulation of the tail.
Touch outside of receptive eld has no effect (spontaneous activity). Touch in center of receptive eld excites. Touch in surround inhibits. Touch outside of receptive eld has no effect. Touch in center of receptive eld excites. Touch in surround inhibits.
Cortical cell responses Period of stimulation Neuron A Period of stimulation Neuron B
FIGURE 5.5 Identifying Somatosensory Receptive Fields
critical events. Neuroscientists distinguish between phasic receptors, which display this sort of adaptation, and tonic receptors, which show little or no adaptation and thus can signal the duration of a stimulus. (As each of us knows all too well, pain sensors are often tonic receptors, maintaining a high level of activity to help us avoid further injury.) The process of adaptation illustrates the principle we referred to earlier in our discussion of selection and analysis: sensory systems often shift away from accurate portrayal of the external world. In some mechanical receptors, such as the Pacinian
phasic receptor A receptor in which the frequency of action potentials drops rapidly as stimulation is maintained. tonic receptor A receptor in which the frequency of action potentials declines slowly or not at all as stimulation is maintained.
The somatosensory neuron responds to a touch on the fth nger.
The neuron fires rapidly when the stimulus--whether weak, moderate, or strong--is first applied...
Foundations of Brain and Behavior 4e Strong stimulus
...but then it adapts, slowing to a steady rate.
FIGURE 5.6 Sensory Adaptation (After M. Knibestol and A. B. Valbo, 1970. Acta Physiol. Scand. 80: 178.) 2
corpuscle described earlier, adaptation develops from the elasticity of the receptor cell itself. When the corpuscle (which is a separate, accessory structure) is removed, the uncovered sensory nerve fiber does not adapt, but continues discharging action potentials in response to a constant stimulus. SOMETIMES WE NEED RECEPTORS TO BE QUIET We've already noted that survival depends more on sensitivity to important changes than on exact reporting of stimuli. To maintain such sensitivity, we need to suppress unneeded or unimportant sensory activity. As we just discussed, adaptation is one way in which sensory activity is controlled, and we are equipped with two additional suppression systems. One way to suppress sensory activity is simply to physically prevent the stimuli from reaching the sensors. Closing the eyelids provides this function in the visual system; in the auditory system, tiny middle-ear muscles reduce the intensity of sounds that reach the inner ear. A second kind of suppression of sensory inputs is entirely neural in nature. In many sensory and pain pathways, reciprocal neural connections descend from the brain to synapse on lower sensory levels, where they can then inhibit activity in the ascending sensory axons. This central modulation of sensory information, whereby the brain actively controls the information it receives, is a feature of many sensory and pain pathways. Such modulation helps the brain attend to some stimuli more than others.
central modulation of sensory information The process in which higher brain centers, such as the cortex and thalamus, suppress some sources of sensory information and amplify others. dorsal column system A somatosensory system that delivers most touch stimuli to the brain via the dorsal columns of spinal white matter. dermatome A strip of skin innervated by a particular spinal nerve. thalamus The brain regions at the top of the brainstem that trade information with the cortex.
1. In general terms, explain how a sensory event is encoded in action potentials in sensory fibers. 2. Why do some receptor cells respond only to strong stimuli? 3. Describe receptive fields and how scientists detect them. 4. Name and briefly describe a couple of processes that change a sensory neuron's response to stimuli. Successive levels of the CNS process sensory information Sensory information travels from the sensory surface to the highest levels of the brain, and each sensory system--such as touch, vision, or hearing--has its own distinctive pathway from the periphery to successively higher levels of the spinal cord and/ or brain. For example, the somatosensory touch receptors that we've been discussing send their axons--eventually bundled into sensory nerves--from the skin to the dorsal (rear) part of the spinal cord. On entering the cord, the somatosensory projections ascend as part of the spinal cord's dorsal column system, a large wedge of white matter in the dorsal spinal cord (FIGURE 5.7). These axons go all the way up to the brainstem, where they synapse onto neurons that project contralaterally (to the opposite side) and then go to the thalamus. From there, the incoming sensory information is directed to cortex. At all levels, the inputs are organized according to a somatosensory map in which the body surface is divided into discrete bands. Each band, called a dermatome (from the Greek derma, "skin," and tome, "part" or "segment"), is the strip of skin that is innervated by a particular spinal nerve (FIGURE 5.8). This maplike organization of sensory inputs is a feature of several sensory systems, including touch, vision, and hearing. Each station in a sensory pathway accomplishes a basic aspect of information processing. For example, painful stimulation of the finger leads to reflexive withdrawal of the hand, which is mediated by spinal circuits before we even feel any pain. At the brainstem level, other circuits turn the head toward the source of pain. Eventually, sensory pathways reach the cerebral cortex, where the most complex aspects of sensory processing take place, perhaps consciously identifying the source of the pain (darn, another sliver!) and planning a response (where did I leave those tweezers?). For most senses, information reaches the thalamus before being relayed
Midbrain Medial lemniscus Medulla Dorsal columns Spinal cord
4 At this point, the left thalamus will be receiving information about the right side of the body. The thalamus will in turn send this information to the somatosensory cortex.
3 In the medulla, the axon from the periphery makes its rst synapse, innervating a neuron of the dorsal column nuclei. This medullary neuron in turn sends its axon across the midline and up to the thalamus.
2 Once the axon enters the spinal cord dorsal horn, it joins the dorsal column of white matter and ascends to the brain.
FIGURE 5.7 Somatosensory Pathways
1 Touch receptors detect stimulation of the skin and send action potentials along axons that enter dorsal roots of the spinal cord. This axon is part of a unipolar neuron, the cell body of which resides in the dorsal root ganglion.
FIGURE 5.8 Dermatomes (A)
Peripheral nerve Skin surface with parts of three dermatomes
There is some overlap in innervation between adjacent dermatomes.
3 Primary sensory cortex swaps information with nonprimary sensory cortex.
2 The thalamus shares the information with the cerebral cortex; the cortex directs the thalamus to suppress some sensations.
1 Sensory information enters the CNS through the brainstem or spinal cord and then travels to the thalamus.
FIGURE 5.9 Levels of Sensory Processing
primary sensory cortex For a given sensory modality, the region of cortex that receives most of the information about that modality from the thalamus (or, in the case of olfaction, directly from the secondary sensory neurons). nonprimary sensory cortex Also called secondary sensory cortex. For a given sensory modality, the cortical regions receiving direct projections from primary sensory cortex for that modality. primary somatosensory cortex Also called somatosensory 1 or S1. Primarily the postcentral gyrus of the parietal lobe, where sensory inputs from the body surface are mapped.
to the cortex (FIGURE 5.9). Information about each sensory modality is sent to a separate division of the thalamus. One way for the brain to suppress particular stimuli is for the cortex to direct the thalamus to emphasize some sensory information and suppress other information. SENSORY CORTEX IS HIGHLY ORGANIZED Researchers have identified a region designated as primary sensory cortex for each sensory modality--primary somatosensory cortex, primary auditory cortex, and so on--that is generally the initial destination of sensory inputs to the cortex. However, other cortical regions may receive and process the same information, often in collaboration with the primary sensory cortex; sensibly enough (pardon the pun), we call these regions nonprimary sensory cortex (see Figure 5.9). Each cortical sensory region processes different aspects of our Wpaetrscoen/pBtureaeldeloxvpeeriences. The MPinridm'saMryacshoinme atosensory cortex (also called somatosensory 1 or S1) of each hemiFsopuhndearteioinssloocf aBtreadinianndthBeehpaovsiotcre4netral gyrus, the long strip of tissue that lies just posterior Dragon y Media Group MtoMt4he_e05c.e0n9.tarial sulc0u3/s0d2/iv2i0d2i0ng the parietal lobe from the frontal lobe (FIGURE 5.10A). S1 receives touch information from the opposite side of the body. The cells in S1 are arranged as a map of the body (FIGURE 5.10B), but it is a very unusual, distorted map: the size of each region on the map is proportional to the density of sensory receptors found in that region of the skin. Parts of the body where we are especially sensitive to touch (like the hand and fingers) have large representations in S1 compared with less sensitive areas (like the shoulder). This proportional mapping is illustrated in the strange-looking character in FIGURE 5.10C, called a sensory homunculus, in whom the size of each body part reflects the proportion of S1 devoted to that part. We discuss other aspects of cortical organization in A STEP FURTHER 5.1, on the website. Sensory brain regions influence one another and change over time Often the use of one sensory system influences perception from another sensory system. For example, humans detect a visual signal more accurately if it is accompanied by a sound from the same part of space (Hillyard et al., 2016).
