Physiology 5th Ed.


Posture and movement depend on a combination of involuntary reflexes coordinated by the spinal cord and voluntary actions controlled by higher brain centers.

Organization of Motor Function by the Spinal Cord

Posture and movement ultimately depend on contraction of some skeletal muscles while, simultaneously, other muscles remain relaxed. Recall that activation and contraction of skeletal muscles is under the control of the motoneurons that innervate them. The motor system is designed to execute this coordinated response largely through reflexes integrated in the spinal cord.

Motor Units

motor unit is defined as a single motoneuron and the muscle fibers that it innervates. The number of muscle fibers innervated can vary from a few fibers to thousands of fibers, depending on the nature of the motor activity. Thus, for eye movements requiring fine control, motoneurons innervate only a few muscle fibers. For postural muscles involved in large movements, motoneurons innervate thousands of muscle fibers. A motoneuron pool is the set of motoneurons innervating fibers within the same muscle.

The force of contraction of a muscle is graded by recruitment of motor units (size principle). For example, small motoneurons innervate a few muscle fibers, and, because they have the lowest thresholds, they fire first. Small motoneurons also generate the smallest amounts of force. On the other hand, large motoneurons innervate many muscle fibers. They have the highest thresholds to fire action potentials; thus, they fire last. Because large motoneurons innervate many muscle fibers, they also generate the greatest amounts of force. The size principle states that as more motor units are recruited, progressively larger motoneurons are involved and greater tension will be generated.

Types of Motoneurons

There are two types of motoneurons: α motoneurons and γ motoneurons. α Motoneurons innervate extrafusal skeletal muscle fibers. Action potentials in α motoneurons lead to action potentials in the extrafusal muscle fibers they innervate, which results in contraction (see Chapter 1). γ Motoneurons innervate specialized intrafusal muscle fibers, a component of the muscle spindles. The overall function of the muscle spindle is to sense muscle length; the function of the γ motoneurons innervating them is to adjust the sensitivity of the muscle spindles (so that they respond appropriately as the extrafusal fibers contract and shorten). α Motoneurons and γ motoneurons are coactivated (activated simultaneously) so that muscle spindles remain sensitive to changes in muscle length even as the muscle contracts and shortens.

Types of Muscle Fibers

As already noted, there are two types of muscle fibers: extrafusal fibers and intrafusal fibers. Extrafusal fibers constitute the majority of skeletal muscle, are innervated by α motoneurons, and are used to generate force. Intrafusal fibers are specialized fibers that are innervated by γ motoneurons and are too small to generate significant force. Intrafusal fibers are encapsulated in sheaths, forming muscle spindles that run parallel to the extrafusal fibers.

Muscle Spindles

Muscle spindles are distributed among the extrafusal muscle fibers, and they are especially abundant in muscles utilized for fine movements (e.g., muscles of the eye). Muscle spindles are spindle-shaped organs composed of intrafusal muscle fibers and innervated by sensory and motor nerve fibers, as illustrated in Figure 3-31. Muscle spindles are attached to connective tissue and arranged in parallel with the extrafusal muscle fibers.


Figure 3–31 Structure of the muscle spindle. An intrafusal muscle fiber is shown in relation to an extrafusal muscle fiber.

Intrafusal Muscle Fibers of Muscle Spindles

There are two types of intrafusal fibers present in muscle spindles: nuclear bag fibers and nuclear chain fibers (see Fig. 3-31). Generally, both types of fibers are present in every muscle spindle, but nuclear chain fibers are more plentiful than nuclear bag fibers. (There are five or six nuclear chain fibers per muscle spindle, compared with two nuclear bag fibers.) Nuclear bag fibers are larger, and their nuclei are accumulated in a central (“bag”) region. Nuclear chain fibers are smaller, and their nuclei are arranged in rows (“chains”).

