250 wrd

Images.com/Corbis

Learning Objectives

After completing this chapter, you should be able to:

• Draw the elements of a muscle and explain how muscle contraction occurs. • Differentiate between skeletal and smooth muscle. • Take a simple function such as bending your arm and explain the role of antagonist muscles. • Give examples of isometric and isotonic muscle contractions. • Describe the mechanisms underlying the stretch reflex, tendon reflex, withdrawal reflex, crossed extensor

reflex, elimination reflexes, and sexual reflexes. • List several differences between the pyramidal and extrapyramidal motor systems. Describe the movement

disorders associated with damage to the brain, spinal cord, motor neurons, and muscles.

5

Control of Movement

David Sacks/Getty Images

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CHAPTER 55.1 Muscle Structure and Function

Larissa was a beautiful baby with huge brown eyes and dimpled cheeks. Nearly 2 years of age, she was a bright, happy chatterbox, using full sentences to express herself. However, Larissa’s motor development was abnormally slow. She couldn’t sit up unassisted until she was nearly 11 months old, and she still wasn’t walking when her parents brought her in for her 2-year examination. (Most babies can sit up by themselves by the age of 7 months and walk by 15 months.) The pediatrician looked concerned as she examined Larissa. She applied a firm touch to the sole of Larissa’s right foot and frowned as Larissa’s toes fanned out in response, her big toe bending upward. Then she tested Larissa’s left foot. Again, the toes on her left foot fanned in response to the pediatrician’s touch.

The pediatrician explained to Larissa’s parents that the fanning of her toes was called a Babinski reflex and was perfectly normal in young babies. However, a Babinski reflex is normally absent in children as old as Larissa. To determine the cause of the delay in Larissa’s motor development, the pediatrician ordered a number of tests for Larissa, including scans of her brain and spinal cord. MRI scans of Larissa’s spinal cord revealed a tiny, fluid-filled cyst in the cervical region of her spinal cord, a condition known as syringomyelia.

The pediatrician explained that Larissa was probably born with the fluid-filled cyst in her spinal cord and that the cyst was interfering with the transmission of messages from her brain to the motor neurons in her spinal cord. Although surgery was risky, the pediatrician advised Larissa’s parents to consult a pediatric neurosurgeon because the cyst could grow over time, causing Larissa to become severely disabled. Just after her second birthday, Larissa underwent surgery to destroy the cyst in her spinal cord. She began walking soon after the surgery, and her motor development continued normally after that.

5.1 Muscle Structure and Function

The Babinski reflex is one example of a reflex that is seen in very young infants but disappears as the baby gets older. If you firmly touch the bottom of the foot of an infant who is younger than 6 months old, the baby’s toes will extend and spread apart. This fanning of the toes in response to a touch on the bottom of the foot is called a Babinski reflex. By the time the infant is approximately 6 months of age, the cerebral cor- tex develops inhibitory control of motor neurons in the spinal cord. This means that the cerebral cor- tex begins to send inhibitory mes- sages down the spinal cord, which inhibit the Babinski reflex. There- fore, if you stroke the sole of the foot of an older child (one who is older than 6 months of age), the child’s toes will flex and curl inward in response to the touch.

Jennie Woodcock; Reflections Photolibrary/CORBIS

Photo 5.1 Fanning of the toes in response to a touch on the bottom of the foot is called a Babinski reflex. When the foot of an older child is touched, the toes flex and curl.

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CHAPTER 5Section 5.1 Muscle Structure and Function

Clinicians make use of reflexes when testing for damage to the nervous system (Fiorentino, 1973). Adults with intact, or undamaged, nervous systems do not exhibit a Babinski reflex when touched on the sole of their foot. This is a normal response for people with healthy nervous systems. How- ever, those with spinal cord or brain damage do not always curl their toes when tested with a firm touch to the bottom of their feet. The “Case Study” describes the case of a young man named Kevin who damaged his spinal cord in a car accident when he was 19. Touching the bottom of Kevin’s foot produces a Babinski reflex. That is, Kevin’s toes fan out, just like a young baby’s, when the sole of his foot is stroked. Damage to Kevin’s spinal cord has destroyed the axons that carried inhibitory messages to the motor neurons that control Kevin’s feet. Thus, the Babinski reflex is not inhibited when the bottom of Kevin’s foot is touched, and Kevin exhibits the Babinski reflex.

Case Study: Partial Spinal Cord Injury

After graduating from high school, Kevin enlisted in the U.S. Army. He completed his basic training at Fort Sill, Oklahoma, and then continued training at Fort Stewart in Georgia. On his 19th birthday, Kevin received orders to go to Afghanistan. Although his parents expressed concern about his deployment to a war zone, he was eager to go to Afghani- stan with his company. One day, about 2 months after arriving in Afghanistan, Kevin was driving an armored Jeep in a convoy that was traveling from Bagram Airfield to Kabul. The convoy suddenly came under fire. The truck immediately in front of Kevin’s Jeep was struck and came to an abrupt halt. Kevin tried to stop his vehicle, but it skidded on the

dusty road and slammed into the disabled truck. In the impact, Kevin was flung against the steer- ing wheel, breaking his sternum, or breastbone, and several ribs. In addition, Kevin’s spinal cord was injured at the T4 level.

The damage to his spinal cord was limited to the ventral aspect. This meant that Kevin’s motor function was impaired, but his sensory function was left intact. Kevin’s injury is referred to as an incomplete spinal cord injury. Some axons at the T4 level, the point of injury, survived in spite of the damage, especially those in the dorsal region of Kevin’s spinal cord.

Today the effects of the spinal cord damage are obvious. Kevin can stand on his legs, but he cannot walk without support. His gait is spastic, characterized by overextension of the joints in his legs. Motor function of the autonomic nervous system is also affected. For example, Kevin does not sweat any place on his body below the level of T4.

iStockphoto/Thinkstock

Photo 5.2 How has his partial spinal cord injury affected Kevin’s movement?

Movement is the result of muscle contractions, and muscles are controlled by the nervous sys- tem. Damage to the nervous system, then, disrupts normal muscle function. In this chapter we will examine normal muscle function and disorders that cause abnormal muscle function. We will also consider the roles of the brain and spinal cord in controlling movement, and we will compare reflexes with voluntary movement. Let’s start by looking at the structure and function of muscles.

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CHAPTER 5Section 5.1 Muscle Structure and Function

Like all body tissues, muscles are composed of cells. Each cell is called a muscle fiber (Figure 5.1). Muscle fibers are similar to all cells in that they have a nucleus, mitochondria, and other typical cellular components.

Figure 5.1: Muscles and muscle fibers

Muscles are composed of cells, and each cell is called a muscle fiber.

Bone

Tendon

Muscle fibers

Muscle

What causes muscle contractions? To begin to answer this question, recall that muscle fibers resem- ble neurons in one important aspect. Like neurons, each muscle fiber has a chemically sensitive region known as an endplate. The endplate of a muscle fiber contains receptor sites for the neu- rotransmitter acetylcholine. Axons from motor neurons terminate on the endplates of muscle fibers, and acetylcholine is released from the terminal buttons of the motor neurons whenever the motor neurons get excited and fire. This means that motor neurons initiate muscle contraction by releasing acetylcholine into the junction between the axon terminal button and the muscle fiber, called the neuromuscular junction (Figure 5.2). When acetylcholine binds with its receptor sites on the muscle fiber, it causes myosin and actin filaments to slide past each other, shortening the fiber (Figure 5.2).

Figure 5.2: The neuromuscular junction

During a muscle contraction, actin filaments slide along the myosin filaments, shortening the muscle fiber.

Z-line Myosin filaments Actin filaments

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CHAPTER 5Section 5.1 Muscle Structure and Function

Figure 5.3: The role of muscle filaments in muscle contraction

The axons of motor neurons synapse with motor endplates on muscle fibers.

Motor axon

Muscle fibers

Motor endplates

Contraction of a muscle occurs when its fibers shorten. Please keep in mind that each muscle con- tains hundreds or thousands of muscle fibers. Each muscle fiber receives innervation from one axon, which means that each motor neuron stimulates contraction in only one muscle. However, an axon from a motor neuron often branches near its terminus, and individual branches terminate on end- plates of different fibers. That is, one motor neuron can innervate many different fibers in one muscle (see Figure 5.3).