Trunk Neck Head Shoulder Arm Elbow Forearm Hand
The homunculus (literally, "little man") depicts the body surface with each area drawn in proportion to the size of its representation in the primary somatosensory cortex. (C)
Digit 5 4 3 2 Thumb Eyes Nose Face Upper lip Lower lip Chin
The order and size of cortical representations of different regions of skin vary; information from the hand and ngers takes up much more room than does information from the shoulder.
Many sensory areas in the brain--called association areas--process a mixture of inputs from different modalities. Some "visual" cells, for instance, also respond to auditory or touch stimuli. The convergence of information from different sensory systems on these polymodal neurons allows different sensory systems to interact (B. E. Stein and Stanford, 2008). And for a few people, a stimulus in one sensory modality may evoke an additional perception in another sensory modality, as when seeing a number evokes a color, or music literally becomes a matter of taste, where each note has both a sound and a flavor (Beeli et al., 2005). This condition is known as synesthesia. For more information and an example of synesthesia, see A STEP FURTHER 5.2, on the website. At one time, most researchers thought that sensory regions of cortex were fixed early in life. Now, however, we know that cortical maps are highly plastic, changing considerably as a result of experience (D. T. Blake et al., 2006). For example, two artists born without arms who used their toes extensively had distinct maps of each toe, unlike control participants (Dempsey-Jones et al., 2019). Professional musicians who play stringed instruments have expanded cortical representations of their left fingers, presumably because they use these fingers to depress the strings for precisely the right notes (Münte et al., 2002). Brain imaging also reveals cortical reorganization in people who lose a hand in adulthood (FIGURE 5.11). One man received a transplanted hand
FIGURE 5.10 Representation of the Body Surface in Somatosensory Cortex
polymodal neuron A neuron upon which information from more than one sensory system converges. synesthesia A condition in which stimuli in one modality evoke the involuntary experience of an additional sensation in another modality.
Foundations of BrainAanrmd Behavior 4eCentral
(B) After the loss of one hand, the cortical regions representing the upper arm and face expand, taking over the cortical region previously representing the missing hand.
FIGURE 5.11 Plasticity in Somatosensory Cortex (After T. T. Yang et al., 1994. NeuroReport 5: 701.)
Region formerly stimulated by receptors in the hand now responds to touch on face or arm.
pain The discomfort normally associated with tissue damage.
(from a deceased accident victim) 35 years after losing his own. Despite the length of time that had passed, his brain reorganized in just a few months to receive sensation from the hand in the appropriate part of S1 (Frey et al., 2008). Some changes in cortical maps occur after weeks or months of use or disuse; they may arise from the growth of new synapses and dendrites or from the loss of others.
1. Name the main somatosensory (touch) pathway to the brain, describe its organization, and name its main components. 2. Where is the primary somatosensory cortex located? How is it organized? 3. Discuss interactions between sensory modalities--for example, effects of auditory inputs on visual perception.
Doesn't That Hurt? Although it might seem like a blessing, people with congenital insensitivity to pain, like the "Human Pincushion" pictured here, tend to die young as a consequence of repeated body injuries.
5.2Pain: The Body's Emergency Signaling System This next section describes the system bringing us the unpleasant but adaptive sensation of pain. Studying this material should enable you to: 5.2.1 List and describe the three separate components of pain experience. 5.2.2 Describe the neuronal receptor cells that detect painful stimuli and the molecular receptor proteins they use. 5.2.3 Trace the neuronal pathway that transmits pain information from the periphery to the brain, as well as the neuronal pathway by which the brain can modulate pain. 5.2.4 Discuss the various methods for controlling pain, including advantages and disadvantages of each. One important aspect of body sensation is at best a mixed blessing. The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." Pain forcefully guides our behavior in several ways that minimize the risk to our bodies (Melzack et al., 2001). Immediate, short-term pain causes us to withdraw from the source, often reflexively, thus preventing further damage. Longer-lasting pain encourages behaviors, such as sleep, inactivity, grooming, feeding, and drinking, that promote recuperation. And the pain-related social communication--grimacing, groaning, shrieking, and the rest of the miserable lineup--provides a warning to kin and elicits caregiving behaviors from them, including grooming, defending, and feeding. Learning, experience, emotion, and culture all affect our perception of pain in striking ways, and these factors may strongly influence people's descriptions of pain, ranging from an apparent absence of pain in badly injured soldiers and athletes, to the anguish of a child with a paper cut. A widely used quantitative measure of pain perception--the McGill Pain Questionnaire (Main, 2016)--asks people to select words that tap three different dimensions of pain: 1. The sensory-discriminative dimension (e.g., throbbing, gnawing, shooting) 2. The motivational-affective (emotional) dimension (e.g., tiring, sickening, fearful) 3. An overall cognitive-evaluative dimension (e.g., no pain, mild, excruciating) Researchers found that people use different constellations of descriptors in various forms of pain: tooth pain is described differently from arthritic pain, which in turn is
described differently from menstrual pain. This more detailed analysis provides better information for the diagnosis and treatment of illness. A discrete pain pathway projects from body to brain Most tissues of the body (but not all) contain receptors specialized for detecting painful stimuli. These receptors are particularly well studied in the skin; in this section we discuss some features of these receptors, along with the peripheral and CNS pathways that mediate pain. PERIPHERAL RECEPTORS GET THE INITIAL MESSAGE When tissue is injured, the affected cells release chemicals that activate nearby pain receptors, called nociceptors, on free nerve endings specialized to detect damage. These chemicals also cause inflammation (FIGURE 5.12). Many different substances in injured tissue--serotonin, histamine, and various enzymes and peptides, to name just a few--can stimulate these nociceptors. Different nociceptors respond to various stimuli, such as pain and/ or changes in temperature. Identification of the nociceptor that detects physical damage was aided through careful study of the family of a Pakistani boy who died in tragic circumstances-- performing dangerous pranks because he could feel no pain. Scientists isolated a mutation in a gene (called SCN9A) that appears to be responsible for his congenital insensitivity to pain (CIP). Children with CIP require constant monitoring to prevent them from poking out their eyes or pulling out their teeth (Oppenheim, 2006). The SCN9A gene encodes a sodium channel expressed in free nerve endings that serve as nociceptors (J. J. Cox et al., 2006), offering a new target for developing high-potency pain medication. Some free nerve endings detect temperature changes. Studies of capsaicin, the chemical that makes chili peppers spicy hot, helped reveal the receptor that signals sudden increases in temperature (this action is the reason spicy food seems to burn)
nociceptor A receptor that responds to stimuli that produce tissue damage or pose the threat of damage.
3 Stimulated mast cells release histamine and a currently unknown, chloroquine-like molecule.
FIGURE 5.12 Peripheral Mediation of Pain
1 Damaged cells release substances that excite free nerve endings that function as nociceptors.
2 Action potentials generated in the periphery can re exively excite blood vessels and mast cells to produce in ammation.
4 Information enters through the dorsal root and synapses on neurons in the dorsal horn.
5 Pain bers release glutamate as a transmitter and substance P as a neuromodulator in the spinal cord. The dorsal horn cells then send information across the midline and up to the thalamus.
transient receptor potential type M3 (TRPM3) A receptor, found in some free nerve endings, that opens its channel in response to rising temperatures. A delta (A) fiber A moderately large, myelinated, and therefore fastconducting axon that usually transmits pain information. C fiber A small, unmyelinated axon that conducts pain information slowly and adapts slowly.
(C. Moore et al., 2018). This receptor, with the not-so-spicy name transient receptor potential vanilloid type 1 (TRPV1, or just vanilloid receptor 1), belongs to a larger family of proteins called transient receptor potential (TRP) ion channels. Mice lacking the gene for TRPV1 still respond to mechanosensory pain, but not to mild heat or capsaicin (Caterina et al., 2000). TRPV1's normal job is to report a rise in temperature to warn us of danger, so chili peppers cleverly evolved capsaicin to ward off mammalian predators--by falsely signaling burning heat. A related receptor, transient receptor potential type M3 (TRPM3), detects even higher temperatures than does TRPV1, but it does not respond to capsaicin (Vriens and Voets, 2018). TRPM3 receptors are found on A delta (A) fibers, which are large-diameter, myelinated axons. Because of the relatively large axon diameter and myelination, action potentials in these fibers reach the spinal cord very quickly. In contrast, the nerve fibers that possess TRPV1 receptors consist of thin, unmyelinated fibers called C fibers. So, when you burn your hand on that hot pan, the initial sharp pain you feel is conducted by the fat A delta fibers activated by their TRPM3 receptors, and the long-lasting dull ache that follows arises from slower C fibers and their TRPV1 receptors. Other members of the TRP family of receptors detect coolness as well as constituents of spices like oregano, cloves, garlic, and wasabi (Jordt et al., 2004; Bautista et al., 2007; Salazar et al., 2008), but their relation to pain receptors remains a delicious mystery (sorry). Stimulating your TRPV1 receptor too much can be hazardous to your health, as we see in Signs & Symptoms next.