Innervation of Muscle Spindles

Muscle spindles are innervated by both sensory (afferent) and motor (efferent) nerves.

image Sensory innervation of the muscle spindle consists of a single group Ia afferent nerve, which innervates the central region of both the nuclear bag fibers and the nuclear chain fibers, and group II afferent nerves, which primarily innervate the nuclear chain fibers. Recall that group Ia fibers are among the largest nerves in the body; thus, they have among the fastest conduction velocities. These fibers form primary endings in a spiral-shaped terminal around the central region of the nuclear bag and nuclear chain fibers. Group II fibers have intermediate diameters and intermediate conduction velocities. Group II fibers form secondary endings primarily on the nuclear chain fibers.

image Motor innervation of the muscle spindle consists of two types of γ motoneurons: dynamic and static. Dynamic γ motoneurons synapse on nuclear bag fibers in “plate endings.” Static γ motoneuronssynapse on nuclear chain fibers in “trail endings,” which spread out over longer distances. γ Motoneurons are smaller and slower than the α motoneurons that innervate the extrafusal fibers. Again, the function of the γ motoneurons (either static or dynamic) is to regulate the sensitivity of the intrafusal muscle fibers they innervate.

Function of Muscle Spindles

Muscle spindles are stretch receptors whose function is to correct for changes in muscle length when extrafusal muscle fibers are either shortened (by contraction) or lengthened (by stretch). Thus, muscle spindle reflexes operate to return muscle to its resting length after it has been shortened or lengthened. To illustrate the function of the muscle spindle reflex, consider the events that occur when a muscle is stretched.

1.     When a muscle is stretched, the extrafusal muscle fibers are lengthened. Because of their parallel arrangement in the muscle, the intrafusal muscle fibers also are lengthened.

2.     The increase in length of the intrafusal fibers is detected by the sensory afferent fibers innervating them. The group Ia afferent fibers (innervating the central region of nuclear bag and nuclear chain fibers) detect the velocityof length change, and the group II afferent fibers (innervating the nuclear chain fibers) detect the length of the muscle fiber. Thus, when the muscle is stretched, the increase in the length of the intrafusal fibers activates both group Ia and group II sensory afferent fibers.

3.     Activation of the group Ia afferent fibers stimulates α motoneurons in the spinal cord. These α motoneurons innervate extrafusal fibers in the homonymous (same) muscle and, when activated, cause the muscle to contract (i.e., to shorten). Thus, the original stretch (lengthening) is opposed when the reflex causes the muscle to contract and shorten. γ Motoneurons are coactivated with the α motoneurons, ensuring that the muscle spindle will remain sensitive to changes in muscle length even during the contraction.

Spinal Cord Reflexes

Spinal cord reflexes are stereotypical motor responses to specific kinds of stimuli, such as stretch of the muscle. The neuronal circuit that directs this motor response is called the reflex arc. The reflex arc includes the sensory receptors; the sensory afferent nerves, which carry information to the spinal cord; the interneurons in the spinal cord; and the motoneurons, which direct the muscle to contract or relax.

The stretch reflex is the simplest of all spinal cord reflexes, having only one synapse between sensory afferent nerves and motor efferent nerves. The Golgi tendon reflex is of intermediate complexity and has two synapses. The most complex of the spinal cord reflexes is the flexor-withdrawal reflex, which has multiple synapses. Characteristics of the three types of spinal cord reflexes are summarized in Table 3-5.

Table 3–5 Muscle Reflexes


Stretch Reflex

The stretch (myotatic) reflex is exemplified by the knee-jerk reflex (Fig. 3-32). The following steps occur in the stretch reflex, which has only one synapse between the sensory afferent nerves (group Ia afferents) and the motor efferent nerves (α motoneurons):


Figure 3–32 Operation of the stretch reflex. Solid lines show excitatory pathways; dashed lines show inhibitory steps. Open neurons are excitatory; filled neurons are inhibitory.

1.     When the muscle is stretched, group Ia afferent fibers in the muscle spindle are activated and their firing rate increases. These group Ia afferents enter the spinal cord and synapse directly on and activate α motoneurons. This pool of α motoneurons innervates the homonymous muscle.

2.     When these α motoneurons are activated, they cause contraction of the muscle that was originally stretched (the homonymous muscle). When the muscle contracts, it shortens, thereby decreasing stretch on the muscle spindle. The muscle spindle returns to its original length, and the firing rate of the group Ia afferents returns to baseline.

3.     Simultaneously, information is sent from the spinal cord to cause contraction of synergistic muscles and relaxation of antagonistic muscles.