Different Muscle Types

You learned in Chapter 2 that there are three types of muscles: skeletal, smooth, and cardiac muscles. Skeletal muscle is the muscle tissue that is connected to the bones and cartilage of the skeleton. Contraction of the skeletal muscles causes the bones of the skeleton to move. They are the muscles that are under our voluntary control and thus are innervated by the somatic nervous system. When I tap my finger on the desktop or smile at a friend, I am using skeletal muscles to perform these voluntary activities.

Smooth muscles are found in the walls of blood vessels and in the walls of many organs, includ- ing the stomach, the small and large intestines, the bladder, and the uterus. They are also found in the skin and in the ducts of glands. As you learned in Chapter 4, smooth muscles control the constriction and dilation of blood vessels and of the pupil of the eye. Smooth muscles are respon- sible for peristalsis, the rhythmic contractions of the digestive organs, and they also control the opening and closing of sphincters and ducts throughout the body. In general, smooth muscles con- tract more slowly, although more efficiently, than skeletal (or striated) muscles. However, smooth muscle contraction has not received as much study as skeletal muscle contraction. Therefore, we will limit our focus to the action of skeletal muscles in the remainder of this chapter.

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CHAPTER 5Section 5.1 Muscle Structure and Function

Skeletal Muscle Function

Skeletal muscles are attached to the bones of the skeleton by tough strands of connective tissue known as tendons. The bones themselves are joined together at joints, which typically are enclosed in a capsule (Figure 5.4). Inside the joint capsule is a greasy fluid that allows bones to slide past each other easily as the bones are moved by contracting muscles. Many joints are structured in such a way that movement around the joint is permitted in two opposing directions only. For example, movement around the elbow joint is limited to flexion and extension of the arm (Figure 5.4). Flexion of a limb refers to a movement that bends the limb, whereas extension is a straightening of the limb.

Figure 5.4: Attachment of muscles to bones around the elbow joint

Extensor and flexor muscles are positioned on opposite sides of a joint. Flexor muscles bend the limb, and extensor muscles straighten the limb.

Humerus

Biceps (flexor muscle)

Radius

Ulna

Joint capsule

Flexor muscle

Triceps (extensor muscle)

Two muscles on either side of the elbow joint, called the biceps and the triceps muscles, produce flexion and extension of the arm. Contraction of the biceps muscle causes the arm to bend at the elbow joint. In contrast, contraction of the triceps muscle produces extension of the arm. Muscles that produce opposite movements around a joint are called antagonists. Thus, the biceps and triceps muscles are antagonist muscles. Likewise, the muscles that open your mouth and the muscles that close it are antagonists.

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CHAPTER 5Section 5.2 Spinal Control of Movement

Please keep in mind that muscles do their work by contracting. My arm bends because my biceps muscle contracts, and my arm straightens because my triceps muscle contracts. Muscle relaxation is a passive process. It occurs when a muscle stops contracting. Motor neurons initiate muscle contraction by releasing acetylcholine at the neuromuscular junction. When a motor neuron stops firing, the associated muscle fibers stop contracting, and muscle relaxation takes place.

Movement occurs when one or more muscles con- tract. For example, as you’ve just learned, contrac- tion of the biceps muscle bends the arm. This type of muscle contraction is called isotonic contraction. As its name implies (iso- means “same” and -tonic means “tone” in Greek), muscle tone remains unchanged during this type of contraction. Isotonic contraction occurs when a muscle shortens in length, pulling the attached bones in the direction of the contraction.

Isometric contraction is another type of contraction. During isometric contraction, the muscle does not shorten but rather remains the same length. How does this happen? The bones remain in a fixed position dur- ing isometric contraction, so the muscle cannot shorten.

Try this out for yourself. First, contract your right biceps muscle isotonically, which will cause your arm to flex. When you do this, keep your left hand on your biceps as you bend your right arm and feel that the muscle tone does not change. Next, contract your right biceps mus- cle isometrically. To do this, you need to assume the stance of a bodybuilder with your right arm in a semi- flexed position. After your arm is in a fixed position, continue to contract your right biceps muscle, keeping your left hand over the right biceps to monitor muscle tone. When a bodybuilder performs an isometric contraction of the biceps muscle, you can see the biceps bulge and pop out of the arm.

5.2 Spinal Control of Movement

Many movements of the arms, trunk, and legs are regulated by spinal cord mechanisms. Think about this for a moment. Consider what happens when you touch something very hot with your bare hand. You immediately jerk your hand away from the hot object, don’t you? This reac- tion happens instantaneously. It happens so fast, in fact, that you don’t have time to think about it. Your reaction occurs so quickly because the painful sensation is processed in the spinal cord. That is, the information about the painful stimulus goes directly to your spinal cord, where it is sent to the motor neurons that stimulate the contraction of muscles that pull your hand away from the painful object (Figure 5.5). It would take far too long for you to react if the information had to travel up the spinal cord to be processed in the brain and then motor directions were sent from the brain to the muscle.

These rapid, automatic responses to specific stimuli that are mediated by the spinal cord are called reflexes. Reflexes can be simple movements, or they can be postural adjustments that involve many muscles. However, reflexes always occur the same way in response to a particular stimulus.

Flirt/SuperStock

Photo 5.3 An isometric contraction causes the muscles to bulge.

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CHAPTER 5Section 5.2 Spinal Control of Movement

The reflex that is described in the preceding paragraph is called the withdrawal reflex, or the flex- ion reflex. This reflex involves an immediate withdrawal movement that is made in response to a painful or noxious stimulus. I am so certain of the speed of this reflex that I once sat and watched my son, Jacob, at 2 years of age, stick his finger into a flame of a candle. I didn’t bother to rush to his aid because I knew that his withdrawal reflex would remove his hand from the flame before I could reach him. (And it did!)

Reflexes also occur in the head and neck, but these are not typically mediated by the spinal cord. Motor nuclei in the brainstem control these reflexes. In this section we will focus solely on spinal reflexes. We will consider reflexes that occur in the head and neck in Chapter 6.

Spinal Reflexes

Review the structure of the spinal cord in Figure 5.5. Sensory information enters the spinal cord through the dorsal root, and the motor neurons are situated in the gray matter in the ventral aspect of the spinal cord. When a withdrawal reflex occurs, an axon carrying sensory information from a receptor relays this information directly to motor neurons, which respond to the informa- tion by initiating muscle contractions that cause flexion.

Figure 5.5: The withdrawal reflex

Axons from receptors in the skin terminate directly on the dendrites of motor neurons. A painful stimu- lus triggers an axon potential in the axon of the receptor, which causes excitatory neurotransmitter molecules to be released into the synapse. The motor neurons in the spinal cord become excited and initiate muscle contractions that pull the limb away from the noxious stimulus.

Biceps (flexor muscle)

Axons of motor neurons

Axons of sensory neurons in skin

Hand

Ventral

Motor neurons

Burning match

Spinal cord Dorsal

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CHAPTER 5Section 5.2 Spinal Control of Movement

The withdrawal reflex is a unisynaptic reflex, involving only one synapse between the receptor and the motor neuron (uni- means “one” in Greek). Most other reflexes are polysynaptic reflexes, involving more than one synapse (poly- means “many” in Greek). Because more synapses are involved in a polysynaptic reflex than in a unisynaptic reflex, there is a greater time lapse between the introduction of the stimulus and the initiation of movement in polysynaptic reflexes. In con- trast, unisynaptic reflexes occur nearly instantaneously, in less than 50 milliseconds.

Interspersed among the muscle fibers in skeletal muscles are special structures called muscle spin- dles. A muscle spindle is composed of several short muscle fibers that are joined to a centralized structure called a nuclear bag (Figure 5.6). A neuron called a stretch receptor is located inside the nuclear bag. This stretch receptor gets excited whenever the muscle spindle is stretched.

Figure 5.6: A muscle spindle

How does the muscle spindle communicate with the spinal cord?