From S. K. Boddhula et al., 2018. BMJ Case Reports. Courtesy of Kulothungan Gunasekaran
The 34-year-old man was a professional eater,
entering contests to see how quickly he could
down huge quantities of food. He'd been moder-
ately successful in this pursuit, but a chili pepper
contest proved to be too much. After eating an
entire "Carolina Reaper" pepper, purposely bred
to be 6 times hotter than a habanero pepper, the
man suffered dry heaves and pain in his neck
followed by a series of thunderclap headaches:
excruciating, sudden-onset headaches that peak
in a minute before subsiding, only to return (Bod-
dhula et al., 2018). MRI scans of the man's brain
showed no abnormalities, but a CAT scan of
blood vessels revealed that several arteries sup-
plying his brain had narrowed to a remarkable
extent (FIGURE 5.13A), which may have caused the headaches. Over the next few days, the man suffered several more thunderclap headaches lasting a few seconds. Once the headaches had stopped, the CAT scan showed that the arteries supplying his brain had expanded to a more
Eating an entire "Carolina Reaper" chili pepper appeared to close off some of the blood vessels supplying this man's brain, which may have caused the sudden, severe headaches he suffered.
normal size (FIGURE 5.13B). The gentleman may have gotten off lightly. People have
FIGURE 5.13 Thunderclap Headache
suffered severe, even fatal, heart attacks after
eating superhot chili peppers (N. Davis, 2018).
(B) Five weeks later, after the headaches had stopped, the blood vessels were much less constricted.
Special neural pathways carry pain information to the brain Nerve fibers carrying information about pain and temperature send their axons to enter the dorsal horns of the spinal cord, where they synapse onto spinal neurons that project across the midline to the opposite side and then up toward the thalamus of the brain, forming the anterolateral system (or spinothalamic system) (FIGURE 5.14). This projection is distinct from the somatosensory system that we discussed earlier (the dorsal column system; see Figure 5.7), but as in that system, each hemisphere receives its inputs from the contralateral side of the body. Within the spinal cord, the arriving pain fibers release the excitatory transmitter glutamate along with a peptide, substance P, that selectively boosts pain signals and remodels pain pathway neurons (Zieglgänsberger, 2019). Mice lacking substance P cannot feel intense pain, but they still feel mild pain (Hökfelt et al., 2001). Pain information is eventually integrated in the cingulate cortex, part of the limbic system we mentioned in Chapter 1 (see Figure 1.14B). The extent of activation in the cingulate (as well as in somatosensory) cortex correlates with how much discomfort different people report in response to the same mildly painful stimulus (Coghill et al., 2003). Different subregions of the cingulate cortex seem to mediate emotional
anterolateral system Also called spinothalamic system. A somatosensory system that carries most of the pain information from the body to the brain. substance P A peptide transmitter that is involved in pain transmission. cingulate cortex Also called cingulum. A region of medial cerebral cortex that lies dorsal to the corpus callosum.
Somatosensory cortex (S1) Thalamic nuclei
FIGURE 5.14 Ascending Pain Pathways in the CNS Pain sensation travels from its origin to the brain via the anterolateral (spinothalamic) system, crossing the midline in the spinal cord.
5 Cingulate cortex is especially activated by pain information.
Forebrain Midbrain Pons Medulla Anterolateral or spinothalamic system Spinal cord
4 Pain information is distributed to many thalamic and cortical areas. Periaqueductal gray 3 Pain information is provided to various brainstem sites, which control pain-related behavior such as vocalization. 2 Axons of dorsal horn neurons cross the midline and ascend the spinal cord in the anterolateral quadrant. 1 Pain information is carried by rapidly conducting myelinated A delta bers and slowly conducting unmyelinated C bers. A and C bers
FIGURE 5.15 Using a Visual Illusion to Relieve Phantom Limb Pain (After V. S. Ramachandran and D. RogersRamachandran, 2000. Arch. Neurol. 57: 317.)
The mirror seems to show that both limbs are intact. The individual is asked to command both hands to move in symmetry, and observe them.
The illusion of controlling the missing hand relieves the phantom sensation that the missing hand is painfully clenched shut.
View Activity 5.2: Ascending Pain Pathways in the CNS
versus sensory aspects of pain (Vogt, 2005); one part of the cingulate cortex becomes active even when we just empathize with a loved one experiencing pain (T. Singer et al., 2004). Sometimes pain persists long after the injury that started it has healed. This neuropathic pain is a disagreeable example of neuroplasticity, where neurons continue to directly signal pain, and indeed amplify the pain signal, in the absence of any tissue damage (Woolf and Salter, 2000). In one example of neuropathic pain called phantom limb pain, patients experience great pain that seems to come from an amputated limb. It is notoriously difficult to treat. One approach that has some success involves using a mirror to trick the brain into believing it is controlling the missing limb (FIGURE 5.15) (Ramachandran and Rogers-Ramachandran, 2000); apparently, visual feedback (even if false) allows the brain to recalibrate the pain signal.
neuropathic pain Pain that persists long after the injury that started it has healed. analgesia Absence of or reduction in pain.
1. Define pain. Why should pain be viewed as a positive adaptation? 2. Provide a general explanation of the way pain receptors work. How do pain Watsorne/cBerepetdolrosvde iffer from touch receptors? The3M. Ninadm'seMaanchdindeistinguish between the two sizes of fibers that carry pain information Foundfartoiomnsthoef BpreairnipahnedryBethoatvhioers4peinal cord. Dragon y Media Group MM44. eS_0k5e.t1c5h.aithe pai0n3/p0a2t/h2w02a0ys from the periphery to the cortex. Pain control can be difficult Throughout history, suffering humans have sought remedies to reduce their experience of pain. It's not easy; even cutting nerves may provide only temporary relief, until the pain system finds a way to restore its signal to the brain. A dominant model of pain transmission, called the gate control theory, hypothesizes that spinal "gates"--modulation sites at which pain can be facilitated or blocked--control the signal that gets through to the brain (Melzack and Wall, 1965). If this theory is right, effective pain relief may depend on finding ways to keep the gates closed, cutting off the pain signal. Popular strategies for analgesia (absence of pain; from the Greek an, "not," and algesis, "feeling of pain") fall into four general categories, which we'll discuss next.
© Meghan Mccarthy/The Palm Beach Post via ZUMA Wire/Alamy Stock Photo
Analgesic drugs are highly effective The opiates (opium-related drugs, like morphine) have been known for centuries to relieve pain sensations. Along with brain-derived painkillers such as the endorphins and other endogenous opioids, opiate drugs bind to specific receptors in the brain to reduce pain (see Chapter 4). Researchers have found that this action is especially pronounced in the brainstem region called the periaqueductal gray (see Figure 5.14); one possibility is that the brainstem system activates the pain-gating mechanism of the spinal cord via descending projections, thereby blocking the transmission of pain signals. Similar benefits can be obtained by (carefully!) injecting opiates directly into the spinal cord; this is called an epidural or intrathecal injection. Although people sometimes become addicted to painkillers, that is usually not true of people who are using them to treat severe pain; in fact, the danger of addiction from the use of morphine to relieve surgical pain has been vastly exaggerated and is estimated to be less than 1% (Brownlee and Schrof, 1997). Unfortunately, those few who do become addicted face a very real danger of death by overdose (Volkow et al., 2018); an opioid epidemic has been made worse by the development of extremely potent opioids such as OxyContin and fentanyl, resulting in more and more deaths (see Figure 3.9). If given in time, opioid antagonists like naloxone (Narcan) can save addicts' lives, so more and more public safety officers carry the drug. Of course, there are other painkilling drugs, but none are as effective as the opiates. Over-the-counter medications like aspirin and acetaminophen (Tylenol) act via non-opiate mechanisms (especially the cyclooxygenase enzymes COX-1 and COX-2) to reduce pain and inflammation. Cannabis reduces pain by stimulating endogenous cannabinoid receptors (CB1 receptors) in the spinal cord and in the brain (Agarwal et al., 2007; Pernía-Andrade et al., 2009). Electrical stimulation can sometimes relieve pain In transcutaneous electrical nerve stimulation (TENS), mild electrical stimulation is applied to nerves around the injury sites to relieve pain. The exact mechanism of this pain relief is not clear, but one possibility is that TENS closes the spinal "gate" for pain that Melzack and Wall (1965) described. Recall, for example, the last time you stubbed your toe. In addition to expelling a string of expletives, you may have vigorously rubbed the injured area, bringing a little relief. TENS is a more efficient way of stimulating those adjacent nerves, and it may bring dramatic relief lasting for hours (Vance et al., 2014). We know that TENS acts at least in part by releasing endogenous opioids, because administration of the opioid antagonist naloxone partially blocks this analgesic action (Gonçalves et al., 2014). Placebos effectively control pain in some people, but not all In some people, simply believing that they are receiving a proven treatment can effectively relieve pain. In a classic example of this placebo effect, when participants who had just had their wisdom teeth extracted were given morphine or a placebo, fully a third of those receiving the placebo experienced pain relief (J. D. Levine et al., 1978). But when the placebo was coadministered with a drug that blocks opioid receptors (naloxone), the participants did not experience the benefits of the placebo effect. This latter finding strongly implies that placebos work by activating the brain's endogenous opioid system. In fact, functional brain imaging indicates that opioids and placebos activate the same brain regions (Petrovic et al., 2002; D. J. Scott et al., 2008). For reasons unknown, some people consistently experience relief from placebos while others do not (FIGURE 5.16).
