Most “voluntary” movements initiated by the cerebral cortex are achieved when the cortex activates “patterns” of function stored in lower brain areas—the cord, brain stem, basal ganglia, and cerebellum. These lower centers, in turn, send specific control signals to the muscles.
For a few types of movements, however, the cortex has almost a direct pathway to the anterior motor neurons of the cord, bypassing some motor centers on the way. This is especially true for control of the fine dexterous movements of the fingers and hands. This chapter and Chapter 56 explain the interplay among the different motor areas of the brain and spinal cord to provide overall synthesis of voluntary motor function.
Motor Cortex and Corticospinal Tract
Figure 55-1 shows the functional areas of the cerebral cortex. Anterior to the central cortical sulcus, occupying approximately the posterior one third of the frontal lobes, is the motor cortex. Posterior to the central sulcus is the somatosensory cortex (an area discussed in detail in earlier chapters), which feeds the motor cortex many of the signals that initiate motor activities.
Figure 55-1 Motor and somatosensory functional areas of the cerebral cortex. The numbers 4, 5, 6, and 7 are Brodmann’s cortical areas, as explained in Chapter 47.
The motor cortex itself is divided into three subareas, each of which has its own topographical representation of muscle groups and specific motor functions: (1) the primary motor cortex, (2) the premotor area, and (3) the supplementary motor area.
Primary Motor Cortex
The primary motor cortex, shown in Figure 55-1, lies in the first convolution of the frontal lobes anterior to the central sulcus. It begins laterally in the sylvian fissure, spreads superiorly to the uppermost portion of the brain, and then dips deep into the longitudinal fissure. (This area is the same as area 4 in Brodmann’s classification of the brain cortical areas, shown in Figure 47-5.)
Figure 55-1 lists the approximate topographical representations of the different muscle areas of the body in the primary motor cortex, beginning with the face and mouth region near the sylvian fissure; the arm and hand area, in the midportion of the primary motor cortex; the trunk, near the apex of the brain; and the leg and foot areas, in the part of the primary motor cortex that dips into the longitudinal fissure. This topographical organization is demonstrated even more graphically in Figure 55-2, which shows the degrees of representation of the different muscle areas as mapped by Penfield and Rasmussen. This mapping was done by electrically stimulating the different areas of the motor cortex in human beings who were undergoing neurosurgical operations. Note that more than one half of the entire primary motor cortex is concerned with controlling the muscles of the hands and the muscles of speech. Point stimulation in these hand and speech motor areas on rare occasion causes contraction of a single muscle; most often, stimulation contracts a group of muscles instead. To express this in another way, excitation of a single motor cortex neuron usually excites a specific movement rather than one specific muscle. To do this, it excites a “pattern” of separate muscles, each of which contributes its own direction and strength of muscle movement.
Figure 55-2 Degree of representation of the different muscles of the body in the motor cortex.
(Redrawn from Penfield W, Rasmussen T: The Cerebral Cortex of Man: A Clinical Study of Localization of Function. New York: Hafner, 1968.)
Premotor Area
The premotor area, also shown in Figure 55-1, lies 1 to 3 centimeters anterior to the primary motor cortex, extending inferiorly into the sylvian fissure and superiorly into the longitudinal fissure, where it abuts the supplementary motor area, which has functions similar to those of the premotor area. The topographical organization of the premotor cortex is roughly the same as that of the primary motor cortex, with the mouth and face areas located most laterally; as one moves upward, the hand, arm, trunk, and leg areas are encountered.
Nerve signals generated in the premotor area cause much more complex “patterns” of movement than the discrete patterns generated in the primary motor cortex. For instance, the pattern may be to position the shoulders and arms so that the hands are properly oriented to perform specific tasks. To achieve these results, the most anterior part of the premotor area first develops a “motor image” of the total muscle movement that is to be performed. Then, in the posterior premotor cortex, this image excites each successive pattern of muscle activity required to achieve the image. This posterior part of the premotor cortex sends its signals either directly to the primary motor cortex to excite specific muscles or, often, by way of the basal ganglia and thalamus back to the primary motor cortex.
A special class of neurons called mirror neurons becomes active when a person performs a specific motor task or when he or she observes the same task performed by others. Thus, the activity of these neurons “mirrors” the behavior of another person as though the observer was performing the specific motor task. Mirror neurons are located in the premotor cortex and the inferior parietal cortex (and perhaps in other regions of the brain) and were first discovered in monkeys. However, brain imaging studies indicate that these neurons are also present in humans and may serve the same functions as observed in monkeys—to transform sensory representations of acts that are heard or seen into motor representations of these acts. Many neurophysiologists believe that these mirror neurons may be important for understanding the actions of other people and for learning new skills by imitation. Thus, the premotor cortex, basal ganglia, thalamus, and primary motor cortex constitute a complex overall system for the control of complex patterns of coordinated muscle activity.
Supplementary Motor Area
The supplementary motor area has yet another topographical organization for the control of motor function. It lies mainly in the longitudinal fissure but extends a few centimeters onto the superior frontal cortex. Contractions elicited by stimulating this area are often bilateral rather than unilateral. For instance, stimulation frequently leads to bilateral grasping movements of both hands simultaneously; these movements are perhaps rudiments of the hand functions required for climbing. In general, this area functions in concert with the premotor area to provide body-wide attitudinal movements, fixation movements of the different segments of the body, positional movements of the head and eyes, and so forth, as background for the finer motor control of the arms and hands by the premotor area and primary motor cortex.
Some Specialized Areas of Motor Control Found in the Human Motor Cortex
A few highly specialized motor regions of the human cerebral cortex (shown in Figure 55-3) control specific motor functions. These regions have been localized either by electrical stimulation or by noting the loss of motor function when destructive lesions occur in specific cortical areas. Some of the more important regions are the following.
Figure 55-3 Representation of the different muscles of the body in the motor cortex and location of other cortical areas responsible for specific types of motor movements.