Tendon

Muscle spindle

Intrafusal fibers

Nuclear bag

Stretch (annulospiral receptor)

Extrafusal fibers

Extrafusal motor neuron fiber

Intrafusal motor neuron fiber

Sensory axon

Ventral

Spinal cord Dorsal

The Stretch Reflex Have you ever watched someone falling asleep during a lengthy presentation? As that person starts to drop off to sleep, his or her head begins to fall forward. But the head goes down only so far when it jerks back up again. This sequence might occur many times, over and over again: The head begins to sink, then it springs back up quickly, waking the napper momentarily.

Let’s consider what is happening to this sleepy audience member. The head begins to fall forward because muscles in the back of the neck and shoulders lose their muscle tone as the person falls asleep. The head continues to drop until these muscles are stretched so much that stretch

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CHAPTER 5Section 5.2 Spinal Control of Movement

receptors in the muscle spindles fire. When the stretch receptors get excited, they activate motor neurons, which stimulate muscle fiber contraction to restore muscle tone. This reflex is called the stretch reflex. This reflex can be elicited whenever a muscle is stretched. A gentle tap below the kneecap, for example, stretches the extensor muscle in the leg, causing the muscle to contract and the leg to extend.

The Tendon Reflex Recall that tendons connect muscles to bones of the skeleton. Stretch receptors, called Golgi ten- don organs, are located in tendons. The purpose of a Golgi tendon organ is to provide feedback to the nervous system about muscle contraction. When a muscle contracts powerfully, the tendon that attaches the muscle to the skeleton is stretched, which stretches the Golgi tendon organ. Like all stretch receptors, Golgi tendon organs get excited when stretched. Their axons carry informa- tion about tendon stretching to the spinal cord, where they terminate on inhibitory interneurons (Figure 5.7). The overall effect of stretching the Golgi tendon organ is to inhibit muscle contraction in a muscle that is contracting too vigorously.

Figure 5.7: Golgi tendon organ reflex

When excited, the Golgi tendon organs stimulate inhibitory cells in the spinal cord, which inhibit firing of motor neurons and thus inhibit contraction of the muscle.

Golgi tendon organ

Tendon

Tendon Golgi tendon organ

Joint capsule

Ventral

Spinal cord Dorsal

Inhibitor cell

Thus, two feedback systems relay information about muscle function to the spinal cord. Stretch receptors in the muscle spindles fire when the muscle relaxes and muscle fibers stretch, and the Golgi tendon organ fires when its respective muscle contracts too vigorously, stretching the tendon. The stretch receptor and the Golgi tendon organ stimulate opposite effects in the spinal cord. The stretch receptor in the muscle spindles produces muscle contraction. The Golgi tendon organ, in

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CHAPTER 5Section 5.2 Spinal Control of Movement

For Further Thought: Movement and the Raphe Nucleus

An area in the hindbrain called the raphe nucleus releases serotonin when stimulated. Barry Jacobs (1994; Jacobs & Fornal, 1997, 1999) has demonstrated that the activity of these serotonin neurons is closely related to motor activity. For example, some sero- tonin neurons in the raphe nucleus begin to fire right before a movement is initiated. In addition, many serotonin neurons increase their firing rate as the rate of muscle con- tractions increases. If a person walks rapidly, neurons in the raphe nucleus fire faster than if the same person walks at a more leisurely pace. This is especially true for repetitive movements like chewing or running.

Most of Jacobs’s experiments have focused on the activity of neurons in the raphe nuclei of cats because in the past others have studied this area of the cat’s brain, and its properties are well known. Jacobs observed that, when a cat runs on a treadmill, serotonin neurons in the raphe nucleus fire at the same rate as the animal’s gait. These neurons appear to be associated with gross motor functions rather than fine motor control. Thus, neurons in the raphe nucleus appear to enable gross movements of the torso and limbs but not movements of the eyes or fingers.

When a cat hears a sudden noise, such as the slamming of a door, the cat stops what it is doing and turns toward the source of the sound to determine its significance. This “what is it?” reaction is called an orienting response. During an orienting response, when the cat stops all movement to concentrate on a particular stimulus, serotonin neurons in the raphe nucleus do not fire. These same neurons become active again when the individual begins to move once more. Hence, serotonin neurons in the raphe nucleus increase their firing rate when large muscle groups are contracting and decrease their firing rate when movement ceases or when the individual makes a “what is it?” response to an environmental distraction.

contrast, inhibits the firing of motor neurons, causing a decrease in muscle contraction. Together, these two feedback systems maintain the correct muscle tone necessary for optimum muscle function.

These two feedback systems also send information to the brain about the contraction and relax- ation of muscles in the body. This information allows the brain to plan future movements based on the present state of the muscles. In addition, information from the muscles, particularly infor- mation from contracting muscles, can affect neurotransmitter function. For example, repetitive muscle contractions increase serotonin activity in the brain (see the “For Further Thought” box).

iStockphoto/Thinkstock

Photo 5.4 This cat stopped all movement to focus on something he saw that could be a potential threat to him.

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CHAPTER 5Section 5.2 Spinal Control of Movement

Other Spinal Reflexes

The importance of reflexes has been recognized for centuries. Investigators in the 17th and 18th centuries studied and cataloged most of the reflexes that are known today (Swazey, 1969). For example, in the mid-1700s Robert Whytt, at the University of Edinburgh, studied spinal reflexes in decapitated frogs and tortoises. You see, frogs without heads are frogs without brains, which means that any elicited behavior in these specially prepared subjects is mediated by the spinal cord. Whytt studied a number of reflexes that could be produced in headless frogs, including the withdrawal reflex and the scratch reflex. As its name implies, the scratch reflex is a scratching movement made by one of the frog’s limbs when the frog’s skin is tickled. Stimulation of sensory receptors on the frog’s skin is translated into action potentials that travel down axons to the spinal cord, where they excite motor neurons that initiate contractions in muscles that produce scratch- ing movements by the frog’s limb. This scratching behavior occurs even when the brain is absent.

Probably the most important and most comprehensive study of reflexes was conducted by the British physician and scientist Sir Charles Scott Sherrington. From 1884 to 1935 Sherrington stud- ied many reflexes, including the withdrawal reflex, the scratch reflex, and the knee jerk reflex, in monkeys, dogs, and cats. He is credited with introducing the term synapse.

The Crossed Extensor Reflex One spinal reflex that Sherrington studied intensively is the crossed extensor reflex. This reflex is an example of Sherrington’s concept of the integrative action of neurons because it typically occurs in conjunction with another reflex, the withdrawal reflex. Consider what happens when you step on a sharp object when walking in your bare feet. Immediately, the involved leg flexes to withdraw the injured foot from the sharp object. This is the withdrawal reflex. But what about the other leg? If one leg is flexed, it is important that the other leg remain extended. Otherwise, you will tumble to the floor.

The crossed extensor reflex is stimulated by the onset of the withdrawal reflex. The sensory recep- tor that initiates the withdrawal reflex also excites interneurons that cross the midline of the spinal cord (Figure 5.8). These interneurons, in turn, excite the motor neurons that innervate extensor muscles in the opposite leg. As a result, when one limb is withdrawn from a noxious stimulus, the other limb extends to support the weight of the body.

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CHAPTER 5Section 5.2 Spinal Control of Movement

Figure 5.8: The crossed extensor reflex

A painful stimulus to one limb causes flexion of that limb (withdrawal reflex) and extension of the oppo- site limb (crossed extensor reflex).

Axons cross over midline to stimulate motor neurons on contralateral side

Flexion of injured limb

Contraction of flexor

Contraction of extensor

Extension of uninjured limb

Dorsal

Ventral

Urination and Defecation No one has to teach babies how to soil their diapers. Their elimination functions happen naturally. That’s because these functions are under spinal control. Spinal animals, whose brains have been surgically severed from their spinal cords, continue to defecate and urinate, even assuming typical elimination positions. In spinal animals and in young infants, urination and defecation are caused by stretch reflexes. Let’s consider the urination and defecation reflexes separately.