The stretch reflex is illustrated by the knee-jerk reflex, which is initiated by tapping the patellar tendon, causing the quadriceps muscle to stretch. When the quadriceps and its muscle spindles are stretched, group Ia afferent fibers are stimulated. These group Ia afferent fibers synapse on and activate α motoneurons in the spinal cord. These α motoneurons innervate and cause contraction of the quadriceps (the muscle that originally was stretched). As the quadriceps muscle contracts and shortens, it forces the lower leg to extend in the characteristic knee-jerk reflex.

Golgi Tendon Reflex

The Golgi tendon reflex is a disynaptic spinal cord reflex, which is also called the inverse myotatic reflex (inverse or opposite of the stretch reflex).

The Golgi tendon organ is a stretch receptor found in tendons, which senses contraction (shortening) of muscle and activates group Ib afferent nerves. Golgi tendon organs are arranged in series with the extrafusal muscle fibers (contrasting the parallel arrangement of muscle spindles in the stretch reflex). The steps in the Golgi tendon reflex are shown in Figure 3-33 and are described as follows:


Figure 3–33 Operation of the Golgi tendon reflex. Solid lines show excitatory pathways; dashed lines show inhibitory steps. Open neurons are excitatory; filled neurons are inhibitory.

1.     When the muscle contracts, the extrafusal muscle fibers shorten, activating the Golgi tendon organs attached to them. In turn, the group Ib afferent fibers that synapse on inhibitory interneurons in the spinal cord are activated. These inhibitory interneurons synapse on the α motoneurons.

2.     When the inhibitory interneurons are activated (i.e., activated to inhibit), they inhibit firing of the α motoneurons, producing relaxation of the homonymous muscle (the muscle that originally was contracted).

3.     As the homonymous muscle relaxes, the reflex also causes synergistic muscles to relax and antagonistic muscles to contract.

An exaggerated form of the Golgi tendon reflex is illustrated by the clasp-knife reflex. This reflex is abnormal and occurs when there is an increase in muscle tone (e.g., hypertonicity or spasticity of muscle). When a joint is passively flexed, the opposing muscles initially resist this passive movement. However, if the flexion continues, tension increases in the opposing muscle and activates the Golgi tendon reflex, which then causes the opposing muscles to relax and the joint to close rapidly. The initial resistance to flexion followed by a rapid flexion is similar to the way a pocket knife closes: At first the knife closes slowly against high resistance, and then it quickly snaps shut.

Flexor-Withdrawal Reflex

The flexor-withdrawal reflex is a polysynaptic reflex that occurs in response to tactile, painful, or noxious stimulus. Somatosensory and pain afferent fibers initiate a flexion reflex that causes withdrawal of the affected part of the body from the painful or noxious stimulus (e.g., touching a hand to a hot stove and then rapidly withdrawing the hand). The reflex produces flexion on the ipsilateral side (i.e., side of the stimulus) and extension on the contralateral side (Fig. 3-34). The steps involved in the flexor-withdrawal reflex are explained as follows:


Figure 3–34 Operation of the flexor-withdrawal reflex. Solid lines show excitatory pathways; dashed lines show inhibitory steps. Open neurons are excitatory; filled neurons are inhibitory.

1.     When a limb touches a painful stimulus (e.g., hand touches a hot stove), flexor reflex afferent fibers (groups II, III, and IV) are activated. These afferent fibers synapse on multiple interneurons in the spinal cord (i.e., polysynaptic reflex).

2.     On the ipsilateral side of the pain stimulus, reflexes are activated that cause flexor muscles to contract and extensor muscles to relax. This portion of the reflex produces flexion on the ipsilateral side (e.g., withdrawal of the hand from the hot stove).

3.     On the contralateral side of the pain stimulus, reflexes are activated that cause extensor muscles to contract and flexor muscles to relax. This portion of the reflex produces extension on the contralateral side and is called the crossed-extension reflex. Thus, if the painful stimulus occurs on the left side, the left arm and leg will flex or withdraw and the right arm and leg will extend to maintain balance.