Life Saver Naloxone is sometimes called the "Lazarus drug" for its ability to revive people dying of a narcotic overdose in less than a minute. endorphin One of three kinds of endogenous opioids. naloxone A potent antagonist of opiates that is often administered to people who have taken drug overdoses. transcutaneous electrical nerve stimulation (TENS) The delivery of electrical pulses through electrodes attached to the skin, which excite nerves that supply the region to which pain is referred. placebo effect Relief of a symptom, such as pain, that results following a treatment that is known to be ineffective or inert. This region, rich in endogenous opioid receptors, is more active in people who respond well to placebos.
From D. J. Scott et al., 2008 Arch. Gen. Psych. 65: 220
FIGURE 5.16 Placebos Affect Opioid Systems in the Brain
TABLE 5.2 Types of Pain Relief
PSYCHOGENIC Placebo Hypnosis Stress Cognitive (learning, coping strategies) PHARMACOLOGICAL Opiates Spinal block Anti-inflammatory drugs Cannabinoids STIMULATION TENS/mechanical Acupuncture Central gray
May activate endorphin-mediated pain control system Alters brain's perception of pain Uses both opioid and non-opioid mechanisms May activate endorphin-mediated pain control system Bind to opioid receptors in periaqueductal gray and spinal cord Blocks pain signals in spinal cord Block chemical inflammatory signals at the site of injury (see Figure 5.12) Act in nociceptor endings, spinal cord, and brain On large fibers, blocks or alters pain signal to brain Activates endogenous opioids and/or placebo-like effect, possibly modulating effect on activity of peripheral pain pathways Electrically activates endorphin-mediated pain control systems, blocking pain signal in spinal cord
acupuncture The insertion of needles at designated points on the skin to alleviate pain or neurological malfunction.
Activation of endogenous opioids relieves pain Although the ancient pain-relieving technique acupuncture remains very popular, only a minority of people using acupuncture achieve lasting relief from chronic pain. In those people for whom acupuncture is effective, a release of endorphins may be an important part of the process, since treatment with naloxone often blocks acupuncture's effectiveness (Staud and Price, 2006). Acupuncture thus resembles placebos in this regard. Although many rules govern needle placement in acupuncture, systematic research indicates that the placement of the needles actually has little to do with its effects on pain (Linde et al., 2009). The expectation that the needles will relieve pain appears to be the important factor, presumably inducing a release of endogenous opioids. Likewise, stressful life events can produce significant analgesia; for example, tales abound of gravely wounded soldiers who feel no pain for some time after their injuries occur (Bowman, 1997). Research in animals indicates that stress activates both an opioid-dependent form of analgesia, which can be blocked by naloxone, and another, non-opioid analgesia system that has not yet been characterized (but may rely on endocannabinoids) (A. G. Hohmann et al., 2005). These endogenous analgesic systems allow a wounded individual to fight or escape rather than be overwhelmed with pain. Pain relief remains a major challenge for neuroscience research. Chronic pain can have dramatic effects on the brain: for example, the prefrontal cortex in people with chronic back pain shrinks much faster than normal, as if the patients are rapidly aging (Apkarian et al., 2004). The wide range of pain relief strategies (summarized in TABLE 5.2), some of which reflect desperation in the face of great anguish, testifies to the elusive nature of pain. As we learn more about how the brain controls pain, we can hope for better, safer analgesics in the future.
1. What is the most effective pharmacological method of pain control? How and where do these drugs work in the brain? 2. How is TENS thought to work to control pain? 3. Compare and contrast placebos and acupuncture for pain. Discuss the possibility that they act on the same neural system.
This chapter concludes with the system that enables the brain to move the body, allowing us to interact with the world. Learning this information means you can:
5.3.1 Discuss the importance of motor planning and sensory feedback in controlling behavior.
5.3.2 Trace the pathways by which the brain sends commands to individual muscles.
5.3.3 Distinguish between the two main types of sensory feedback from muscles to
5.3.4 Discuss the interaction of various cortical and subcortical brain regions in
body part, usually resulting from a brief
5.3.5 Describe the behavioral symptoms and underlying pathology of two major
Our apparently effortless adult motor abilities--such as reaching out and picking up an object, walking across the room, sipping a cup of coffee--require complex muscular systems with constant feedback from the body. Ian, whom we met at the beginning of the chapter, knows this all too well. Our survey of motor control starts with a discussion of a theoretical framework for studying motor behavior, followed by a tour of the anatomy and pathology of movement.
stimulus (e.g., an eye blink in response to a puff of air). act Complex behavior, as distinct from a simple movement. motor plan Also called motor program. A plan for a series of muscular contractions, established in the nervous system
When you think about it, all behavior must involve movements--contractions of prior to its execution.
muscles that provide our sole means of interacting with the world around us. Early electromyography (EMG)
discoveries suggested that reflexes--simple, unvarying, and unlearned responses
The electrical recording of muscle activity.
to sensory stimuli such as touch, pressure, and
pain--might be the basic units of behavior. It was
thought that more-complex behaviors, or acts,
such as getting dressed, walking, or speaking a
sentence, might result from simply connecting
together different reflexes, the sensation from
The flaws of this perspective soon became
apparent: for most acts we have a plan in which
several units (arm movements, leg movements,
speech sounds) are placed in a larger pattern (the
intended complete act), and they are not always
produced in the same (or even the correct) order. So, researchers realized that acts require a motor plan (or motor program), a complex set of com-
mands to muscles that is established before an act occurs. Feedback from movements informs and fine-tunes the motor program as the execution is unfolding, but the basic sequence of movements
When asked to pull up on the lever, the person rst adjusts their
is planned. Examples of behaviors that exhibit this kind of internal plan range from highly skilled acts, such as piano playing, to the simple
legs to steady themselves--an example of a simple motor
escape behaviors of animals such as crayfish.
Researchers can track the simple movements that make up an act by recording the electrical activity of muscles as they contract--a technique called electromyography (EMG)--and
the moment-to-moment positions of the body.
The EMG recordings in FIGURE 5.17 show that
FIGURE 5.17 Electromyography (After D. Purves et al., 2001. Neuro
a person pulling a lever will adjust his legs just
science [2nd ed.]. Oxford University Press/Sinauer. Sunderland, MA.)
162CHAPTER5 antagonist A muscle that counteracts the effect of another muscle. synergist A muscle that acts together with another muscle.
before moving his arm--an example of motor planning. Motor plans resemble engineering concepts that are applied to the operation of machines. In designing machines, engineers commonly have two goals: (1) accuracy, to prevent or minimize error; and (2) speed, to complete a task quickly and efficiently. Improvements in one goal usually come at some cost to the other goal; in other words, there is a trade-off between speed and accuracy, and this trade-off is also apparent in motor planning by the nervous system. The neuromuscular system consists of the muscles of the body plus a collection of brain mechanisms and nerves that prepare and execute motor plans and obtain feedback information from the sensory system for use in error correction. The system is organized according to a distinct hierarchy: 1. The skeletal system and the muscles attached to it determine which movements are possible. 2. The spinal cord controls skeletal muscles in response to motor commands from the brain or, in the case of simple reflexes, in direct response to sensory inputs. 3. The brainstem integrates motor commands from higher levels of the brain and transmits them to the spinal cord. It also relays sensory information about the body from the spinal cord to the forebrain. 4. Some of the main commands for action are initiated in the primary motor cortex. 5. Areas adjacent to the primary motor cortex, nonprimary motor cortex, provide an additional source of motor commands, acting indirectly via primary motor cortex and through direct connections to lower levels of the motor hierarchy. At the very top of the movement hierarchy is the prefrontal cortex, which is crucial to the formulation of behavioral plans. 6. Other brain regions--the cerebellum and basal ganglia, via the thalamus-- modulate the activities of the other parts of the control system. Through the remainder of the chapter we'll look at the elements of this hierarchy, as outlined in FIGURE 5.18, in a bit more detail.