The organ that collects urine, called the bladder, is lined with smooth muscle. Like all muscles, the muscle in the bladder wall contains stretch receptors. As the bladder fills with urine, the wall of the bladder becomes stretched, causing the stretch receptors to fire. The axons of these stretch receptors terminate on motor neurons in the spinal cord that control bladder muscles. Stretching of stretch receptors in the bladder produces contraction of the bladder muscle, which forces urine out of the body through a passageway called the urethra. Thus, the bladder empties as a result of a stretch reflex.

Defecation involves a stretch reflex, too. The large intestine, including the region (called the rec- tum) closest to the anus, is also lined with smooth muscles and stretch receptors. As the rec- tum fills with feces, the walls of the rectum stretch, causing stretch receptors to fire. The stretch

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CHAPTER 5Section 5.2 Spinal Control of Movement

receptors stimulate motor neurons in the spinal cord that initiate contraction of rectal muscles, expelling feces from the body.

Toilet training takes urination and defecation out of reflexive control and places it under conscious control. A child being toilet trained learns to use skeletal muscles to open and close the sphincter muscles of the bladder and anus. This training cannot be done with a very young child because the frontal lobes are not developed enough to take control of bladder and bowel function.

People with spinal cord injuries typically have incomplete communication between the brain and neurons in the spinal cord. Often, following the injury, they lose conscious control of their bladder and bowels. However, the stretch reflexes that produce urination and defecation remain intact. Some people with spinal cord injuries can learn to control bladder function by taking advantage of the intact stretch reflex in the bladder. For example, the bladder wall can be stretched by tug- ging on the skin of the abdomen. Thus, people with spinal cord injuries can initiate urination by stretching the abdominal wall.

Sexual Reflexes Many of the components of sexual activity, including erection of the penis and ejaculation, are under spinal control (Agmo, 1999). Adequate stimulation will produce penile erection in men with spinal cord injuries and in male animals whose brains have been surgically separated from their spinal cords. Continued stimulation will induce ejaculation of semen in these male subjects. Sen- sory receptors associated with the penis excite motor neurons in the sacral area of the spinal cord that cause dilation of blood vessels, producing erection of the penis. Genital receptors also excite motor neurons that cause the rhythmic contraction of muscles associated with ejaculation in the male and orgasmic response in the female.

Some sexual response can be brought under conscious control. For example, thinking erotic thoughts can produce sexual excitement leading to penile erection in the man or engorgement of the clitoris and vaginal lubrication in the woman. However, these responses can also be stimu- lated reflexively and are difficult, if not impossible, to stop after they have begun. For that reason, premature ejaculation cannot be halted when it occurs, because the motor neurons that initiate the ejaculatory muscle contractions have been excited reflexively. A man who is trying to prevent premature ejaculation must do so by sending inhibitory signals from his brain down to the motor neurons in his spinal cord. Another way to control premature ejaculation is the use of anesthetic creams that are applied to the genital area to reduce sensation in that area and thus decrease stimulation of sensory neurons that excite the ejaculatory motor neurons.

We have examined a number of reflexes that involve sensory neurons in the peripheral nervous system and motor neurons in the spinal cord. These reflexes serve to protect the body, to produce postural adjustments, or to support important biological functions such as respiration, elimina- tion, and reproduction. All of these reflexes take place without prompting from higher brain struc- tures and do not require conscious control. However, you should keep in mind that motor neurons receive innervation both from the peripheral nervous system and from the brain. That is, skeletal muscles that are under reflexive control can also be brought under conscious control. In the final sections of this chapter, we will look at how the brain controls movement.

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CHAPTER 5Section 5.3 Control of Movement by the Brain

5.3 Control of Movement by the Brain

The brain controls movement by means of two motor systems: the pyramidal motor system and the extrapyramidal motor system. These two systems arise from different regions of the brain, and each has many distinguishing features, which we will examine. However, these systems do not act independently because there is a good deal of communication between the pyramidal and extrapyramidal systems. In addition, both systems terminate on motor neurons, the final common path to the skeletal muscles.

The Pyramidal Motor System

The pyramidal motor system arises from the primary motor cortex in the frontal lobe (Figure 5.9). It sends information to the motor neurons by way of axons that leave the primary motor cortex and extend without synapsing to the appropriate motor neurons. From the primary motor cortex to the motor neurons in the spinal cord, the axons of the pyramidal system are bundled together in a tract known as the corticospinal tract. Look at this term: corticospinal tract. This is a tract that runs from the cerebral cortex (cortico) to the spinal cord.

Recall that the left hemisphere of the brain controls the right side of the body and that the right hemisphere controls the left side of the body. This means that the corticospinal tracts arising from the left and right hemispheres have to cross over to the other side of the brain. The axons from the left primary motor cortex cross over to the right side of the brain, and those from the right primary motor cortex cross over to the left side, in pyramid-shaped structures on the ventral surface of the medulla. The pyramidal system gets its name from these pyramids in the medulla where the crossover of the corticospinal tract occurs.

Figure 5.9: The motor cortex in the frontal lobe

Neurons in the motor cortex stimulate motor neurons that control specific muscles in the body.

Toes Central sulcus

Abdomen

Chest

Leg

Body

Arm

Anus and vagina

Knee

Hip

Shoulder

Elbow

Wrist

Fingers and thumb

Ear Eyelid

Nose Closure

of jaw

Face

Neck

Tongue Mouth

Ankle

Leg

Body

Arm

Face

Neck

Tongue Mouth

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CHAPTER 5Section 5.3 Control of Movement by the Brain

The primary motor cortex is organized topographically, as you learned in Chapter 1. Each mus- cle in the body is controlled by neurons located in specific places in the primary motor cortex. Figure 5.9 illustrates the location of neurons in the primary motor cortex of a chimpanzee that control particular body parts, the result of research conducted by Sherrington and his colleague, Grunbaum, in 1901 and 1902. Recall from Chapter 1 that Fritsch and Hitzig mapped the primary motor cortex of the dog in 1863 and that Penfield mapped the human primary motor cortex in the 1940s. Research conducted in many species (for example, Sherrington and Grunbaum studied the primary motor cortex of the chimpanzee, orangutan, and gorilla) confirms that the primary motor cortex is organized in such a way that the location of the neurons is essentially the same for all mammalian species, with neurons at the top of the primary motor cortex controlling the feet of the hind limbs and neurons at the bottom of the primary motor cortex controlling the face and mouth.

The function of the pyramidal motor system is fine motor control of skeletal muscles. Using scis- sors requires fine motor control of the muscles of the hands and fingers, for example. Neurons in the primary motor cortex organize the movements necessary to open and close scissors and send commands to the appropriate motor neurons in the spinal cord. Under direction of the primary motor cortex, these motor neurons stimulate muscles in the hand, producing movements that open and close the scissors smoothly and accurately. Whenever you learn a new motor task that requires fine motor control, the primary motor cortex directs the motor neurons, thereby regulat- ing the muscle contractions needed to produce the new movement.

The Extrapyramidal Motor System

The function of the extrapyramidal motor system is to coordinate gross movements and postural adjustments. This system generally develops before the pyramidal system because gross motor control is learned before fine motor control. For example, children learn to patty-cake before they learn to hold a crayon. In addition, not all gross move- ments develop at the same time. A baby learns to hold her head upright before she masters the ability to sit, and she learns to sit before she stands.

The extrapyramidal system arises from many parts of the brain, including the cerebral cortex, the thal- amus, the cerebellum, the basal ganglia, and the reticular formation. As its name implies, the extrapy- ramidal system is distributed outside the pyramidal system and does not pass through the pyramids in the medulla (extra- means “outside” in Latin). And, unlike the pyramidal system, the extrapyramidal system syn- apses profusely, permitting much intercommunication among the structures in the forebrain, midbrain, and hindbrain that comprise the extrapyramidal motor system. The basal ganglia and the cerebellum perhaps play the most important roles in the extrapyramidal motor system. Let’s examine the roles of these struc- tures separately. Belinda Images/SuperStock

Photo 5.5 A baby learning to sit is a func- tion of the extrapyramidal motor system.