4.     A persistent neural discharge, called an afterdischarge, occurs in the polysynaptic reflex circuits. As a result of the afterdischarge, the contracted muscles remain contracted for a period of time after the reflex is activated.

Control of Posture and Movement by the Brain Stem

Descending motor pathways (i.e., those descending from the cerebral cortex and brain stem) are divided among the pyramidal tract and the extrapyramidal tract. Pyramidal tracts are corticospinal and corticobulbar tracts that pass through the medullary pyramids and descend directly onto lower motoneurons in the spinal cord. All others are extrapyramidal tracts. The extrapyramidal tracts originate in the following structures of the brain stem:

image The rubrospinal tract originates in the red nucleus and projects to motoneurons in the lateral spinal cord. Stimulation of the red nucleus produces activation of flexor muscles and inhibition of extensor muscles.

image The pontine reticulospinal tract originates in nuclei of the pons and projects to the ventromedial spinal cord. Stimulation has a generalized activating effect on both flexor and extensor muscles, with its predominant effect on extensors.

image The medullary reticulospinal tract originates in the medullary reticular formation and projects to motoneurons in the spinal cord. Stimulation has a generalized inhibitory effect on both flexor and extensor muscles, with the predominant effect on extensors.

image The lateral vestibulospinal tract originates in the lateral vestibular nucleus (Deiters’ nucleus) and projects to ipsilateral motoneurons in the spinal cord. Stimulation produces activation of extensors and inhibition of flexors.

image The tectospinal tract originates in the superior colliculus (tectum or “roof” of the brain stem) and projects to the cervical spinal cord. It is involved in control of neck muscles.

Both the pontine reticular formation and the lateral vestibular nucleus have powerful excitatory effects on extensor muscles. Therefore, lesions of the brain stem above the pontine reticular formation and lateral vestibular nucleus, but below the midbrain, cause a dramatic increase in extensor tone, called decerebrate rigidity. Lesions above the midbrain do not cause decerebrate rigidity.


The cerebellum, or “little brain,” regulates movement and posture and plays a role in certain kinds of motor learning. The cerebellum helps control the rate, range, force, and direction of movements (collectively known as synergy). Damage to the cerebellum results in lack of coordination.

The cerebellum is located in the posterior fossa just below the occipital lobe. It is connected to the brain stem by three cerebellar peduncles, which contain both afferent and efferent nerve fibers.

There are three main divisions of the cerebellum: the vestibulocerebellum, the spinocerebellum, and the pontocerebellum. The vestibulocerebellum is dominated by vestibular input and controls balance and eye movements. The spinocerebellum is dominated by spinal cord input and controls synergy of movement. The pontocerebellum is dominated by cerebral input, via pontine nuclei, and controls the planning and initiation of movements.

Layers of the Cerebellar Cortex

The cerebellar cortex has three layers, which are described in relation to its output cells, the Purkinje cells (Fig. 3-35). The layers of the cerebellar cortex are as follows:


Figure 3–35 Structures of the cerebellar cortex shown in cross section.

image The granular layer is the innermost layer. It contains granule cells, Golgi II cells, and glomeruli. In the glomeruli, axons of mossy fibers from the spinocerebellar and pontocerebellar tracts synapse on dendrites of granule and Golgi type II cells.

image The Purkinje cell layer is the middle layer. It contains Purkinje cells, and its output is always inhibitory.

image The molecular layer is the outermost layer. It contains outer stellate cells, basket cells, dendrites of Purkinje and Golgi II cells, and axons of granule cells. The axons of granule cells form parallel fibers, which synapse on the dendrites of Purkinje cells, basket cells, outer stellate cells, and Golgi type II cells.