Broca’s Area and Speech
Figure 55-3 shows a premotor area labeled “word formation” lying immediately anterior to the primary motor cortex and immediately above the sylvian fissure. This region is called Broca’s area. Damage to it does not prevent a person from vocalizing but makes it impossible for the person to speak whole words rather than uncoordinated utterances or an occasional simple word such as “no” or “yes.” A closely associated cortical area also causes appropriate respiratory function, so respiratory activation of the vocal cords can occur simultaneously with the movements of the mouth and tongue during speech. Thus, the premotor neuronal activities related to speech are highly complex.
“Voluntary” Eye Movement Field
In the premotor area immediately above Broca’s area is a locus for controlling voluntary eye movements. Damage to this area prevents a person from voluntarily moving the eyes toward different objects. Instead, the eyes tend to lock involuntarily onto specific objects, an effect controlled by signals from the occipital visual cortex, as explained in Chapter 51. This frontal area also controls eyelid movements such as blinking.
Head Rotation Area
Slightly higher in the motor association area, electrical stimulation elicits head rotation. This area is closely associated with the eye movement field; it directs the head toward different objects.
Area for Hand Skills
In the premotor area immediately anterior to the primary motor cortex for the hands and fingers is a region that is important for “hand skills.” That is, when tumors or other lesions cause destruction in this area, hand movements become uncoordinated and nonpurposeful, a condition called motor apraxia.
Transmission of Signals from the Motor Cortex to the Muscles
Motor signals are transmitted directly from the cortex to the spinal cord through the corticospinal tract and indirectly through multiple accessory pathways that involve the basal ganglia, cerebellum, and various nuclei of the brain stem. In general, the direct pathways are concerned more with discrete and detailed movements, especially of the distal segments of the limbs, particularly the hands and fingers.
Corticospinal (Pyramidal) Tract
The most important output pathway from the motor cortex is the corticospinal tract, also called the pyramidal tract, shown in Figure 55-4. The corticospinal tract originates about 30 percent from the primary motor cortex, 30 percent from the premotor and supplementary motor areas, and 40 percent from the somatosensory areas posterior to the central sulcus.
Figure 55-4 Corticospinal (pyramidal) tract.
(Modified from Ranson SW, Clark SL: Anatomy of the Nervous System. Philadelphia: WB Saunders, 1959.)
After leaving the cortex, it passes through the posterior limb of the internal capsule (between the caudate nucleus and the putamen of the basal ganglia) and then downward through the brain stem, forming the pyramids of the medulla. The majority of the pyramidal fibers then cross in the lower medulla to the opposite side and descend into the lateral corticospinal tracts of the cord, finally terminating principally on the interneurons in the intermediate regions of the cord gray matter; a few terminate on sensory relay neurons in the dorsal horn, and a very few terminate directly on the anterior motor neurons that cause muscle contraction.
A few of the fibers do not cross to the opposite side in the medulla but pass ipsilaterally down the cord in the ventral corticospinal tracts. Many, if not most, of these fibers eventually cross to the opposite side of the cord either in the neck or in the upper thoracic region. These fibers may be concerned with control of bilateral postural movements by the supplementary motor cortex.
The most impressive fibers in the pyramidal tract are a population of large myelinated fibers with a mean diameter of 16 micrometers. These fibers originate from giant pyramidal cells, called Betz cells, that are found only in the primary motor cortex. The Betz cells are about 60 micrometers in diameter, and their fibers transmit nerve impulses to the spinal cord at a velocity of about 70 m/sec, the most rapid rate of transmission of any signals from the brain to the cord. There are about 34,000 of these large Betz cell fibers in each corticospinal tract. The total number of fibers in each corticospinal tract is more than 1 million, so these large fibers represent only 3 percent of the total. The other 97 percent are mainly fibers smaller than 4 micrometers in diameter that conduct background tonic signals to the motor areas of the cord.
Other Fiber Pathways from the Motor Cortex
The motor cortex gives rise to large numbers of additional, mainly small, fibers that go to deep regions in the cerebrum and brain stem, including the following:
1. The axons from the giant Betz cells send short collaterals back to the cortex itself. These collaterals are believed to inhibit adjacent regions of the cortex when the Betz cells discharge, thereby “sharpening” the boundaries of the excitatory signal.
2. A large number of fibers pass from the motor cortex into the caudate nucleus and putamen. From there, additional pathways extend into the brain stem and spinal cord, as discussed in the next chapter, mainly to control body postural muscle contractions.
3. A moderate number of motor fibers pass to red nuclei of the midbrain. From these, additional fibers pass down the cord through the rubrospinal tract.
4. A moderate number of motor fibers deviate into the reticular substance and vestibular nuclei of the brain stem; from there, signals go to the cord by way of reticulospinal and vestibulospinal tracts, and others go to the cerebellum by way of reticulocerebellar and vestibulocerebellar tracts.
5. A tremendous number of motor fibers synapse in the pontile nuclei, which give rise to the pontocerebellar fibers, carrying signals into the cerebellar hemispheres.
6. Collaterals also terminate in the inferior olivary nuclei, and from there, secondary olivocerebellar fibers transmit signals to multiple areas of the cerebellum.
Thus, the basal ganglia, brain stem, and cerebellum all receive strong motor signals from the corticospinal system every time a signal is transmitted down the spinal cord to cause a motor activity.
Incoming Sensory Fiber Pathways to the Motor Cortex
The functions of the motor cortex are controlled mainly by nerve signals from the somatosensory system but also, to some degree, from other sensory systems such as hearing and vision. Once the sensory information is received, the motor cortex operates in association with the basal ganglia and cerebellum to excite an appropriate course of motor action. The more important incoming fiber pathways to the motor cortex are the following:
1. Subcortical fibers from adjacent regions of the cerebral cortex, especially from (a) the somatosensory areas of the parietal cortex, (b) the adjacent areas of the frontal cortex anterior to the motor cortex, and (c) the visual and auditory cortices.