The motor cortex receives information from other cortical areas and sends commands to the thalamus and brainstem.
Primary motor cortex Nonprimary motor cortex Basal ganglia
The cerebellum and basal ganglia adjust the commands received from other parts of the motor control system. Cerebellum
The brainstem passes commands from the cortex to the spinal cord.
Muscles Muscles of face, of body head, and neck
FIGURE 5.18 The Hierarchy of Movement Control
1. Distinguish among reflexes, movements, and acts. 2. Discuss the importance of sensory feedback for the control of movements. How are speed and accuracy related, in the context of movement control? 3. What is a motor plan? 4. Identify the six major levels of the motor control hierarchy. Muscles and the skeleton work together to move the body Our skeleton, like those of other species with bones, is articulated with joints that vary in their planes of movement--ranging from "universal" joints, like the hip or shoulder, to joints that act more like hinges and move mostly in one direction, such as the elbow or knee. Around a joint, different muscles, connected to the bones by tendons, are arranged in a reciprocal fashion such that when one muscle group contracts, it stretches the other group; that is, the muscles are antagonists. Some groups of muscles, called synergists, may work together to move a limb in one direction. A simple example of muscle action around a joint is shown in FIGURE 5.19. The movement of a limb is determined by the degree and rate of contraction in some muscles and relaxation
in others, or we can lock a limb in position by contracting opposing muscles at the same time. The muscles that we use for movement of the skeleton are called skeletal muscles. Because they have a striped appearance on microscopic examination, due to overlapping layers of contractile proteins called myosin and actin, skeletal muscles are said to be made of striate muscle. (Smooth muscle, which has a different appearance and is found in visceral organs and blood vessels, is not generally involved in voluntary behavior, so we will not concern ourselves with it here.) Contraction of the muscle increases the overlap of the actin and myosin filaments within muscle fibers, and as these filaments slide past each other, the muscle fiber shortens. Most muscles consist of a specific mixture of two types of fibers: slow-twitch fibers that contract with relatively low intensity but fatigue slowly, and fast-twitch fibers that contract strongly but fatigue quickly. Through training, endurance athletes enhance the slow-twitch properties of their muscles (Putman et al., 2004). Muscles contract because motor neurons (or motoneurons) of the spinal cord and brainstem (see Figure 1.7 and Figure 1.8) send action potentials along their axons and axon collaterals to terminate at specialized synapses, called neuromuscular junctions, that are found on muscle fibers (FIGURE 5.20). The production of an action potential by a motor neuron triggers a release of the neurotransmitter acetylcholine (ACh) at all of the
(A) Spinal motor neurons send their axons out the ventral roots to the periphery. (B) Muscle Axon of ber motor neuron
The Sensorimotor System 163 (B) Because muscles exert force only by contracting, muscle attachments determine the resulting movement.
arm, while the biceps The triceps extends the xion exes it. Because these two muscles mediate opposite movements, they are known as antagonists.
FIGURE 5.19 The Arrangement of Muscles around the Elbow
motor neuron Also called motoneuron. A neuron that transmits neural messages to muscles (or glands). neuromuscular junction The region where the motor neuron terminal meets its target muscle fiber. It is the point where the nerve transmits its message to the muscle fiber. acetylcholine (ACh) A neurotransmitter that is produced and released by the autonomic nervous system, by motor neurons, and by neurons throughout the brain.
Neuromuscular junctions (C) Axon terminal branch Motor end plate Muscle ber Myosin
Watson/NBerervedelove The Mind's Machine Foundations of Brain and Behavior 3e
Figure: 05.19
Near the muscle, each axon splits into several collaterals, each of which innervates a separate muscle ber within the muscle.
FIGURE 5.20 The Innervation of Muscle
Intrafusal muscle ber (B) Innervation of a Golgi tendon organ
The receptors in the body of a muscle are muscle spindles.
A typical muscle spindle has sensory endings that signal current muscle length and its rate of change. The spindle can change its length to suit conditions.
The Golgi tendon organs monitor tension in the muscle.
final common pathway The motor neurons of the brain and spinal cord, so called because they receive and integrate all motor signals from the brain to direct movement. proprioception Body sense; information about the position and movement of the body.
motor neuron's axon terminals. The motor neuron, together with all of the muscle fibers it innervates, is known as a motor unit; the fibers respond to the release of ACh by triggering the molecular events that cause actin and myosin to produce contraction (see Figure 5.20). Some large motor units--where motor neurons innervate thigh muscle, for example--may involve hundreds or thousands of muscle fibers. But muscles that require more precise control--muscles of the face, for example--tend to have much smaller motor units, with each motor neuron controlling only a few muscle fibers. Many people experience "jumping nerves" in the eyelids when they're fatigued (from studying neuroscience, maybe). This tiny but incredibly annoying twitch, called a fasciculation, is actually a misfiring facial motor unit. A fasciculation in the thigh, in contrast, produces a much larger twitch. Within the spinal cord, motor neurons tend to have large cell bodies and very widespread dendritic fields because they receive and integrate inputs from so many different sources--incoming sensory inputs, as well as descending signals from the brain--that form thousands of synapses onto the motor neurons. Virtually all motor neuron axons are myelinated, so their action potentials reach their target muscles quickly. In a somewhat dramatic turn of phrase, neuroscientists refer to motor neurons as the final common pathway: the sole route through which the spinal cord and brain can control our many muscles. SENSORY FEEDBACK FROM MUSCLES, TENDONS, AND JOINTS REGULATES MOVEMENT To produce rapid coordinated movements of the body, the brain and spinal cord continually monitor the state of the muscles, the positions of the limbs, and the instructions being issued by the motor centers. This collection of information about body movements and positions is called proprioception (from the Latin proprius, "own," and recipere, "to receive"). Ian, whom we met at the start of this chapter, was attacked by a virus that selectively killed proprioceptive axons; his predicament illustrates how important this "sixth sense" is for movement. Let's consider
two proprioceptors--muscle spindles and Golgi tendon organs--that monitor muscle length and muscle tension. The muscle spindle is basically a capsule, buried within the other fibers of the muscle, that contains a special kind of muscle fiber called an intrafusal fiber (from the Latin intra, "within," and fusus, "spindle") (FIGURE 5.21A). When a muscle is stretched beyond its relaxed state, so it is lengthened--imagine someone handing you a heavy book, causing your arm to bend downward and lengthening the biceps muscle-- sensory endings within the spindle fiber become excited and trigger action potentials in sensory nerves. This proprioceptive signal informs the spinal cord and brain about the extent and rate of change in the length of the muscle, and therefore about the load being imposed. Interestingly, a special motor neuron controls the length of the intrafusal fiber, adjusting it according to the movements being planned by the brain--in a sense, calibrating the muscle spindle to the expected limb position. While muscle spindles respond primarily to length, the other proprioceptive receptors for muscle--Golgi tendon organs--are especially sensitive to the tension of the muscle as it shortens. Loads that are strong enough to stretch the tough tendon are sensed by the nerve endings of the Golgi tendon organ that weave through the tendon (FIGURE 5.21B). It takes a pretty strong load to stretch a tendon to this degree, so it makes sense that the primary function of Golgi tendon organs is to monitor the force of muscle contractions, providing a second source of sensory information about the muscles (FIGURE 5.22). This arrangement makes the Golgi tendon organs useful in another important way: they detect overloads that threaten to tear muscles and tendons, and they can cause a reflexive relaxation of the affected muscles, protecting the muscles (and causing you to drop that book). Another familiar example of a stretch reflex is the knee-jerk (or patellar) reflex that we discussed in Chapter 2 (see Figure 2.14). Classic studies in physiology emphasized the importance of information from muscle spindles and Golgi tendon organs for controlling movement. Mott (1895) and
muscle spindle A muscle receptor that lies parallel to a muscle and sends impulses to the central nervous system when the muscle is lengthened. intrafusal fiber Any of the small muscle fibers that lie within each muscle spindle. Golgi tendon organ A type of receptor found within tendons that sends impulses to the central nervous system when a muscle contracts.