Input to the Cerebellar Cortex

Two systems provide excitatory input to the cerebellar cortex: the climbing fiber system and the mossy fiber system. Each system also sends collateral branches directly to deep cerebellar nuclei, in addition to their projections to the cerebellar cortex. Excitatory projections from the cerebellar cortex then activate secondary circuits, which modulate the output of the cerebellar nuclei via the Purkinje cells.

image Climbing fibers originate in the inferior olive of the medulla and project directly onto Purkinje cells. These fibers make multiple synaptic connections along the dendrites of Purkinje cells, although each Purkinje cell receives input from only one climbing fiber. These synaptic connections are powerful! A single action potential from a climbing fiber can elicit multiple excitatory bursts, called complex spikes,in the dendrites of the Purkinje cell. It is believed that climbing fibers “condition” the Purkinje cells and modulate their responses to mossy fiber input. Climbing fibers also may play a role in cerebellar learning.

image Mossy fibers constitute the majority of the cerebellar input. These fibers include vestibulocerebellar, spinocerebellar, and pontocerebellar afferents. Mossy fibers project to granule cells, which are excitatory interneurons located in collections of synapses called glomeruli. Axons from these granule cells then ascend to the molecular layer, where they bifurcate and give rise to parallel fibers. Parallel fibers from the granule cells contact the dendrites of manyPurkinje cells, producing a “beam” of excitation along the row of Purkinje cells. The dendritic tree of each Purkinje cell may receive input from as many as 250,000 parallel fibers! In contrast to the climbing fiber input to the Purkinje dendrites (which produce complex spikes), the mossy fiber input produces single action potentials called simple spikes. These parallel fibers also synapse on cerebellar interneurons (basket, stellate, and Golgi II).

Interneurons of the Cerebellum

The function of cerebellar interneurons is to modulate Purkinje cell output. With the exception of granule cells, all of the cerebellar interneurons are inhibitory. Granule cells have excitatory input to basket cells, stellate cells, Golgi II cells, and Purkinje cells. Basket cells and stellate cells inhibit Purkinje cells (via parallel fibers). Golgi II cells inhibit granule cells, thereby reducing their excitatory effect on Purkinje cells.

Output of the Cerebellar Cortex

The only output of the cerebellar cortex is via axons of Purkinje cells. The output of the Purkinje cells is always inhibitory because the neurotransmitter released at these synapses is γ-aminobutyric acid (GABA) (see Chapter 1). Axons of Purkinje cells project topographically to deep cerebellar nuclei and to lateral vestibular nuclei. This inhibitory output of the cerebellar cortex regulates the rate, range, force, and direction of movement (synergy).

Disorders of the Cerebellum

Cerebellar lesions result in an abnormality of movement called ataxia. Cerebellar ataxia is a lack of coordination due to errors in rate, range, force, and direction of movement. Ataxia can be exhibited in one of several ways. There may be a delayed onset of movement or poor execution of the sequence of a movement, causing the movement to appear uncoordinated. A limb may overshoot its target or stop before reaching its target. Ataxia may be expressed as dysdiadochokinesia, in which a person is unable to perform rapid, alternating movements. Intention tremors may occur perpendicular to the direction of a voluntary movement, increasing near the end of the movement. (Intention tremors seen in cerebellar disease differ from the resting tremors seen in Parkinson disease.) The rebound phenomenon is the inability to stop a movement; for example, if a person with cerebellar disease flexes his forearm against a resistance, he may be unable to stop the flexion when the resistance is removed.

Basal Ganglia

The basal ganglia are the deep nuclei of the telencephalon: caudate nucleus, putamen, globus pallidus, and amygdala. There also are associated nuclei including the ventral anterior and ventral lateral nuclei of the thalamus, the subthalamic nucleus of the diencephalon, and the substantia nigra of the midbrain.

The main function of the basal ganglia is to influence the motor cortex via pathways through the thalamus. The role of the basal ganglia is to aid in planning and execution of smooth movements. The basal ganglia also contribute to affective and cognitive functions.

The pathways into and out of the basal ganglia are complex, as illustrated in Figure 3-36. Almost all areas of the cerebral cortex project topographically onto the striatum including a critical input from the motor cortex. The striatum then communicates with the thalamus and then back to the cortex via two different pathways.