2. Subcortical fibers that arrive through the corpus callosum from the opposite cerebral hemisphere. These fibers connect corresponding areas of the cortices in the two sides of the brain.
3. Somatosensory fibers that arrive directly from the ventrobasal complex of the thalamus. These relay mainly cutaneous tactile signals and joint and muscle signals from the peripheral body.
4. Tracts from the ventrolateral and ventroanterior nuclei of the thalamus, which in turn receive signals from the cerebellum and basal ganglia. These tracts provide signals that are necessary for coordination among the motor control functions of the motor cortex, basal ganglia, and cerebellum.
5. Fibers from the intralaminar nuclei of the thalamus. These fibers control the general level of excitability of the motor cortex in the same way they control the general level of excitability of most other regions of the cerebral cortex.
Red Nucleus Serves as an Alternative Pathway for Transmitting Cortical Signals to the Spinal Cord
The red nucleus, located in the mesencephalon, functions in close association with the corticospinal tract. As shown in Figure 55-5, it receives a large number of direct fibers from the primary motor cortex through the corticorubral tract, as well as branching fibers from the corticospinal tract as it passes through the mesencephalon. These fibers synapse in the lower portion of the red nucleus, the magnocellular portion, which contains large neurons similar in size to the Betz cells in the motor cortex. These large neurons then give rise to the rubrospinal tract, which crosses to the opposite side in the lower brain stem and follows a course immediately adjacent and anterior to the corticospinal tract into the lateral columns of the spinal cord.
Figure 55-5 Corticorubrospinal pathway for motor control, showing also the relation of this pathway to the cerebellum.
The rubrospinal fibers terminate mostly on the interneurons of the intermediate areas of the cord gray matter, along with the corticospinal fibers, but some of the rubrospinal fibers terminate directly on anterior motor neurons, along with some corticospinal fibers. The red nucleus also has close connections with the cerebellum, similar to the connections between the motor cortex and the cerebellum.
Function of the Corticorubrospinal System
The magnocellular portion of the red nucleus has a somatographic representation of all the muscles of the body, as is true of the motor cortex. Therefore, stimulation of a single point in this portion of the red nucleus causes contraction of either a single muscle or a small group of muscles. However, the fineness of representation of the different muscles is far less developed than in the motor cortex. This is especially true in human beings, who have relatively small red nuclei.
The corticorubrospinal pathway serves as an accessory route for transmission of relatively discrete signals from the motor cortex to the spinal cord. When the corticospinal fibers are destroyed but the corticorubrospinal pathway is intact, discrete movements can still occur, except that the movements for fine control of the fingers and hands are considerably impaired. Wrist movements are still functional, which is not the case when the corticorubrospinal pathway is also blocked.
Therefore, the pathway through the red nucleus to the spinal cord is associated with the corticospinal system. Further, the rubrospinal tract lies in the lateral columns of the spinal cord, along with the corticospinal tract, and terminates on the interneurons and motor neurons that control the more distal muscles of the limbs. Therefore, the corticospinal and rubrospinal tracts together are called the lateral motor system of the cord, in contradistinction to a vestibuloreticulospinal system, which lies mainly medially in the cord and is called the medial motor system of the cord, as discussed later in this chapter.
“Extrapyramidal” System
The term extrapyramidal motor system is widely used in clinical circles to denote all those portions of the brain and brain stem that contribute to motor control but are not part of the direct corticospinal-pyramidal system. These include pathways through the basal ganglia, the reticular formation of the brain stem, the vestibular nuclei, and often the red nuclei. This is such an all-inclusive and diverse group of motor control areas that it is difficult to ascribe specific neurophysiologic functions to the so-called extrapyramidal system as a whole. In fact, the pyramidal and extrapyramidal systems are extensively interconnected and interact to control movement. For these reasons, the term “extrapyramidal” is being used less often both clinically and physiologically.
Excitation of the Spinal Cord Motor Control Areas by the Primary Motor Cortex and Red Nucleus
Vertical Columnar Arrangement of the Neurons in the Motor Cortex
In Chapters 47 and 51, we pointed out that the cells in the somatosensory cortex and visual cortex are organized in vertical columns of cells. In like manner, the cells of the motor cortex are organized in vertical columns a fraction of a millimeter in diameter, with thousands of neurons in each column.
Each column of cells functions as a unit, usually stimulating a group of synergistic muscles, but sometimes stimulating just a single muscle. Also, each column has six distinct layers of cells, as is true throughout nearly all the cerebral cortex. The pyramidal cells that give rise to the corticospinal fibers all lie in the fifth layer of cells from the cortical surface. Conversely, the input signals all enter by way of layers 2 through 4. And the sixth layer gives rise mainly to fibers that communicate with other regions of the cerebral cortex itself.
Function of Each Column of Neurons
The neurons of each column operate as an integrative processing system, using information from multiple input sources to determine the output response from the column. In addition, each column can function as an amplifying system to stimulate large numbers of pyramidal fibers to the same muscle or to synergistic muscles simultaneously. This is important because stimulation of a single pyramidal cell can seldom excite a muscle. Usually, 50 to 100 pyramidal cells need to be excited simultaneously or in rapid succession to achieve definitive muscle contraction.
Dynamic and Static Signals Are Transmitted by the Pyramidal Neurons
If a strong signal is sent to a muscle to cause initial rapid contraction, then a much weaker continuing signal can maintain the contraction for long periods thereafter. This is the usual manner in which excitation is provided to cause muscle contractions. To do this, each column of cells excites two populations of pyramidal cell neurons, one called dynamic neurons and the other static neurons. The dynamic neurons are excited at a high rate for a short period at the beginning of a contraction, causing the initial rapid development of force. Then the static neurons fire at a much slower rate, but they continue firing at this slow rate to maintain the force of contraction as long as the contraction is required.