Intrafusal muscle ber Low level of excitation of both receptors
Spindle activity Golgi tendon organ activity
FIGURE 5.22 Activation of Muscle Receptors
Tendon organ excited; spindle not excited
When a load is imposed on the muscle, muscle receptors are excited as shown here.
166CHAPTER5 View Animation 5.4: The Stretch Reflex Circuit
4 The muscle spindle also excites interneurons that inhibit triceps motor neurons, causing the triceps to relax when the biceps contracts.
3 The action potentials synapse onto motor neurons in the spinal cord that cause the biceps to contract, restoring the arm to its original position.
1 A weight dropped into the hand stretches the biceps muscle.
2 The stretch excites the muscle spindle, which sends action potentials to the dorsal spinal cord. Triceps muscle
FIGURE 5.23 The Stretch Reflex Circuit
stretch reflex The contraction of a muscle in response to stretch of that muscle. pyramidal system Also called corticospinal system. The motor system that includes neurons within the cerebral cortex and their axons, which form the pyramidal tract.
Sherrington (1898) showed that severing the sensory fibers from a monkey's arm muscles causes the monkey to stop using the affected limb, even if the connections from motor neurons to the muscles are preserved. The arm dangles, apparently useless. But if the good arm is restrained, the animal soon learns to use the affected arm, and indeed it can become quite dexterous (Taub, 1976). Monkeys manage to do this the same way Ian does, by guiding their movements with visual feedback about how the arm is moving. In fact, we all supplement our proprioceptive information with feedback from other sensory channels, like vision. WaTtshone/sBpreiendlaovlecord mediates "automatic" responses ThaenMdindr'es cMeaicvheinse inputs from the brain Foundations of Brain and Behavior 4e DrTaogorneayllMyeudniadGerrosutpand the physiology of movement, we need to understand how the MM"f4ine_a0l5c.2o3m.aimon p0a8t/h3w1/a2y0"20is controlled by the CNS. The lowest level of this hierarchy is the spinal cord, where relatively simple circuits produce reflexive behavioral responses to sensory stimuli. A straightforward example is the stretch reflex, illustrated in FIGURE 5.23, that can be elicited by stretching any muscle. In this case, dropping a load into the outstretched hand causes a sudden stretch of the biceps muscle, which is detected by muscle spindles. In the spinal cord, the incoming sensory information from the spindles has two immediate effects: it stimulates motor neurons of the biceps, causing a contraction, and it simultaneously inhibits the antagonistic motor neurons that connect to the triceps muscle on the back of the arm. The reflex thus generates a compensatory movement to bring the hand and arm back to their intended position. Not all spinal circuits are quite this simple; for example, the rhythmic movements of walking are governed by spinal circuits that may involve many neurons across multiple spinal segments.
(A) Pyramidal motor system Frontal cortex Pyramid of medulla Fibers cross to the opposite side in the medulla and descend in the corticospinal tracts. Ventral corticospinal tract
Frontal lobe Cerebral cortex Upper medulla Lower medulla Spinal cord
(B) Representation of the body in primary motor cortex (M1)
Shoulder Neck Trunk Hip Leg Knee Ankle Feet Toes Genitalia
M1 is a strip just in front of the central sulcus. Regions controlling different parts of the body are shown here in relative sequence and size.
FIGURE 5.24 The Pyramidal System and Primary Motor Cortex (B after C. N. Prudente et al., 2015. J. Neurosci. 35: 9163.)
Although muscles of the head are controlled directly by the brain, via the cranial nerves (see Figure 1.7), the muscles of the rest of the body are ultimately controlled by commands from the brain and spinal cord via the somatic nerves. The brain sends these commands through two major pathways: the pyramidal system and the extrapyramidal system. The pyramidal system (or corticospinal system) consists of neuronal cell bodies within the frontal cortex and their axons, which pass through the brainstem, forming the pyramidal tract to the spinal cord (FIGURE 5.24A). In a cross section of the medulla, the tract is a wedge-shaped anterior protuberance (pyramid) on each side of the midline. Because the left and right pyramidal tracts each cross over to the other side, the right cortex controls the left side of the body while the left cortex controls the right. Lesions anywhere in the pyramidal tract will cause paralysis in the muscles controlled by the damaged neurons. Many of the axons of the pyramidal tract originate from neurons in the primary motor cortex (M1), which consists mainly of the precentral gyrus, just anterior to the central sulcus (FIGURE 5.24B). We will return to the topic of motor cortex a little later. Many other axon pathways run from the forebrain to the brainstem and spinal cord. Because these tracts are outside the pyramids of the medulla, they and their connections are lumped together as the extrapyramidal system. In general, lesions of the Wexattsroanp/yBrraeemdliodvael system do not prevent the movement of individual joints and limbs, The Mind's Machine Fbouunt dthateioynds oofiBnrtaeinrfaenrde Bweihtahvisopri4neal reflexes, usually exaggerating them, and they interDferargeown ityhMseydsitaeGmrosutphat regulate and fine-tune motor behavior. Many of these extrapyMraMm4eid_0a5l.2p4r.aoijection0s8/p3a1s/s20to20the spinal cord via specialized motor regions (the reticular formation and red nucleus) of the midbrain and brainstem; as we'll see shortly, the basal ganglia are an important point of origin for extrapyramidal projections. Spinal injuries due to vehicular accidents, violence, falls, and sports injuries are all too common, and they often cause heartbreaking disabilities. Because the spinal cord
Here, the gure's body parts are proportional to the amount of motor cortex devoted to the corresponding muscles, although this sort of mapping oversimpli es the organization of the motor cortex. extrapyramidal system A motor system that includes the basal ganglia and some closely related brainstem structures. Axons of this system pass into the spinal cord outside the pyramids of the medulla.
168CHAPTER5 1 Each horizontal line represents one action potential from this particular M1 neuron.
-500 0 500 1,000 ms 2 This cell is silent before movements of the arm toward the right...
3 ...but res vigorously before the arm is moved to the left or straight up.
FIGURE 5.25 Directional Tuning of Motor Cortex Cells (After A. P. Georgopoulos et al., 1982. J. Neurosci. 2: 1527. © 1982 Society for Neuroscience.)
the precentral gyrus. Watson/Breedlove precentraTlhgeyMruinsd's TMhaechstirnipe of frontal cortex, jusFtoinunfrdoanttioonfstohfeBcraeinntraanldsuBlechuasv,ior 4e
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carries all of the instructions from the brain to the muscles, an injury that completely severs the cord results in immediate and permanent paralysis below the level of injury. Depending on the extent of destruction of the spinal cord below the injury site, spinal reflexes may or may not be lost as well (in fact, reflexes may become stronger because of the loss of descending inhibition from the brain). Over 250,000 people in the United States have spinal cord injuries (Richards et al., 2017), and thousands more occur each year, mostly in young people. Although much remains to be discovered, the hope of reconnecting the injured spinal cord no longer seems far-fetched, as discussed in A STEP FURTHER 5.3, on the website. Motor cortex plans and executes movements--and more The primary motor cortex of humans--M1--is a major source of axons forming the pyramidal tract. Like S1, the primary somatosensory cortex that we discussed earlier in the chapter, M1 occupies a single large cortical gyrus: the precentral gyrus, located immediately in front of the central sulcus (M1 is thus a part of the frontal lobe; see Figure 5.24B). And like S1, M1 is organized as a map of the contralateral side of the body. So, electrical stimulation of a discrete region of the left M1 will cause movement in the corresponding region of the right side of the body. Once again, the map is distorted, in the sense that the parts of the body that we control most precisely--hands, lips, tongue--are overrepresented in M1. FIGURE 5.24C shows the motor homunculus, a figure drawn using the body proportions represented in M1. But although the M1 map helps us understand the basic organization of motor cortex, recent research indicates that the map is really an oversimplification. The mapping of individual body regions in M1 isn't nearly as clear-cut and discrete as traditional M1 maps suggest. In fact, there is a fair bit of intermingling of body regions in the map, because many body parts coordinate with one another across regions of M1 (Rathelot and Strick, 2006).
From M. H. Monfils et al., 2005. Neuroscientist 11: 471. Courtesy of J. Kleim
This map illustrates forelimb control in a rat's motor cortex, prior to training.
FIGURE 5.26 Motor Learning Causes Remapping of Motor Cortex
After 10 days of training on a task requiring precise reaching and grasping, the representation of the digits and wrist (green) has expanded into areas previously associated with the shoulder and elbow (blue).