Figure 3–36 Pathways in the basal ganglia. The relationship between the cerebral cortex, the basal ganglia, and the thalamus are shown. Solid blue lines show excitatory pathways; dashed brown lines show inhibitory pathways. The overall output of the indirect pathway is inhibition, and the overall output of the direct pathway is excitation. (Modified from Kandel ER, Schwartz JH, Jessell TM: Principles of Neural Science, 4th ed. New York, McGraw-Hill, 2000.)

image Indirect pathway. In the indirect pathway, the striatum has inhibitory input to the external segment of the globus pallidus, which has inhibitory input to the subthalamic nuclei. The subthalamic nuclei project excitatory input to the internal segment of the globus pallidus and the pars reticulata of the substantia nigra, which send inhibitory input to the thalamus. The thalamus then sends excitatory input back to the motor cortex. In this pathway, the inhibitory neurotransmitter is GABA, and the excitatory neurotransmitter is glutamate. The overall output of the indirect pathway is inhibitory, as illustrated in the summary diagram at the bottom of the figure.

image Direct pathway. In the direct pathway, the striatum sends inhibitory input to the internal segment of the globus pallidus and the pars reticulata of the substantia nigra, which send inhibitory input to the thalamus. As in the indirect pathway, the thalamus sends excitatory input back to the motor cortex. Again, the inhibitory neurotransmitter is GABA, and the excitatory neurotransmitter is glutamate. The overall output of the direct pathway is excitatory, as shown in the summary diagram at the bottom of the figure.

The outputs of the indirect and direct pathways from the basal ganglia to the motor cortex are opposite and carefully balanced: The indirect path is inhibitory, and the direct path is excitatory. A disturbance in one of the pathways will upset this balance of motor control, with either an increase or a decrease in motor activity. Such an imbalance is characteristic of diseases of the basal ganglia.

In addition to the basic circuitry of the indirect and direct pathways, there is an additional connection, back and forth, between the striatum and the pars compacta of the substantia nigra. The neurotransmitter for the connection back to the striatum is dopamine. This additional connection between the substantia nigra and the striatum means that dopamine will be inhibitory (via D2 receptors) in the indirect pathway and excitatory (via D1 receptors) in the direct pathway.

Diseases of the Basal Ganglia

Diseases of the basal ganglia include Parkinson disease and Huntington disease. In Parkinson disease, cells of the pars compacta of the substantia nigra degenerate, reducing inhibition via the indirect pathway and reducing excitation via the direct pathway. The characteristics of Parkinson disease are explainable by dysfunction of the basal ganglia: resting tremor, slowness and delay of movement, and shuffling gait. Treatment of Parkinson disease includes replacement of dopamine by treatment with L-dopa (the precursor to dopamine) or administration of dopamine agonists such as bromocriptine. Huntington disease is a hereditary disorder caused by destruction of striatal and cortical cholinergic neurons and inhibitory GABAergic neurons. The neurologic symptoms of Huntington disease are choreic (writhing) movements and dementia. There is no cure.

Motor Cortex

Voluntary movements are directed by the motor cortex, via descending pathways. The motivation and ideas necessary to produce voluntary motor activity are first organized in multiple associative areas of the cerebral cortex and then transmitted to the supplementary motor and premotor cortices for the development of a motor plan. The motor plan will identify the specific muscles that need to contract, how much they need to contract, and in what sequence. The plan then is transmitted to upper motoneurons in the primary motor cortex, which send it through descending pathways to lower motoneurons in the spinal cord. The planning and execution stages of the plan are also influenced by motor control systems in the cerebellum and basal ganglia.

The motor cortex consists of three areas: primary motor cortex, supplementary motor cortex, and premotor cortex.

image Premotor cortex and supplementary motor cortex (area 6) are the regions of the motor cortex responsible for generating a plan of movement, which then is transferred to the primary motor cortex for execution. The supplementary motor cortex programs complex motor sequences and is active during “mental rehearsal” of a movement, even in the absence of movement.

image Primary motor cortex (area 4) is the region of the motor cortex responsible for execution of a movement. Programmed patterns of motoneurons are activated from the primary motor cortex. As upper motoneurons in the motor cortex are excited, this activity is transmitted to the brain stem and spinal cord, where lower motoneurons are activated and produce coordinated contraction of the appropriate muscles (i.e., the voluntary movement). The primary motor cortex is topographically organized and is described as the motor homunculus. This topographic organization is dramatically illustrated in jacksonian seizures, which are epileptic events originating in the primary motor cortex. The epileptic event usually begins in the fingers of one hand, progresses to the hand and arms, and eventually spreads over the entire body (i.e., the “jacksonian march”).