The neurons of the red nucleus have similar dynamic and static characteristics, except that a greater percentage of dynamic neurons is in the red nucleus and a greater percentage of static neurons is in the primary motor cortex. This may be related to the fact that the red nucleus is closely allied with the cerebellum, and the cerebellum plays an important role in rapid initiation of muscle contraction, as explained in the next chapter.
Somatosensory Feedback to the Motor Cortex Helps Control the Precision of Muscle Contraction
When nerve signals from the motor cortex cause a muscle to contract, somatosensory signals return all the way from the activated region of the body to the neurons in the motor cortex that are initiating the action. Most of these somatosensory signals arise in (1) the muscle spindles, (2) the tendon organs of the muscle tendons, or (3) the tactile receptors of the skin overlying the muscles. These somatic signals often cause positive feedback enhancement of the muscle contraction in the following ways: In the case of the muscle spindles, if the fusimotor muscle fibers in the spindles contract more than the large skeletal muscle fibers contract, the central portions of the spindles become stretched and, therefore, excited. Signals from these spindles then return rapidly to the pyramidal cells in the motor cortex to signal them that the large muscle fibers have not contracted enough. The pyramidal cells further excite the muscle, helping its contraction to catch up with the contraction of the muscle spindles. In the case of the tactile receptors, if the muscle contraction causes compression of the skin against an object, such as compression of the fingers around an object being grasped, the signals from the skin receptors can, if necessary, cause further excitation of the muscles and, therefore, increase the tightness of the hand grasp.
Stimulation of the Spinal Motor Neurons
Figure 55-6 shows a cross section of a spinal cord segment demonstrating (1) multiple motor and sensorimotor control tracts entering the cord segment and (2) a representative anterior motor neuron in the middle of the anterior horn gray matter. The corticospinal tract and the rubrospinal tract lie in the dorsal portions of the lateral white columns. Their fibers terminate mainly on interneurons in the intermediate area of the cord gray matter.
Figure 55-6 Convergence of different motor control pathways on the anterior motor neurons.
In the cervical enlargement of the cord where the hands and fingers are represented, large numbers of both corticospinal and rubrospinal fibers also terminate directly on the anterior motor neurons, thus allowing a direct route from the brain to activate muscle contraction. This is in keeping with the fact that the primary motor cortex has an extremely high degree of representation for fine control of hand, finger, and thumb actions.
Patterns of Movement Elicited by Spinal Cord Centers
From Chapter 54, recall that the spinal cord can provide certain specific reflex patterns of movement in response to sensory nerve stimulation. Many of these same patterns are also important when the cord’s anterior motor neurons are excited by signals from the brain. For example, the stretch reflex is functional at all times, helping to damp any oscillations of the motor movements initiated from the brain, and probably also providing at least part of the motive power required to cause muscle contractions when the intrafusal fibers of the muscle spindles contract more than the large skeletal muscle fibers do, thus eliciting reflex “servo-assist” stimulation of the muscle, in addition to the direct stimulation by the corticospinal fibers.
Also, when a brain signal excites a muscle, it is usually unnecessary to transmit an inverse signal to relax the antagonist muscle at the same time; this is achieved by the reciprocal innervation circuit that is always present in the cord for coordinating the function of antagonistic pairs of muscles.
Finally, other cord reflex mechanisms, such as withdrawal, stepping and walking, scratching, and postural mechanisms, can each be activated by “command” signals from the brain. Thus, simple command signals from the brain can initiate many normal motor activities, particularly for such functions as walking and attaining different postural attitudes of the body.
Effect of Lesions in the Motor Cortex or in the Corticospinal Pathway—The “Stroke”
The motor control system can be damaged by the common abnormality called a “stroke.” This is caused by either a ruptured blood vessel that hemorrhages into the brain or by thrombosis of one of the major arteries supplying the brain. In either case, the result is loss of blood supply to the cortex or to the corticospinal tract where it passes through the internal capsule between the caudate nucleus and the putamen. Also, experiments have been performed in animals to selectively remove different parts of the motor cortex.
Removal of the Primary Motor Cortex (Area Pyramidalis)
Removal of a portion of the primary motor cortex—the area that contains the giant Betz pyramidal cells—causes varying degrees of paralysis of the represented muscles. If the sublying caudate nucleus and adjacent premotor and supplementary motor areas are not damaged, gross postural and limb “fixation” movements can still occur, but there is loss of voluntary control of discrete movements of the distal segments of the limbs, especially of the hands and fingers. This does not mean that the hand and finger muscles themselves cannot contract; rather, the ability to control the fine movements is gone. From these observations, one can conclude that the area pyramidalis is essential for voluntary initiation of finely controlled movements, especially of the hands and fingers.
Muscle Spasticity Caused by Lesions That Damage Large Areas Adjacent to the Motor Cortex
The primary motor cortex normally exerts a continual tonic stimulatory effect on the motor neurons of the spinal cord; when this stimulatory effect is removed, hypotonia results. Most lesions of the motor cortex, especially those caused by a stroke, involve not only the primary motor cortex but also adjacent parts of the brain such as the basal ganglia. In these instances, muscle spasm almost invariably occurs in the afflicted muscle areas on the opposite sideof the body (because the motor pathways cross to the opposite side). This spasm results mainly from damage to accessory pathways from the nonpyramidal portions of the motor cortex. These pathways normally inhibit the vestibular and reticular brain stem motor nuclei. When these nuclei cease their state of inhibition (i.e., are “disinhibited”), they become spontaneously active and cause excessive spastic tone in the involved muscles, as we discuss more fully later in the chapter. This is the spasticity that normally accompanies a “stroke” in a human being.