By recording from M1 neurons in monkeys making arm movements, we can
eavesdrop on the commands originating there (FIGURE 5.25). Many M1 cells change
their firing rates according to the direction of the movement, but for any one cell, dis-
charge rates are highest in one particular direction. Only by averaging the activity of
hundreds of M1 neurons at once can we predict the direction of arm movements with
reasonable accuracy. But of course, millions of M1 neurons are available, so in principle
a larger sampling would provide a more accurate prediction.
Motor representations in M1 are not static; they change as a result of training. For
example, M1 is wider in piano players, especially in the hand area, than in nonmu-
sicians. The younger the musician was at the start of musical training, the larger the
gyrus is in adulthood (Amunts et al., 1997), so this expansion of M1 seems to be in
response to the experience of musical training. Studies using transcranial magnetic
stimulation (TMS) (see Chapter 1) to noninvasively stimulate cortical neurons have
shown that the movements produced by a patch of M1 may change with repeated use
or as a result of motor learning. In rats,
this cortical plasticity associated with (A) Lateral view
motor learning has been directly observed by means of sophisticated mapping of the motor cortex before and after extended training of a new skill (Monfils
Wartysomn/oBtroeerdcloovretex, that make additional The Mind's Machine FocurnudcatiiaolnscoofnBtrraiibnuatnidonBeshtaoviomr o4etor control. DrNagoonn pyrMimedairayGrmouoptor systems can con-
MMtr4ieb_u05te.26t.oai beha0v8i/o2r6/d20ir2e0ctly, through
spinal cord systems, as well as indirect-
of nonprimary motor cortex emphasizes two main regions: the supplementary motor area (SMA), which lies mainly on
Premotor cortex lies just anterior to primary motor cortex (M1). Shown here as one area for
the medial aspect of the hemisphere, and the premotor cortex, which is anterior to the primary motor cortex (FIGURE 5.27).
clarity, the premotor cortex is actually a mosaic of subareas with distinct properties.
nonprimary motor cortex Frontal lobe regions adjacent to the primary motor cortex that contribute to motor control and modulate the activity of the primary motor cortex. supplementary motor area (SMA) A region of nonprimary motor cortex that receives input from the basal ganglia and modulates the activity of the primary motor cortex. premotor cortex A region of nonprimary motor cortex just anterior to the primary motor cortex.
FIGURE 5.27 Human Motor Cortical Areas
Supplementary motor cortex (SMA) lies mainly on the medial surface of the cerebral hemispheres. The SMA and premotor cortex together make up nonprimary motor cortex.
170CHAPTER5 plegia Paralysis; the loss of the ability to move. paresis Muscular weakness, often the result of damage to motor cortex. apraxia An impairment in the ability to carry out complex movements, even though there is no muscle paralysis. mirror neuron A neuron that is active both when an individual makes a particular movement and when that individual sees another individual make the same movement.
The SMA seems important for the initiation of movement sequences, especially when they're being executed according to an internal preprogrammed plan (Tanji, 2001). In contrast, the premotor cortex seems to be activated when motor sequences are guided by external events (Svoboda and Li, 2018). However, evidence is mounting that premotor cortex is not a single system, but really a mosaic of different units, controlling groups of motor behaviors that cluster together into major categories: defensive movements, feeding behavior, and so on (Graziano, 2006; Graziano and Aflalo, 2007). This organization suggests that motor and premotor areas mostly map behaviors, rather than mapping specific movements, as in M1. Strokes or other injuries in motor areas of the cortex result in plegia (paralysis) or paresis (weakness) of voluntary movements, usually on the contralateral side of the body (hemiplegia or hemiparesis). Damage to nonmotor zones of the cerebral cortex, such as some regions of parietal or frontal association cortex, produces more-complicated changes in motor control, such as apraxia (from the Greek a, "not," and praxis, "action"), the inability to carry out complex movements even though paralysis or weakness is not evident and language comprehension and motivation are intact. There are several subtypes of apraxia, but in general it's as though the patient is unable to work out the sequence of movements required to perform a desired behavior--a high-level motor-programming problem.
1. Describe the arrangement of muscles and joints that allows movement. 2. Briefly describe the main components of a motor unit. 3. Define proprioception. Explain how two specialized sensors in muscle provide feedback about the muscle's current state. 4. Provide a summary of the path taken by motor fibers innervating the skeletal musculature--from the level of the brain, through the spinal cord, to the muscle targets. 5. Where is primary motor cortex located, and how is it organized? 6. Distinguish between the pyramidal and extrapyramidal systems. 7. What are some of the contributions of nonprimary motor cortex?
Mirror neurons in premotor cortex track movements in others
A subregion of premotor cortex (called F5) may contain a population of remarkable neurons that seem to fulfill two functions. These neurons fire shortly before a monkey makes a very particular movement of the hand and arm to reach for an object; different neurons fire during different reaching movements. The data thus suggest that these neurons trigger specific movements. But these neurons also seem to fire whenever the monkey sees another monkey (or a human) make that same movement (FIGURE 5.28). These cells are called mirror neurons because they fire as though
the monkey were imagining doing the same thing as the other individual. Mirror neurons are also found in adult humans (Buccino et al., 2004) and children (Lepage and Theoret, 2006), both in the premotor cortex and in other cortical locations. Because the activity of these neurons suggests that they are important in the understanding of other individuals' actions (Rizzolatti and Craighero, 2004), an intriguing notion is that mirror neurons could be part of a neural system for empathy. Thus, there has been a great deal of speculation about the function of mirror
neurons in the imitating behavior of human infants, the evolution of language, and other behavior (Gallese and Sinigaglia, 2011). Some have speculated that people with autism spectrum disorder, which is characterized by a failure to anticipate other people's thinking and actions, may have a deficit in mirror neuron activity (J. H. Williams et al., 2006). Note, however, that the specific functions ascribed to mirror neurons remain somewhat controversial (Caramazza et al., 2014).
RESEARCHERS AT WORK(continued) Question The researchers hypothesized that neurons of the premotor cortex, in a ventral subregion called F5, encode specific and detailed movements rather than muscle contractions. Experiment The activity of single F5 neurons was recorded while the monkey made reaching movements.
Result The neurons fired shortly before the monkey made a specific movement, in accordance with the initial hypothesis. But to the experimenters' surprise, the neurons also became active when the monkey simply watched an experimenter perform the same movement, as if the monkey was imagining making the movement.
The neuron is less responsive if there is no object to be picked up. Time Conclusion These "mirror neurons" may be part of a system for analyzing the behavior of others (Umilta et al., 2001). FIGURE 5.28 Mirror Neurons (After M. A. Umilta et al., 2001. Neuron 31: 155.) Watson/Breedlove The Mind's Machine Foundations of Brain and Behavior 4e
Extrapyramidal systems regulate and fine-tune motor commands
Earlier we noted that extrapyramidal projec-
tions--the motor fibers outside the pyramidal
tracts--are especially important in modulation
and ongoing control of movement. Two of the
most important sources of extrapyramidal fibers
are the basal ganglia and the cerebellum.
As we saw in Chapter 1, the basal ganglia
are a group of several interconnected forebrain
nuclei (especially the caudate nucleus, putamen,
and globus pallidus), with strong inputs from the
substantia nigra and the subthalamic nucleus. The
basal ganglia receive inputs, via the thalamus,
from wide expanses of the cortex forming a loop from the cortex through the basal ganglia and
thalamus and back to the cortex (FIGURE 5.29).
The basal ganglia help control the amplitude and
direction of movement, and changes in activity in
FIGURE 5.29 Subcortical Systems Involved in Movement
regions of the basal ganglia appear to be important for the initiation of movement. Much of the
motor function of the basal ganglia appears to be
the modulation of activity started by other brain
circuits, such as the motor pathways of the cortex (see Figure 5.24). The basal ganglia
View Activity 5.3: Subcortical Systems Involved
are especially important for movements performed by memory, in contrast to those guided by sensory control.
Inputs to the cerebellum come both from sensory sources and from other brain
motor systems. Sensory inputs include the muscle and joint receptors and the vestib-
basal ganglia A group of forebrain nuclei, including caudate nucleus, globus pallidus, and putamen, found deep within the cerebral hemispheres. cerebellum A structure located at the back of the brain, dorsal to the pons, that is involved in the central regulation of movement and in some forms of learning. ataxia A loss of movement coordination, often caused by disease of the
ular, somatosensory, visual, and auditory systems. Both pyramidal and nonpyramidal pathways contribute inputs to the cerebellum and in turn receive outputs--all of which are inhibitory--from the deep nuclei of the cerebellum. The cerebellum helps establish and fine-tune neural programs for skilled movements, especially the kinds of rapid, repeated movements that become automatic. Remarkably, some people appear to be born without a cerebellum, yet develop normal motor skills (FIGURE 5.30), presumably because of the great plasticity of the brain during development. In addition to its role in motor function, the cerebellum is also crucial for some types of learning (Katz and Steinmetz, 2002), as we'll discuss in more detail in Chapter 13.