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CHAPTER 5Section 5.3 Control of Movement by the Brain

The Cerebellum As you learned in Chapter 4, the function of the cerebellum is to coordinate movement in response to sensory stimuli. The cerebellum receives sensory information from muscles and tendons, from the reticular formation, from the inner ear, and from the eyes, nose, and ears. The muscles and tendons inform the cerebellum about the state of all the muscles in the body. Therefore, the cerebellum knows which muscles are contracted and which are relaxed before it sends out com- mands to motor neurons.

The reticular formation responds whenever the nervous system is exposed to a new or impor- tant stimulus. It relays information about the important stimulus to the cerebellum, and the cerebellum organizes the response. For example, when my reticular formation detects that my name has been spoken, it alerts my cerebellum. In response, my cerebellum stops my ongoing behavior and turns my head in the direction where my name was spoken. From the inner ear, the cerebellum gets information about balance. The cerebellum coordinates muscle contrac- tions to restore balance whenever we start to fall. The receptors in the eyes, ears, and nose all send information to the cerebellum about the presence of objects in the environment. After communicating with the cerebrum and the basal ganglia, the cerebellum coordinates move- ments toward or away from those objects.

No one is certain exactly how the cerebellum coordinates movement. Undoubtedly, accurate movements require that both the force and timing of muscle contractions are carefully controlled. And, research with patients with cerebellar injuries indicates that the cerebellum is intimately involved in regulating the force and timing of muscle contractions (Wickelgren, 1998b).

The organization of the cerebellum gives us some clues about how it might coordinate movement (Figure 5.10). The cerebellum’s outer layer, called the cerebellar cortex, appears to govern coordi- nation of movement (Bastian, Living, Kaufman, & Thach, 1998). The cerebellar cortex contains five types of neurons (Purkinje, Golgi, stellate, basket, and granule cells), but only the axons of Purkinje cells carry information out of the cerebellum. Each Purkinje cell in the cerebellar cortex is believed to control one specific muscle in the body. Linking the Purkinje cells are millions of parallel axons that run through the cerebellar cortex. The parallel axons are thought to activate certain muscles simultaneously, producing coordinated movement.

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CHAPTER 5Section 5.3 Control of Movement by the Brain

Figure 5.10: Organization of the cerebellum

The cerebellar cortex contains a number of different neurons, including Purkinje, stellate, basket, granu- lar, and Golgi cells. The Purkinje cells carry information out of the cerebellum.

Parallel fiber

Mossy fiber

Climbing fiber

Axon terminals of a basket cell

Purkinje cell

Stellate cell

Basket cell

Granular cell Golgi cell

Dorsal view of cerebellum

Anterior lobe

Posterior lobe

L R

The cerebellum is especially adept at coordinating rapid, well-learned movements. For exam- ple, when you are first learning to play a musical scale on the piano, your primary motor cortex directs the movement of your fingers on the piano keyboard. After you have learned the scale, however, control shifts to the cerebellum. In fact, the cerebellum appears to take over control of all well-learned movements, allowing the individual to perform the movements subconsciously, without involvement of the cerebrum. Often, when I drive to work in the morning, I get into my car, put the car in gear, and suddenly find myself pulling into the parking lot at the university. I don’t remember anything about the drive: I don’t remember stopping for red lights or passing any landmarks. That’s because I used my cerebellum to drive while I used my cerebrum to think about upcoming events of the day.

The Basal Ganglia The basal ganglia play an important role in relaying information to and from the cerebral cor- tex, although the specific functions of the basal ganglia with respect to movement are unclear (Schmidt & Kretschmer, 1997). Recall from Chapter 4 that the basal ganglia are actually a group of nuclei, or clusters of neuronal cell bodies, located beneath the cerebral cortex. Information comes into the basal ganglia from the cerebral cortex, is processed there, and then is sent back to the cerebral cortex. At least five independent pathways have been identified in the basal ganglia (Weiner & Lang, 1995). For example, one circuit receives information from the somatosensory cor- tex. Another circuit gets input from association areas in the cerebral cortex and relays that input to the prefrontal cortex. Researchers believe that the most important function of the basal ganglia is to inhibit specific regions of the cerebral cortex associated with movement to stop movements before they begin (Folstein, 1989).

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CHAPTER 5Section 5.4 Movement Disorders

5.4 Movement Disorders

Damage to muscles, motor neurons, the spinal cord, the pyramidal system, or the extrapyra-midal system can cause a movement disorder. Let’s look at the types of disorders associated with damage to each of these structures or systems.

Damage to Muscles

Skeletal muscles must be intact and healthy in order to function properly. For example, when a muscle is separated from the skeleton, as happens with a torn tendon, contraction of the muscle does not produce the expected movement. Another disorder, muscular dystrophy, causes wast- ing of the muscle fibers, which weakens muscular contraction. There are several forms of muscu- lar dystrophy, each of which is most prevalent in certain age groups. However, all forms of this disorder appear to have a genetic basis, and all result in progressive muscle weakness and physical disability. A cure for muscular dystrophy appears to be right around the corner. Scientists have discovered a way to block the genetic error that causes muscular dystrophy, and drugs are under development to produce this blockage in people who inherit the flawed gene (Nakamori & Thorn- ton, 2011; Wheeler et al., 2009). Myasthenia gravis is a movement disorder associated with the progressive degeneration of acetylcholine receptors located at neuromuscular junctions. It is an autoimmune disease in which antibodies attack and destroy acetylcholine receptors on skeletal muscles, leaving the afflicted individual with muscle weakness and rapidly fatiguing muscle con- tractions. This disorder occurs most often in women between the ages of 20 and 30, although men are more likely than women to develop the disorder after the age of 40. Although no cure for myasthenia gravis presently exists, the disorder can be treated with drugs that increase the amount of acetylcholine that is available at the synapse to stimulate the remaining neuromuscular receptor sites. A blood-filtering process, known as plasmapheresis, is also used to remove the muscle-attacking antibodies from the blood (Spring & Spies, 2001).

Damage to Motor Neurons

Motor neurons, as you learned earlier in this chapter, are the final common path leading to muscles. Damage to motor neurons would most certainly affect movement adversely. One disorder, known as amyotrophic lateral sclerosis (ALS), is caused by the degeneration of motor neurons in the spinal cord and brain. (This disorder, which typ- ically first appears in middle or late adulthood, is also referred to as Lou Gehrig’s disease, named after the famous baseball player who was stricken with it.) As more and more

Everett Collection/SuperStock

Photo 5.6 Lou Gehrig’s disease is named after baseball player Lou Gehrig, who was forced to retire due to his illness.

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CHAPTER 5Section 5.4 Movement Disorders

motor neurons die, the symptoms of ALS progress from muscle weakness to muscle wasting and extreme impairment of movement. Abnormal, excessive glutamate activity is thought to produce the motor neuron degeneration seen in ALS (Plaitakis & Shashidharan, 1995). Currently, no treat- ment or cure is available for individuals with ALS (Charles & Swash, 2001).

Damage to the Spinal Cord

Spinal cord injuries can produce a range of disorders, depending on the location of the injury. Damage to the cervical spinal cord is a common injury that occurs in diving, skiing, and automobile accidents. Crushing or tearing of the cervical spinal cord typically results in quadriplegia. As its name implies, quadriplegia involves paralysis, or loss of motor function, of all four limbs (quattuor means “four” in Latin).

Often, damage to the cervical spinal cord does not result in total loss of movement in the arms and hands. Recall from Chapter 4 that innervation for most muscles is typically spread over several segments of the spinal cord. For example, the motor neurons that control muscles in the arms and hands are scattered over segments C5, T2, and T3. Damage to the spinal cord at C6, for example, would impair biceps muscle fibers that receive innervation from motor neurons in T2 and T3. However, those muscle fibers in the biceps that receive innervation from motor neurons in C5 would be spared, and weak control of the biceps muscle would be observed with a C6 injury.

Damage to the thoracic or lumbar area of the spinal cord usually produces paraplegia. In paraplegia the hind limbs lose their motor function. The forelimbs, or arms, escape impairment in paraplegia because the cervical spinal cord is not injured and remains intact. However, damage to the thoracic or lumbar area interrupts communication between the brain and the motor neurons that control muscles in the legs and feet. Thus, voluntary movement of the legs and feet is impaired.