Role of the Brain Stem in Controlling Motor Function
The brain stem consists of the medulla, pons, and mesencephalon. In one sense, it is an extension of the spinal cord upward into the cranial cavity because it contains motor and sensory nuclei that perform motor and sensory functions for the face and head regions in the same way that the spinal cord performs these functions from the neck down. But in another sense, the brain stem is its own master because it provides many special control functions, such as the following:
1. Control of respiration
2. Control of the cardiovascular system
3. Partial control of gastrointestinal function
4. Control of many stereotyped movements of the body
5. Control of equilibrium
6. Control of eye movements
Finally, the brain stem serves as a way station for “command signals” from higher neural centers. In the following sections, we discuss the role of the brain stem in controlling whole-body movement and equilibrium. Especially important for these purposes are the brain stem’s reticular nuclei and vestibular nuclei.
Support of the Body Against Gravity—Roles of the Reticular and Vestibular Nuclei
Figure 55-7 shows the locations of the reticular and vestibular nuclei in the brain stem.
Figure 55-7 Locations of the reticular and vestibular nuclei in the brain stem.
Excitatory-Inhibitory Antagonism Between Pontine and Medullary Reticular Nuclei
The reticular nuclei are divided into two major groups: (1) pontine reticular nuclei, located slightly posteriorly and laterally in the pons and extending into the mesencephalon, and (2) medullary reticular nuclei, which extend through the entire medulla, lying ventrally and medially near the midline. These two sets of nuclei function mainly antagonistically to each other, with the pontine exciting the antigravity muscles and the medullary relaxing these same muscles.
Pontine Reticular System
The pontine reticular nuclei transmit excitatory signals downward into the cord through the pontine reticulospinal tract in the anterior column of the cord, as shown in Figure 55-8. The fibers of this pathway terminate on the medial anterior motor neurons that excite the axial muscles of the body, which support the body against gravity—that is, the muscles of the vertebral column and the extensor muscles of the limbs.
Figure 55-8 Vestibulospinal and reticulospinal tracts descending in the spinal cord to excite (solid lines) or inhibit (dashed lines) the anterior motor neurons that control the body’s axial musculature.
The pontine reticular nuclei have a high degree of natural excitability. In addition, they receive strong excitatory signals from the vestibular nuclei, as well as from deep nuclei of the cerebellum. Therefore, when the pontine reticular excitatory system is unopposed by the medullary reticular system, it causes powerful excitation of antigravity muscles throughout the body, so much so that four-legged animals can be placed in a standing position, supporting the body against gravity without any signals from higher levels of the brain.
Medullary Reticular System
The medullary reticular nuclei transmit inhibitory signals to the same antigravity anterior motor neurons by way of a different tract, the medullary reticulospinal tract, located in the lateral column of the cord, as also shown in Figure 55-8. The medullary reticular nuclei receive strong input collaterals from (1) the corticospinal tract, (2) the rubrospinal tract, and (3) other motor pathways. These normally activate the medullary reticular inhibitory system to counterbalance the excitatory signals from the pontine reticular system, so under normal conditions the body muscles are not abnormally tense.
Yet some signals from higher areas of the brain can “disinhibit” the medullary system when the brain wishes to excite the pontine system to cause standing. At other times, excitation of the medullary reticular system can inhibit antigravity muscles in certain portions of the body to allow those portions to perform special motor activities. The excitatory and inhibitory reticular nuclei constitute a controllable system that is manipulated by motor signals from the cerebral cortex and elsewhere to provide necessary background muscle contractions for standing against gravity and to inhibit appropriate groups of muscles as needed so that other functions can be performed.
Role of the Vestibular Nuclei to Excite the Antigravity Muscles
All the vestibular nuclei, shown in Figure 55-7, function in association with the pontine reticular nuclei to control the antigravity muscles. The vestibular nuclei transmit strong excitatory signals to the antigravity muscles by way of the lateral and medial vestibulospinal tracts in the anterior columns of the spinal cord, as shown in Figure 55-8. Without this support of the vestibular nuclei, the pontine reticular system would lose much of its excitation of the axial antigravity muscles.
The specific role of the vestibular nuclei, however, is to selectively control the excitatory signals to the different antigravity muscles to maintain equilibrium in response to signals from the vestibular apparatus. We discuss this more fully later in the chapter.
The Decerebrate Animal Develops Spastic Rigidity
When the brain stem of an animal is sectioned below the midlevel of the mesencephalon, but the pontine and medullary reticular systems, as well as the vestibular system, are left intact, the animal develops a condition called decerebrate rigidity. This rigidity does not occur in all muscles of the body but does occur in the antigravity muscles—the muscles of the neck and trunk and the extensors of the legs.
The cause of decerebrate rigidity is blockage of normally strong input to the medullary reticular nuclei from the cerebral cortex, the red nuclei, and the basal ganglia. Lacking this input, the medullary reticular inhibitor system becomes nonfunctional; full overactivity of the pontine excitatory system occurs, and rigidity develops. We shall see later that other causes of rigidity occur in other neuromotor diseases, especially lesions of the basal ganglia.
Vestibular Sensations and Maintenance of Equilibrium
Vestibular Apparatus
The vestibular apparatus, shown in Figure 55-9, is the sensory organ for detecting sensations of equilibrium. It is encased in a system of bony tubes and chambers located in the petrous portion of the temporal bone, called the bony labyrinth. Within this system are membranous tubes and chambers called the membranous labyrinth. The membranous labyrinth is the functional part of the vestibular apparatus.
Figure 55-9 Membranous labyrinth and organization of the crista ampullaris and the macula.
The top of Figure 55-9 shows the membranous labyrinth. It is composed mainly of the cochlea (ductus cochlearis); three semicircular canals; and two large chambers, the utricle and saccule. The cochlea is the major sensory organ for hearing (see Chapter 52) and has little to do with equilibrium. However, the semicircular canals, the utricle, and the saccule are all integral parts of the equilibrium mechanism.
“Maculae”—Sensory Organs of the Utricle and Saccule for Detecting Orientation of the Head with Respect to Gravity
Located on the inside surface of each utricle and saccule, shown in the top diagram of Figure 55-9, is a small sensory area slightly over 2 millimeters in diameter called a macula. The macula of the utricle lies mainly in the horizontal plane on the inferior surface of the utricle and plays an important role in determining orientation of the head when the head is upright. Conversely, the macula of the saccule is located mainly in a vertical plane and signals head orientation when the person is lying down.