DAMAGE TO EXTRAPYRAMIDAL SYSTEMS IMPAIRS MOVEMENT Different con-
stellations of symptoms are associated with damage to the various extrapyramidal
motor structures. The exact consequences of cerebellar damage depend on the part of
the cerebellum that has been damaged, but common motor symptoms include char-
acteristic abnormalities of gait and posture, especially ataxia (loss of coordination) of
the legs. Other cerebellar lesions may cause decomposition of movement (in which
gestures are broken up into individual segments instead of being executed smoothly)
or difficulties with gaze and visual tracking of objects. The anatomy of the cerebellum
and the symptomatology of cerebellar disease are discussed in more detail in A STEP
Two diseases that target the basal ganglia reveal important aspects of extrapyra-
midal contributions to motor control. Patients with Parkinson's disease show pro-
gressive degeneration of dopamine-containing cells in the substantia nigra. Loss of
these neurons, which project to the caudate nucleus and putamen, is associated with
a cluster of symptoms that are all too familiar: slow movement, tremors of the hands
FIGURE 5.30 A Woman without a
and face while at rest, a rigid bearing, and diminished facial expressions. Patients who
have Parkinson's show few spontaneous actions and have great difficulty in all motor
efforts, no matter how routine. Exercise can slow the progression of Parkinson's, and studies indicate that dance therapy, using music to encourage movement, helps patients with Parkinson's (Kalyani et al., 2019). Whereas damage to the basal ganglia in Parkinson's disease reduces movement, other kinds of basal ganglia disorders cause the opposite: excessive movement. The first symptoms of Huntington's disease are subtle behavioral changes: clumsiness, and twitches in the fingers and face. Subtlety is rapidly lost as the illness progresses; a continuing stream of involuntary jerks engulfs the entire body. Aimless movements of the eyes, jerky leg movements, and writhing of the body make even routine activity a major challenge, exacerbated in later stages of the disease by intellectual deterioration. The neuroanatomical basis of this disorder is widespread destruction of the basal ganglia, including the caudate nucleus and the putamen (rather than just the substantia nigra, which greatly reduces movement in Parkinson's). Although much remains to be discovered, there is more reason than ever to look forward to the introduction of effective treatments for motor disorders. Scientists are learning more and more about what goes wrong in Parkinson's and Huntington's diseases, and their continuing research efforts may pave the way to new therapies.
decomposition of movement Difficulty of movement in which gestures are broken up into individual segments instead of being executed smoothly. It is a symptom of cerebellar lesions. Parkinson's disease A degenerative neurological disorder, characterized by tremors at rest, muscular rigidity, and reduction in voluntary movement, caused by loss of the dopaminergic neurons of the substantia nigra. substantia nigra A brainstem structure that is a major source of dopaminergic projections to the basal ganglia. Huntington's disease A genetic disorder, with onset in middle age, in which the destruction of basal ganglia results in a syndrome of abrupt, involuntary writhing movements and changes in mental functioning.
1. What are mirror neurons, and what is their significance? 2. What are the symptoms of Parkinson's disease, and what brain changes cause it? 3. What are the symptoms of Huntington's disease, and what brain changes cause it? 4. Children of people with Huntington's disease have a fifty-fifty chance of inheriting the gene causing it. If you had a parent with Huntington's, would you want to take the test to see if you carry the disease? Recommended Reading Ballantyne, J. C., Fishman, S. M., and Rathmell, J. P. (Eds.). (2018). Bonica's Management of Pain (5th ed.). Philadelphia, PA: Lippincott. Cole, J. (2016). Losing Touch: A Man without His Body. Oxford, UK: Oxford University Press. Cytowic, R. E. (2018). Synesthesia. Cambridge, MA: MIT Press. McMahon, C., Koltzenberg, M., Tracey, I., and Turk, D. C. (2013). Wall and Melzack's Textbook of Pain (6th ed.). Philadelphia, PA: Saunders. Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W., et al. (Eds.). (2017). Neuroscience (6th ed.). Sunderland, MA: Oxford University Press/Sinauer. (See Unit III:"Movement and Its Central Control,"Chapters 16-21.) Turk, D. C., and Gatchel, R. J. (Eds.). (2018). Psychological Approaches to Pain Management: A Practitioner's Handbook (3rd ed.). New York, NY: Guilford Press. Walsh, R. A., de Bie, R. M., and Fox, S. H. (2017). Movement Disorders: What Do I Do Now? (2nd ed.). New York, NY: Oxford University Press. Wolfe, J. M., Kluender, J. R., Levi, D. M., Bartoshuk, L. M., et al. (2021). Sensation & Perception (6th ed.). Sunderland, MA: Oxford University Press/Sinauer.
You should be able to relate each summary to the adjacent illustration, including structures and processes. The online version of this Visual Summary includes links to figures, animations, and activities that will help you consolidate the material.
1 Receptor cells in sensory organs furnish only selected information to the brain. For example, our skin contains several kinds of touch receptors, each specialized for detecting a specific stimulus. Species tend to sense only those environmental stimuli that are important to them. Review Figures 5.2 and 5.3, Animation 5.2, Activity 5.1
2 Sensory transduction is the conversion of an environmental stimulus into a receptor potential in sensory receptors, leading to the activation of sensory neurons. The receptive field of a neuron is the region in space where a stimulus will change the firing of that cell. The receptive fields of neurons may be very different at successive levels of the sensory pathway. Review Figures 5.5 and 5.6, Animation 5.3
3 The succession of levels in a sensory pathway allows for increasingly elaborate kinds of processing. Touch information from the skin courses through a distinct spinal pathway, the dorsal column system. Review Figures 5.7 and 5.8 5 Free nerve endings detect mechanical damage or temperature changes because they have specialized receptor proteins that detect these conditions. Pain, temperature, and itch information enters the spinal cord, crosses the midline, and ascends through the anterolateral system (or spinothalamic system) to the brain. Review Figures 5.12 and 5.14, Activity 5.2 7 Motor control systems are organized into a hierarchy that consists of the skeletal system and associated muscles, the spinal cord, the brainstem, and various parts of the brain, including the primary (M1) and nonprimary motor cortices, the cerebellum, and the basal ganglia. Review Figure 5.18 9 Muscle spindles and Golgi tendon organs--sensory receptors in the muscles and tendons, respectively--transmit crucial information about muscle activities to the central nervous system. The sensitivity of the muscle spindle can be adjusted by efferent impulses that control the length of the spindle. Review Figures 5.21-5.23, Animation 5.4
Trunk Neck Head Shoulder Arm Elbow Forearm Hand Digit 5 4 3 2 Thumb Eyes Nose Face Upper lip Lower lip Chin
At the level of the cerebral cortex are multiple maps of the body surface. Primary somatosensory cortex, or S1, located in the postcentral gyrus, contains a map of the contralateral body, which overrepresents highly sensitive body regions. Review Figures 5.9 and 5.10
6 Pain sensation, detected by nociceptors, is subject to many modulating influences, including regions of the brain and spinal cord that employ endogenous opioids such as endorphins. Opioid systems are also active in the placebo effect and in other techniques, such as acupuncture. Review Figure 5.16
Primary motor cortex Nonprimary motor cortex Basal ganglia Thalamus Brainstem Spinal cord Muscles Muscles of face, of body head, and neck
Cerebral cortex Upper medulla Lower medulla Spinal cord
8 Muscles around a joint work in pairs. Antagonists work in opposition; synergists work together. Action potentials travel over motor neuron axons to reach muscle fibers at the neuromuscular junction, releasing acetylcholine (ACh) to trigger muscle contraction. Review Figures 5.19 and 5.20 10 The fibers of the pyramidal system (or corticospinal system) originate mainly in the primary motor cortex (M1) and adjacent regions and run directly to spinal motor neurons or to interneurons in the spinal cord. Disproportionate amounts of M1, in the precentral gyrus, are devoted to finely controlled muscles. Review Figures 5.24-5.27
Caudate nucleus Putamen Globus pallidus Subthalamic nucleus
11 The extrapyramidal system, consisting of brain regions that modulate movement, includes the basal ganglia (caudate nucleus, putamen, globus pallidus), substantia nigra, some major brainstem nuclei (thalamic nuclei, reticular formation, and red nucleus), and the cerebellum. Review Figure 5.29, Activity 5.3
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