Most spinal cord injuries do not involve complete breaks of the spinal cord. In most cases only partial damage occurs. People with partial damage to the spinal cord are often ambulatory, or able to walk, with or without assistance (Little, Ditunno, Stiens, & Harris, 1999). Keep in mind that sen- sory axons enter the spinal cord on the dorsal side. Thus, damage to the spinal cord can produce sensory, as well as motor, impairment.

Whenever damage to the spinal cord occurs, spinal shock, a condition in which no reflexes can be elicited, is observed immediately following the injury. Spinal shock can last for hours, days, or weeks following the injury and involves a total loss of spinal reflex activity. As you learned earlier in this chapter, spinal reflexes remain intact following surgical severance of the spinal cord. How- ever, immediately following damage to the spinal cord, no reflexes can be elicited. It appears that the spinal cord goes into a state of shock following disconnection from the brain.

In rats, dogs, and cats, spinal reflexes return within a few hours or days of the spinal injury, although the animal remains paralyzed and cannot engage in voluntary movement. Unfortunately, for monkeys, apes, and humans, recovery from spinal shock does not typically occur (Creed, Denny- Brown, Eccles, Liddell, & Sherrington, 1932). Following injury to the spinal cord, primates do not recover spinal reflexes as fully as lower animals do. Even the withdrawal reflex cannot ordinarily

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CHAPTER 5Section 5.4 Movement Disorders

be elicited. In humans the urination and defecation reflexes shut down immediately following spinal cord injury, and the injured patients require urinary catheterization (a tube placed into the bladder to remove urine) and special assistance in bowel function to maintain elimination of wastes. It appears that motor neurons in the spinal cords of primates rely profoundly on innerva- tion from the brain. When this innervation is interrupted because of damage to the spinal cord, the motor neurons cannot function normally, and reflexive action is disrupted.

Damage to the Pyramidal System

Damage to any part of the pyramidal system will affect movement, especially fine motor control. The primary motor cortex, which is located at the top of the brain directly under the skull, is par- ticularly vulnerable to damage from trauma, such as a blow to the head. Discrete damage to the primary motor cortex will affect only a small set of muscles. For example, a small tumor on the most superior aspect of the primary motor cortex will impair walking or foot movement, whereas a tumor on the inferior aspect of the primary motor cortex will affect jaw movement. Recent research has demonstrated that the primary motor cortex is more flexible than originally believed. When one area of the primary motor cortex is damaged, other areas of the primary motor cortex can take over the function of the damaged area.

Damage to any part of the corticospinal tract results in transient flaccid paralysis. Let’s take the term transient flaccid paralysis apart. You know what paralysis is: an inability to move voluntarily. The word transient refers to the fact that this paralysis is temporary, and the word flaccid means that there is a loss of muscle tone. Damage to the pyramidal system results in a temporary state of paralysis in which the patient has no muscle tone. The limbs feel like limp noodles when tested. If, following an automobile accident, a person comes into the emergency room on a stretcher and is paralyzed with a loss of muscle tone, you can be sure that the injured individual has suffered damage to the pyramidal motor system.

Transient flaccid paralysis usually lasts for only a few days or weeks following pyramidal damage. It is gradually replaced by a more permanent state of hyperreflexia, in which the injured individual has extremely reactive reflexes. For example, when a knee jerk reflex is tested immediately following pyramidal damage, no reflex is elicited. However, when tested for a knee jerk reflex several weeks following pyramidal injury, the patient will typically give an extremely strong extension response.

The primary motor cortex receives information from other areas of the cerebrum, including the prefrontal cortex, the parietal lobe, and the temporal lobe. Sometimes damage to these areas of the brain will have an adverse effect on the functioning of the primary motor cortex and on fine motor control. In one disorder, called apraxia, the individual cannot organize movements into a productive sequence (Roy & Square, 1994). For example, when given an envelope and a sheet of paper, the person with apraxia cannot figure out how to fold the paper and put it into the enve- lope, even after being shown how to do it. The person with apraxia cannot complete a series of movements that must be carried out sequentially. The primary motor cortex is typically intact and undamaged in apraxia, but other areas of the cortex are impaired, particularly those areas of the parietal and prefrontal cortex in the left hemisphere that relay information to the primary motor cortex about the sequence of movements to be performed.

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CHAPTER 5Section 5.4 Movement Disorders

Damage to the Extrapyramidal System

Recall that many diverse brain structures comprise the extrapyramidal system. Damage to any of these structures produces impairment of the motor system. In contrast to the pyramidal system, damage to the extrapyramidal motor system does not produce transient flaccid paralysis. Instead, immediately following extrapyramidal damage, hyperreflexia and spasticity are observed in the injured person. Spasticity interferes with normal smooth movement of the limbs. As the injured person attempts to move a limb, the limb moves in a jerky fashion until rigidity sets in, halting movement altogether.

Let me give you an example. Consider the knee jerk reflex. Let’s take a person with extrapyrami- dal damage and test the knee jerk reflex. Tapping the tendon beneath the kneecap stretches the extensor (or quadriceps) muscle in the leg, as you’ve already learned. When this tendon is tapped, stretch receptors in the extensor muscle initiate a vigorous contraction of that muscle, and the leg extends. However, when the extensor muscle contracts vigorously, it violently stretches the flexor muscle of the leg. In a person with extrapyramidal damage, the stretch reflex in the flexor muscle occurs forcefully, flexing the leg and powerfully stretching the extensor muscle. Stretching the extensor muscle sets off the stretch reflex in the extensor muscle once again, causing extreme contraction of the extensor muscle and stretching of the flexor muscle.

Damage to the Basal Ganglia

Damage to particular extrapyramidal structures produces specific movement disorders. For exam- ple, damage to the basal ganglia causes a number of problems, including tics and choreas. Tics are brief, involuntary contractions of skeletal muscles produced by the basal ganglia (Leckman, Pauls, & Cohen, 1995). Usually these tics are confined to the head and neck and typically consist of a twitch in one or more facial or shoulder muscles. Choreas involve more elaborate involuntary movements of the head, arms, and legs. Hemiballismis is a form of chorea that includes uncon- trolled flailing of the arms and legs.

These uncontrolled movements, especially choreas and hemiballismus, are observed in some indi- viduals with cerebral palsy. Cerebral palsy is a movement disorder that is caused by damage to the motor areas of the cerebrum, including the motor cortex and basal ganglia (Hadders-Algra, 2001). Although the cause of most cases of cerebral palsy is unknown, it can develop in infants before birth or shortly after birth (Collins, Lorenz, Jetton, & Paneth, 2001; Schendel, 2001). Many different forms of cerebral palsy exist, depending on the extent and location of cerebral damage. Damage to the basal ganglia in cerebral palsy can result in spasticity, disturbed control of balance, and uncontrolled movements.

Huntington’s Disease Perhaps the best-known chorea is the disorder known as Huntington’s chorea or Huntington’s disease, which we discussed in Chapter 1. Functioning of the basal ganglia becomes disrupted in Huntington’s disease, producing tics and uncontrollable muscle contractions early in the disease and culminating in dementia and psychosis in the end stages of the illness. Research has demonstrated that Huntington’s disease is linked to a dominant gene on chromosome 4, which increases dopa- mine activity in the basal ganglia (Fischer, 1997; Nicholson & Faull, 1996; Trottier & Mandel, 2001).

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CHAPTER 5Section 5.4 Movement Disorders

This image illustrates the brain atrophy, or destruction of tissue, that is seen in Huntington’s disease.

No known cure exists for Hunting- ton’s disease at present. In the early stages of the illness, antipsy- chotic medication, which reduces the activity of dopamine in the brain, is used to treat the involun- tary muscle contractions. However, no treatment helps much in the end stages of the illness. If gluta- mate overactivity is responsible for the degeneration of neurons in the basal ganglia, drugs that treat epilepsy by decreasing glutamate activity or increasing GABA activ- ity might prove useful for treating and even preventing Huntington’s disease (Fischer, 1997).