Each macula is covered by a gelatinous layer in which many small calcium carbonate crystals called statoconia are embedded. Also in the macula are thousands of hair cells, one of which is shown in Figure 55-10; these project ciliaup into the gelatinous layer. The bases and sides of the hair cells synapse with sensory endings of the vestibular nerve.
Figure 55-10 Hair cell of the equilibrium apparatus and its synapses with the vestibular nerve.
The calcified statoconia have a specific gravity two to three times the specific gravity of the surrounding fluid and tissues. The weight of the statoconia bends the cilia in the direction of gravitational pull.
Directional Sensitivity of the Hair Cells—Kinocilium
Each hair cell has 50 to 70 small cilia called stereocilia, plus one large cilium, the kinocilium, as shown in Figure 55-10. The kinocilium is always located to one side, and the stereocilia become progressively shorter toward the other side of the cell. Minute filamentous attachments, almost invisible even to the electron microscope, connect the tip of each stereocilium to the next longer stereocilium and, finally, to the kinocilium.
Because of these attachments, when the stereocilia and kinocilium bend in the direction of the kinocilium, the filamentous attachments tug in sequence on the stereocilia, pulling them outward from the cell body. This opens several hundred fluid channels in the neuronal cell membrane around the bases of the stereocilia, and these channels are capable of conducting large numbers of positive ions. Therefore, positive ions pour into the cell from the surrounding endolymphatic fluid, causing receptor membrane depolarization. Conversely, bending the pile of stereocilia in the opposite direction (backward to the kinocilium) reduces the tension on the attachments; this closes the ion channels, thus causing receptor hyperpolarization.
Under normal resting conditions, the nerve fibers leading from the hair cells transmit continuous nerve impulses at a rate of about 100 per second. When the stereocilia are bent toward the kinocilium, the impulse traffic increases, often to several hundred per second; conversely, bending the cilia away from the kinocilium decreases the impulse traffic, often turning it off completely. Therefore, as the orientation of the head in space changes and the weight of the statoconia bends the cilia, appropriate signals are transmitted to the brain to control equilibrium.
In each macula, each of the hair cells is oriented in a different direction so that some of the hair cells are stimulated when the head bends forward, some are stimulated when it bends backward, others are stimulated when it bends to one side, and so forth. Therefore, a different pattern of excitation occurs in the macular nerve fibers for each orientation of the head in the gravitational field. It is this “pattern” that apprises the brain of the head’s orientation in space.
Semicircular Ducts
The three semicircular ducts in each vestibular apparatus, known as the anterior, posterior, and lateral (horizontal) semicircular ducts, are arranged at right angles to one another so that they represent all three planes in space. When the head is bent forward about 30 degrees, the lateral semicircular ducts are approximately horizontal with respect to the surface of the earth; the anterior ducts are in vertical planes that project forward and 45 degrees outward,whereas the posterior ducts are in vertical planes that project backward and 45 degrees outward.
Each semicircular duct has an enlargement at one of its ends called the ampulla, and the ducts and ampulla are filled with a fluid called endolymph. Flow of this fluid through one of the ducts and through its ampulla excites the sensory organ of the ampulla in the following manner: Figure 55-11 shows in each ampulla a small crest called a crista ampullaris. On top of this crista is a loose gelatinous tissue mass, the cupula. When a person’s head begins to rotate in any direction, the inertia of the fluid in one or more of the semicircular ducts causes the fluid to remain stationary while the semicircular duct rotates with the head. This causes fluid to flow from the duct and through the ampulla, bending the cupula to one side, as demonstrated by the position of the colored cupula in Figure 55-11. Rotation of the head in the opposite direction causes the cupula to bend to the opposite side.
Figure 55-11 Movement of the cupula and its embedded hairs at the onset of rotation.
Into the cupula are projected hundreds of cilia from hair cells located on the ampullary crest. The kinocilia of these hair cells are all oriented in the same direction in the cupula, and bending the cupula in that direction causes depolarization of the hair cells, whereas bending it in the opposite direction hyperpolarizes the cells. Then, from the hair cells, appropriate signals are sent by way of the vestibular nerve to apprise the central nervous system of a change in rotation of the head and the rate of change in each of the three planes of space.
Function of the Utricle and Saccule in the Maintenance of Static Equilibrium
It is especially important that the hair cells are all oriented in different directions in the maculae of the utricles and saccules so that with different positions of the head, different hair cells become stimulated. The “patterns” of stimulation of the different hair cells apprise the brain of the position of the head with respect to the pull of gravity. In turn, the vestibular, cerebellar, and reticular motor nerve systems of the brain excite appropriate postural muscles to maintain proper equilibrium.
This utricle and saccule system functions extremely effectively for maintaining equilibrium when the head is in the near-vertical position. Indeed, a person can determine as little as half a degree of dysequilibrium when the body leans from the precise upright position.
Detection of Linear Acceleration by the Utricle and Saccule Maculae
When the body is suddenly thrust forward—that is, when the body accelerates—the statoconia, which have greater mass inertia than the surrounding fluid, fall backward on the hair cell cilia, and information of dysequilibrium is sent into the nervous centers, causing the person to feel as though he or she were falling backward. This automatically causes the person to lean forward until the resulting anterior shift of the statoconia exactly equals the tendency for the statoconia to fall backward because of the acceleration. At this point, the nervous system senses a state of proper equilibrium and leans the body forward no farther. Thus, the maculae operate to maintain equilibrium during linear acceleration in exactly the same manner as they operate during static equilibrium.
The maculae do not operate for the detection of linear velocity. When runners first begin to run, they must lean far forward to keep from falling backward because of initial acceleration, but once they have achieved running speed, if they were running in a vacuum, they would not have to lean forward. When running in air, they lean forward to maintain equilibrium only because of air resistance against their bodies; in this instance, it is not the maculae that make them lean but air pressure acting on pressure end-organs in the skin, which initiate appropriate equilibrium adjustments to prevent falling.
Detection of Head Rotation by the Semicircular Ducts
When the head suddenly begins to rotate in any direction (called angular acceleration), the endolymph in the semicircular ducts, because of its inertia, tends to remain stationary while the semicircular ducts turn. This causes relative fluid flow in the ducts in the direction opposite to head rotation.
Figure 55-12 shows a typical discharge signal from a single hair cell in the crista ampullaris when an animal is rotated for 40 seconds, demonstrating that (1) even when the cupula is in its resting position, the hair cell emits a tonic discharge of about 100 impulses per second; (2) when the animal begins to rotate, the hairs bend to one side and the rate of discharge increases greatly; and (3) with continued rotation, the excess discharge of the hair cell gradually subsides back to the resting level during the next few seconds.
Figure 55-12 Response of a hair cell when a semicircular canal is stimulated first by the onset of head rotation and then by stopping rotation.
The reason for this adaptation of the receptor is that within the first few seconds of rotation, back resistance to the flow of fluid in the semicircular duct and past the bent cupula causes the endolymph to begin rotating as rapidly as the semicircular canal itself; then, in another 5 to 20 seconds, the cupula slowly returns to its resting position in the middle of the ampulla because of its own elastic recoil.
When the rotation suddenly stops, exactly opposite effects take place: The endolymph continues to rotate while the semicircular duct stops. This time, the cupula bends in the opposite direction, causing the hair cell to stop discharging entirely. After another few seconds, the endolymph stops moving and the cupula gradually returns to its resting position, thus allowing hair cell discharge to return to its normal tonic level, as shown to the right in Figure 55-12. Thus, the semicircular duct transmits a signal of one polarity when the head begins to rotate and of opposite polarity when it stops rotating.
“Predictive” Function of the Semicircular Duct System in the Maintenance of Equilibrium
Because the semicircular ducts do not detect that the body is off balance in the forward direction, in the side direction, or in the backward direction, one might ask: What is the semicircular ducts’ function in the maintenance of equilibrium? All they detect is that the person’s head is beginning or stopping to rotate in one direction or another. Therefore, the function of the semicircular ducts is not to maintain static equilibrium or to maintain equilibrium during steady directional or rotational movements. Yet loss of function of the semicircular ducts does cause a person to have poor equilibrium when attempting to perform rapid, intricate changing body movements.
The function of the semicircular ducts can be explained by the following illustration: If a person is running forward rapidly and then suddenly begins to turn to one side, he or she will fall off balance a fraction of a second laterunless appropriate corrections are made ahead of time. But the maculae of the utricle and saccule cannot detect that he or she is off balance until after this has occurred. The semicircular ducts, however, will have already detected that the person is turning, and this information can easily apprise the central nervous system of the fact that the person will fall off balance within the next fraction of a second or so unless some anticipatory correction is made.
In other words, the semicircular duct mechanism predicts that dysequilibrium is going to occur and thereby causes the equilibrium centers to make appropriate anticipatory preventive adjustments. This helps the person maintain balance before the situation can be corrected.
Removal of the flocculonodular lobes of the cerebellum prevents normal detection of semicircular duct signals but has less effect on detecting macular signals. It is especially interesting that the cerebellum serves as a “predictive” organ for most rapid movements of the body, as well as for those having to do with equilibrium. These other functions of the cerebellum are discussed in the following chapter.
Vestibular Mechanisms for Stabilizing the Eyes
When a person changes his or her direction of movement rapidly or even leans the head sideways, forward, or backward, it would be impossible to maintain a stable image on the retinas unless the person had some automatic control mechanism to stabilize the direction of the eyes’ gaze. In addition, the eyes would be of little use in detecting an image unless they remained “fixed” on each object long enough to gain a clear image. Fortunately, each time the head is suddenly rotated, signals from the semicircular ducts cause the eyes to rotate in a direction equal and opposite to the rotation of the head. This results from reflexes transmitted through the vestibular nuclei and the medial longitudinal fasciculus to the oculomotor nuclei. These reflexes are described in Chapter 51.
Other Factors Concerned with Equilibrium
Neck Proprioceptors
The vestibular apparatus detects the orientation and movement only of the head. Therefore, it is essential that the nervous centers also receive appropriate information about the orientation of the head with respect to the body. This information is transmitted from the proprioceptors of the neck and body directly to the vestibular and reticular nuclei in the brain stem and indirectly by way of the cerebellum.
Among the most important proprioceptive information needed for the maintenance of equilibrium is that transmitted by joint receptors of the neck. When the head is leaned in one direction by bending the neck, impulses from the neck proprioceptors keep the signals originating in the vestibular apparatus from giving the person a sense of dysequilibrium. They do this by transmitting signals that exactly oppose the signals transmitted from the vestibular apparatus. However, when the entire body leans in one direction, the impulses from the vestibular apparatus are not opposed by signals from the neck proprioceptors; therefore, in this case, the person does perceive a change in equilibrium status of the entire body.
Proprioceptive and Exteroceptive Information from Other Parts of the Body
Proprioceptive information from parts of the body other than the neck is also important in the maintenance of equilibrium. For instance, pressure sensations from the footpads tell one (1) whether weight is distributed equally between the two feet and (2) whether weight on the feet is more forward or backward.
Exteroceptive information is especially necessary for the maintenance of equilibrium when a person is running. The air pressure against the front of the body signals that a force is opposing the body in a direction different from that caused by gravitational pull; as a result, the person leans forward to oppose this.