Parkinson’s Disease Another well-known illness associated with damage to the basal ganglia is Parkinson’s disease. Parkinson’s disease appears to be caused by destruction of dopamine-producing cells in the sub- stantia nigra in the basal ganglia, resulting in a depletion of dopamine in the basal ganglia. (In 2000 Arvid Carlsson received the Nobel Prize in physiology for his research on dopamine and its role in Parkinson’s disease.) As dopamine levels decline, movement becomes impaired in Parkinson’s disease. The first motor symptoms include tremor, especially of the hands, and unsteadiness and loss of balance, which leads to falls. Rigidity and inability to complete a movement occur later in the course of the illness. Parkinson’s disease is a progressive illness that ultimately leaves persons unable to care for themselves. Because dopamine levels in the brain are diminished in Parkinson’s disease, psychological depression is often a component of the disorder that must be treated.

Parkinson’s disease is most frequently seen in the elderly, although individuals in their 30s or 40s (or, in rare cases, even younger) may be diagnosed with this disorder. In addition, men are more likely to develop this disorder than are women. Actor Michael J. Fox was first diagnosed with Par- kinson’s disease at age 30, whereas Pope John Paul II and former U.S. attorney general Janet Reno developed Parkinson’s later in life.

The exact cause of Parkinson’s disease is unknown. That is, no one can explain how or why dopamine-producing cells in the substantia nigra are destroyed. However, studies of young people in California who inadvertently injected themselves with a bad batch of synthetic heroin that con- tained a lethal by-product, called methyl-phenyl-tetrahydropyridene or MPTP, gave investigators a clue as to how Parkinson’s disease develops. These young drug users developed dramatic cases of Parkinson’s disease after using the MPTP-contaminated drug repeatedly for several days. Several of the afflicted people became so immobile that they could move only their eyes. Following the

Biophoto Associates/Science Source

Photo 5.7 The ventricles are enlarged, and the basal gan- glia and cerebral cortex are much reduced in the brain of an individual with Huntington’s disease (right), compared to the normal brain (left).

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CHAPTER 5Section 5.4 Movement Disorders

discovery of the effects of MPTP in humans, investigators at the National Institute of Mental Health tried to produce the same results in monkeys. They found that injections of MPTP into monkeys produced full-blown Parkinson’s disease in those animals (Burns et al., 1983). Postmortem exami- nation of the monkeys’ brains revealed destruction of the substantia nigra following injection of MPTP.

Scientists have demonstrated that a widely used pesticide, rotenone, produces Parkinson’s-like symptoms in rats (Betarbet et al., 2000; Jackson-Lewis, Blesa, & Przedborski, 2012). Rotenone is structurally similar to MPTP and is found in hundreds of products, including flea and tick pow- ders and plant pesticides. Recently, a number of international research teams have reported an association between Parkinson’s disease and exposure to pesticides in humans (Parrón, Requena, Hernández, & Alarcón, 2011; Spivey, 2011; Wang et al., 2011; Wirdefeldt, Adami, Cole, Trichopou- los, & Mandel, 2011).

Classical antipsychotic drugs, which decrease dopamine activity in the brain, produce symptoms that resemble Parkinson’s disease. These symptoms are labeled extrapyramidal side effects and include tremors, muscular rigidity, and a shuffling gait. The extrapyramidal side effects are believed to be the result of decreased dopamine activity and increased acetylcholine activity in the nervous system. Drugs that decrease acetylcholine activity, called anticholinergic medications, and drugs that increase dopamine activity, called dopaminergic medications, reduce extrapyramidal side effects (Stanilla & Simpson, 2001).

Treatment for Parkinson’s Disease Investigators are still trying to find a cure or lasting treatment for Parkinson’s disease. Because dopamine is depleted in the basal ganglia in Parkinson’s disease, you would think that it would be an easy matter just to give the person a pill containing dopamine. Unfortunately, dopamine can- not cross the blood-brain barrier, so a dopamine pill won’t work. But a precursor of dopamine, a substance that is readily converted to dopamine in the brain, can cross the blood-brain barrier. This precursor is called levo-dopa or L-dopa. L-dopa, when taken orally, enters the bloodstream, crosses the blood-brain barrier, and is converted into dopamine in the brain. This drug is espe- cially helpful in the early stages of the illness. However, L-dopa has a number of unwelcome side effects, including uncontrolled, extraneous muscle contractions, increased blood pressure, occa- sional psychotic symptoms, and headaches (Duty, Henry, Crossman, & Brotchie, 1996). It cannot be used every day, on a long-term basis. Hence, researchers are looking for alternative treatments for Parkinson’s disease.

A number of alternative treatments for Parkinson’s disease appear promising. These treatments are especially useful when patients are receiving the maximal daily dose of L-dopa with no improve- ment in symptoms or when patients develop dyskinesias (movement problems, such as choreas) in response to L-dopa. Alternative drugs therapies, such as glutamate antagonists, are currently under investigation to determine their efficacy in treating Parkinson’s disease. Glutamate hyper- activity has been implicated as an underlying cause of Parkinson’s disease. Thus, reducing gluta- mate activity should decrease clinical manifestations of Parkinson’s disease. Experiments with rats treated with antipsychotic drugs (which block dopamine activity, producing rigidity and immobil- ity in rats) and with monkeys injected with MPTP demonstrate that glutamate antagonists can reduce Parkinsonian symptoms (Alarcon, Bradley, & McKendree-Smith, 2000; Ossowska, Lorenc- Koci, Konieczny, & Wolfarth, 1998; Papa & Chase, 1996; Starr, 1995).

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CHAPTER 5Section 5.5 Chapter Summary

Other treatments for Parkinson’s disease are also under development, including stem cell therapy and deep brain stimulation. Stem cells are specialized cells in the body that are capable of dividing and transforming into different types of cells needed for the growth and repair of body tissues. Implanting stem cells that are capable of transforming into dopamine-producing neurons into the brains of individuals with Parkinson’s disease has been demonstrated to be a successful treatment for many with Parkinson’s (Cooper, Hallett, & Isacson, 2012). Likewise, stimulation of deep brain structures, such as the hypothalamus, substantia nigra, basal ganglia, and hippocampus, has been shown to reduce many of the devastating symptoms of Parkinson’s disease, including tremors, postural problems, and cognitive difficulties (Starr et al., 2010; Uitti, 2012).

Damage to the Cerebellum

Damage to the cerebellum interferes with the ability of this brain structure to coordinate move- ment. Depending on the extent of the damage, movement impairments can vary. For example, tumors in the cerebellum produce a variety of problems related to the location of the tumor. Tumors in the posterior cerebellum disrupt communication with the vestibular system and inter- fere with balance, whereas tumors that affect midline cerebellar structures disturb bilateral coor- dination of the limbs and trunk (Bastian et al., 1998).

People with cerebellar damage show a number of problems, including ataxia, which is an inability to walk or move in a coordinated fashion, and disequilibrium, a loss of balance. Staggering or a foot-dragging gait is evidence of cerebellar damage. Other individuals may be unable to perform rapid, well-learned movements following damage to the cerebellum. Instead, their movements become hesitant and slow.

As you know, the cerebellum is extremely dependent upon the senses as it coordinates move- ment. For example, as I walk across a room, the cerebellum receives information from my eyes about the presence and location of objects in the room, allowing me to cross the room without tripping over shoes and other items on the floor. In Chapter 6 we will examine the various sensory systems, and we will look at a number of sensory disorders that can disrupt cerebellar function.

5.5 Chapter Summary Muscle Structure and Function

• Each muscle cell is called a muscle fiber, which contains contractile tissue. • Each muscle fiber has a chemically sensitive endplate that contains receptors for acetyl-

choline. Acetylcholine stimulates contraction of the muscle fibers in skeletal, smooth, and cardiac muscle.

• The synapse between the axon of a motor neuron and the endplate of a muscle fiber is called a neuromuscular junction.

Different Muscle Types • Skeletal muscles are attached to the bones of the skeleton and produce flexion and exten-

sion movements of the limbs. • Smooth muscles are found in the walls of blood vessels and many internal organs, as well

as in the skin and glands.