Importance of Visual Information in the Maintenance of Equilibrium
After destruction of the vestibular apparatus, and even after loss of most proprioceptive information from the body, a person can still use the visual mechanisms reasonably effectively for maintaining equilibrium. Even a slight linear or rotational movement of the body instantaneously shifts the visual images on the retina, and this information is relayed to the equilibrium centers. Some people with bilateral destruction of the vestibular apparatus have almost normal equilibrium as long as their eyes are open and all motions are performed slowly. But when moving rapidly or when the eyes are closed, equilibrium is immediately lost.
Neuronal Connections of the Vestibular Apparatus with the Central Nervous System
Figure 55-13 shows the connections in the hindbrain of the vestibular nerve. Most of the vestibular nerve fibers terminate in the brain stem in the vestibular nuclei, which are located approximately at the junction of the medulla and the pons. Some fibers pass directly to the brain stem reticular nuclei without synapsing and also to the cerebellar fastigial, uvular, and flocculonodular lobe nuclei. The fibers that end in the brain stem vestibular nuclei synapse with second-order neurons that also send fibers into the cerebellum, the vestibulospinal tracts, the medial longitudinal fasciculus, and other areas of the brain stem, particularly the reticular nuclei.
Figure 55-13 Connections of vestibular nerves through the vestibular nuclei (large oval white area) with other areas of the central nervous system.
The primary pathway for the equilibrium reflexes begins in the vestibular nerves, where the nerves are excited by the vestibular apparatus. The pathway then passes to the vestibular nuclei and cerebellum. Next, signals are sent into the reticular nuclei of the brain stem, as well as down the spinal cord by way of the vestibulospinal and reticulospinal tracts. The signals to the cord control the interplay between facilitation and inhibition of the many antigravity muscles, thus automatically controlling equilibrium.
The flocculonodular lobes of the cerebellum are especially concerned with dynamic equilibrium signals from the semicircular ducts. In fact, destruction of these lobes results in almost exactly the same clinical symptoms as destruction of the semicircular ducts themselves. That is, severe injury to either the lobes or the ducts causes loss of dynamic equilibrium during rapid changes in direction of motion but does not seriously disturb equilibrium under static conditions. It is believed that the uvula of the cerebellum plays a similar important role in static equilibrium.
Signals transmitted upward in the brain stem from both the vestibular nuclei and the cerebellum by way of the medial longitudinal fasciculus cause corrective movements of the eyes every time the head rotates, so the eyes remain fixed on a specific visual object. Signals also pass upward (either through this same tract or through reticular tracts) to the cerebral cortex, terminating in a primary cortical center for equilibrium located in the parietal lobe deep in the sylvian fissure on the opposite side of the fissure from the auditory area of the superior temporal gyrus. These signals apprise the psyche of the equilibrium status of the body.
Functions of Brain Stem Nuclei in Controlling Subconscious, Stereotyped Movements
Rarely, a baby is born without brain structures above the mesencephalic region, a condition called anencephaly. Some of these babies have been kept alive for many months. They are able to perform some stereotyped movements for feeding, such as suckling, extrusion of unpleasant food from the mouth, and moving the hands to the mouth to suck the fingers. In addition, they can yawn and stretch. They can cry and can follow objects with movements of the eyes and head. Also, placing pressure on the upper anterior parts of their legs causes them to pull to the sitting position. It is clear that many of the stereotyped motor functions of the human being are integrated in the brain stem.
Bibliography
Angelaki D.E., Cullen K.E. Vestibular system: the many facets of a multimodal sense. Annu Rev Neurosci. 2008;31:125.
Baker S.N. Oscillatory interactions between sensorimotor cortex and the periphery. Curr Opin Neurobiol. 2007;17:649.
Briggs F., Usrey W.M. Emerging views of corticothalamic function. Curr Opin Neurobiol. 2008;18:403.
Cullen K.E., Roy J.E. Signal processing in the vestibular system during active versus passive head movements. J Neurophysiol. 2004;91:1919.
Fabbri-Destro M., Rizzolatti G. Mirror neurons and mirror systems in monkeys and humans. Physiology (Bethesda). 2008;23:171.
Holtmaat A., Svoboda K. Experience-dependent structural synaptic plasticity in the mammalian brain. Nat Rev Neurosci. 2009;10:647.
Horak F.B. Postural compensation for vestibular loss. Ann N Y Acad Sci. 2009;1164:76.
Klier E.M., Angelaki D.E. Spatial updating and the maintenance of visual constancy. Neuroscience. 2008;156:801.
Lemon R.N. Descending pathways in motor control. Annu Rev Neurosci. 2008;31:195.
Müller U. Cadherins and mechanotransduction by hair cells. Curr Opin Cell Biol. 2008;5:557.
Nachev P., Kennard C., Husain M. Functional role of the supplementary and pre-supplementary motor areas. Nat Rev Neurosci. 2008;9:856.
Nishitani N., Schürmann M., Amunts K., et al. Broca’s region: from action to language. Physiology (Bethesda). 2005;20:60.
Nielsen J.B., Cohen L.G. The Olympic brain. Does corticospinal plasticity play a role in acquisition of skills required for high-performance sports? J Physiol. 2008;586:65.
Pierrot-Deseilligny C. Effect of gravity on vertical eye position. Ann N Y Acad Sci. 2009;1164:155.
Raineteau O. Plastic responses to spinal cord injury. Behav Brain Res. 2008;192:114.
Robles L., Ruggero M.A. Mechanics of the mammalian cochlea. Physiol Rev. 2001;81:1305.
Schieber M.H. Motor control: basic units of cortical output? Curr Biol. 2004;14:R353.
Scott S.H. Inconvenient truths about neural processing in primary motor cortex. J Physiol. 2008;586:1217.
Scott S.K., McGettigan C., Eisner F. A little more conversation, a little less action—candidate roles for the motor cortex in speech perception. Nat Rev Neurosci. 2009;10:295.
Stepien A.E., Arber S. Probing the locomotor conundrum: descending the ‘V’ interneuron ladder. Neuron. 2008;60:1.
Umilta M.A. Frontal cortex: goal-relatedness and the cortical motor system. Curr Biol. 2004;14:R204.