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CHAPTER 5Section 5.5 Chapter Summary

Skeletal Muscle Function • Flexion of a limb refers to a movement that bends the limb, whereas extension is a

straightening of the limb. • Muscles that produce opposite movements around a joint are called antagonists. • Isotonic contraction occurs when a muscle shortens in length, pulling the attached bones

in the direction of the contraction. During isometric contraction, the muscle does not shorten but rather remains the same length, with an increase in muscle tone.

Spinal Control of Movement • The spinal cord mediates rapid, automatic responses to stimuli, called reflexes. • A large number of reflexes are organized in the spinal cord, including the stretch reflex,

tendon reflex, withdrawal reflex, crossed extensor reflex, elimination reflexes, and sexual reflexes.

• The withdrawal, or flexion, reflex involves an immediate withdrawal movement that occurs in response to a painful stimulus.

• In the crossed extensor reflex, one leg extends when the other flexes to withdraw from a painful stimulus.

• Urination and defecation involve a stretch reflex.

Control of Movement by the Brain • The brain controls movement by means of the pyramidal motor system and the extra-

pyramidal motor system. • Arising from the primary motor cortex, the pyramidal system traverses the spinal cord

through the corticospinal tract. Axons leaving the primary motor cortex pass without syn- apsing to target motor neurons in the ventral horn of the spinal cord.

• The extrapyramidal system arises from the cerebral cortex, the basal ganglia, the cer- ebellum, and the reticular formation. The function of the cerebellum is to coordinate well-learned movements and movements made in response to sensory stimuli. The basal ganglia are involved in relaying information to and from the cerebral cortex.

• The pyramidal system develops later than the extrapyramidal system and regulates fine motor control, whereas the extrapyramidal system controls gross postural adjustments and other movements produced by large muscles.

Movement Disorders • Damage to muscles, motor neurons, the spinal cord, the pyramidal system, or the extra-

pyramidal system can result in a movement disorder.

Damage to Muscles • Muscular dystrophy and myasthenia gravis are associated with progressive damage to

muscle fibers.

Damage to Motor Neurons • Amyotrophic lateral sclerosis (ALS) is caused by damage to motor neurons.

Damage to the Spinal Cord • Damage to the cervical spinal cord typically results in quadriplegia, whereas damage to

the thoracic or lumbar spinal cord causes paraplegia.

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CHAPTER 5Web Links

Damage to the Pyramidal System • Damage to the pyramidal system results in transient flaccid paralysis, which eventually is

replaced by hyperreflexia. • Apraxia is also associated with damage to the pyramidal motor system.

Damage to the Extrapyramidal System • Damage to the extrapyramidal system immediately produces hyperreflexia and spasticity.

Damage to the Basal Ganglia • Damage to the basal ganglia can produce tics, choreas as seen in Huntington’s disease,

and Parkinson’s disease. • Parkinson’s disease is caused by destruction of dopamine-producing cells in the substan-

tia nigra. Treatments for Parkinson’s disease include drug therapy, involving L-dopa and glutamate antagonists, and surgical treatments.

Damage to the Cerebellum • Damage to the cerebellum can result in ataxia, disequilibrium, and disruption of rapid,

well-learned movements.

Questions for Thought

1. Why do some reflexes emerge later than others during development? 2. Give an example of how you use isometric muscle contraction every day. Give an exam-

ple of isotonic contraction. 3. If you had a brain tumor at the superior aspect of your primary motor cortex, movement

to which parts of your body might be affected? 4. Explain how the stretch receptors in the muscle spindles and Golgi tendon organs regu-

late muscle tone. 5. Name three differences between the pyramidal and extrapyramidal motor systems. 6. What are the effects of spinal shock?

Web Links

To learn more about infant reflexes and development, visit the MedlinePlus website. Here you will see a general overview of each kind of reflex, descriptions of those that carry on into adult- hood, and any abnormalities that may occur in development. http://www.nlm.nih.gov/medlineplus/

For information on Huntington’s disease, Parkinson’s disease, and other types of movement disorders, visit the Mayo Clinic’s website. This page offers detailed information on symptoms, causes, treatment, and drugs that help those suffering from movement disorders. http://MayoClinic.com/health-information

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CHAPTER 5Key Terms

Key Terms

amyotrophic lateral sclerosis (ALS) A progres- sive disorder caused by degeneration of motor neurons in the spinal cord and brain.

apraxia A disorder caused by cerebral damage in which a person cannot organize movements into a productive sequence and can no longer perform previously familiar movements with the hands.

ataxia An inability to walk in a coordinated fashion.

atrophy A deterioration of tissue.

Babinski reflex A reflex in infants when a touch to the ball of the foot causes the toes to fan (positive) or when a touch to the ball of the foot causes the toes to curl (negative).

cerebellar cortex The cerebellum’s outermost layer, which contains Purkinje, Golgi, stellate, basket, and granule cells.

cerebral palsy A motor disorder caused by damage to the developing brain.

choreas Involuntary contractions that produce movements of the head, arms, and legs.

corticospinal tract A group of axons that car- ries messages from the primary motor cortex to motor neurons in the spinal cord.

crossed extensor reflex A spinal reflex that typically occurs in conjunction with another reflex, the withdrawal reflex; it consists of withdrawing an affected body part from some- thing that is causing pain.

disequilibrium A loss of balance due to impairment of the cerebellum.

extension A movement that straightens a limb.

extrapyramidal motor system The motor system that coordinates gross postural adjust- ments and arises from the cerebral cortex, basal ganglia, cerebellum, and reticular formation.

flexion A movement that bends a limb.

Golgi tendon organ A stretch receptor that provides feedback to the nervous system about muscle contractions.

Huntington’s disease A genetic disorder linked to chromosome 4, which increases dopamine activity in the basal ganglia, producing tics and uncontrollable muscle contractions.

L-dopa A drug used to treat Parkinson’s dis- ease that crosses the blood-brain barrier and is converted to dopamine in the brain.

muscle fiber A muscle cell; it contains a nucleus, mitochondria, and other typical cel- lular components.

muscle spindle A special structure inter- spersed among the muscle fibers in skeletal muscles; it is composed of several short muscle fibers that are joined to a centralized structure called a nuclear bag.

muscular dystrophy A disorder characterized by wasting of the muscle fibers, which causes muscular weakness.

myasthenia gravis A disorder characterized by progressive loss of acetylcholine receptors in the neuromuscular junction.

neuromuscular junction The junction between the axon terminal button and the muscle fiber.

paraplegia A disorder involving loss of motor function to the lower limbs.

Parkinson’s disease A movement disorder caused by destruction of dopamine-producing cells in the substantia nigra, with symptoms of tremor, loss of balance, and rigidity of limbs.

polysynaptic reflexes Reflexes that involve more than one synapse.

primary motor cortex The source of the pyramidal motor system that sends impulses involving fine motor control to motor neurons.

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CHAPTER 5Key Terms

pyramidal motor system The motor system that arises from the primary motor cortex in the frontal lobe and directs fine motor control of skeletal muscles.

quadriplegia A disability involving impairment of motor and sensory functions in all four limbs.

reflexes Rapid, automatic sets of muscle contractions made in response to a particular stimulus.

skeletal muscle Muscle that is controlled by the somatic nervous system and is attached to bones of the skeleton.

smooth muscles Muscles that are controlled by the autonomic nervous system and are found in the walls of blood vessels and in the walls of many organs and glands.

spasticity A disorder that is characterized by disturbed control of balance and uncontrolled movements.

spinal shock A condition seen immediately following damage to the spinal cord in which no spinal reflexes can be elicited.

stretch reflex Contraction of a muscle in response to stretching of the annulospiral receptors in that muscle.

tics Brief, involuntary contractions of specific skeletal muscles produced by damage to the basal ganglia.

transient flaccid paralysis A complete loss of muscle tone, with paralysis, seen immediately after damage to the pyramidal motor system.

unisynaptic reflex A reflex that involves only one synapse.

withdrawal reflex The flexion of a limb in response to a painful or noxious stimulus.

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