Organization of Motor Function

α Motor Neurons

The α motor neurons are large, multipolar neurons that range in size up to 70 µm in diameter (see Fig. 4.10 A ). Their axons leave the spinal cord through the ventral roots, and the brainstem via several cranial nerves, where they are distributed to the appropriate skeletal muscles via peripheral nerves. The α motor neuron axon also projects to other neurons by giving off collateral axons before leaving the CNS. The main axon terminates by synapsing onto the extrafusal muscle fibers. These synapses are called neuromuscular junctions (NMJs) or end plates. Extrafusal fibers are large muscle fibers that make up the bulk of a skeletal muscle and generate its contractile force (a muscle also contains intrafusal fibers whose functions are detailed later in this chapter; also see Chapter 12 ).

A key functional aspect of the motor neuron projection pattern from the CNS is that each neuron’s axon innervates only one muscle, but it branches to innervate multiple fibers within that muscle. Moreover, each extrafusal muscle fiber in mammals is supplied by only one α motor neuron, and thus a motor unit can be defined as an α motor neuron and all of the skeletal muscle fibers that its axon supplies. The motor unit can be regarded as the basic unit of movement because firing of an α motor neuron under normal circumstances leads to activation and contraction of all of the muscle fibers of that particular motor unit. As described previously ( Chapter 6 ), the safety factor of the NMJ is greater than 1, so each action potential in the motor neuron axon triggers an action potential in every muscle fiber of the motor unit.

An important principle is that the average size of the motor unit (i.e., the number of muscle fibers innervated by an axon) varies between muscles, depending on how fine a control of the muscle is required. For finely controlled muscles, such as the eye muscles, an α motor neuron may supply only a few muscle fibers, whereas in a proximal limb muscle, such as the quadriceps femoris, a single α motor neuron may innervate thousands of muscle fibers.

The muscle fibers that belong to a given motor unit are called a muscle unit. All the muscle fibers in a muscle unit are of the same histochemical type (i.e., they are all either slow-twitch [type I] or fast-twitch [type IIA or IIB] fibers). For an in-depth description of muscle fiber types, see Chapter 12 . Of importance in this chapter is that a number of physiological properties are correlated with this histochemical classification scheme. In particular, slow-twitch fibers, which contract and relax slowly, as implied by their name, also generate low-force levels but essentially never fatigue. In contrast, the fast-twitch fiber contract and relax rapidly, generate higher levels of force, and fatigue at varying rates.

The first motor units to be activated in many cases, either by voluntary effort or during reflex action or just to maintain posture, are those with the smallest motor axons. These motor units contain slow-twitch fibers and thus generate the smallest contractile force, allowing the initial contraction to be finely graded. These units tend to be active much of the time, if not continuously, and so their lack of fatigability makes good functional sense.

As more motor units are recruited for a motor act, motor neurons with progressively larger axons become involved, and these axons synapse onto the fast-twitch fibers, thereby generating progressively larger amounts of tension. The most powerful such motor units are typically recruited only for tasks requiring large amounts of force (e.g., sprinting, jumping, and lifting a heavy weight), tasks that people can perform for only for short periods of time.

The orderly recruitment of motor units helps the CNS generate a large range of forces and also maintain relatively precise control at the different force levels. This recruitment pattern is called the size principle because the motor units are recruited in order of motor neuron axon size. The size principle depends on the property of small motor neurons being activated more easily than are large motor neurons. Recall that if an excitatory synapse is active, it opens channels in the postsynaptic membrane and causes an excitatory postsynaptic current (EPSC). The same-size EPSC generates a larger potential change at the initial segment of an axon of a small motor neuron than it does at a larger motor neuron, simply as a consequence of Ohm’s law (V = IR), and due to the smaller motor neurons having higher membrane resistance than larger motor neurons. Because excitatory postsynaptic potentials (EPSPs) in the CNS are small and need to summate to reach threshold for triggering spikes, as the level of synaptic activation rises from zero, the resulting depolarization will reach spiking threshold in smaller motor neurons sooner. As the size principle is usually obeyed, this assumption generally appears to hold; however, there can be exceptions, and in these cases, the descending motor pathways presumably must provide differing levels of synaptic drive to the different-sized motor neurons.

γ Motor Neurons

The γ motor neurons are smaller than α motor neurons; they have a soma diameter of about 35 µm. The γ motor neurons that project to a particular muscle are located in the same regions of the ventral horn as the α motor neurons that supply that muscle. γ Motor neurons do not supply extrafusal muscle fibers; instead, they synapse on specialized striated muscle fibers called intrafusal muscle fibers, which traverse receptors called muscle spindles that are embedded in skeletal muscles. The function of γ motor neurons is to regulate the sensitivity of these receptors (discussed later).

The Myotatic or Stretch Reflex

The stretch reflex, as implied by its name, is a group of motor responses elicited by stretch of a muscle. The knee jerk reflex described previously is a well-known example. The stretch reflex is crucial for the maintenance of posture and helps overcome unexpected impediments during a voluntary movement. Changes in the stretch reflex are involved in actions commanded by the brain, and pathological alterations in this reflex are important signs of neurological disease. The phasic stretch reflex occurs in response to rapid, transient stretches of the muscle, such as those elicited by a physician’s use of a reflex hammer or by an unexpected impediment to an ongoing movement. The tonic stretch reflex occurs in response to a slower or steady stretch applied to the muscle. The receptor responsible for initiating a stretch reflex is the muscle spindle. Muscle spindles are found in almost all skeletal muscles and are particularly concentrated in muscles that exert fine motor control (e.g., the small muscles of the hand and eye). This reflex circuit is a universal mechanism for helping regulate muscle activity.

Structure of the Muscle Spindle

As its name implies, a muscle spindle is a spindle or fusiform-shaped organ composed of a bundle of specialized muscle fibers richly innervated both by sensory axons and by motor axons ( Fig. 9.2 ). A muscle spindle is about 100 µm in diameter and up to 10 mm long. The innervated part of the muscle spindle is encased in a connective tissue capsule. Muscle spindles lie between regular muscle fibers and are typically located near the tendinous insertion of the muscle. The ends of the spindle are attached to the connective tissue within the muscle (endomysium). The key point is that muscle spindles are connected in parallel with the regular muscle fibers and thus are able to sense changes in the length of the muscle.

The muscle fibers within the spindle are called intrafusal fibers, to distinguish them from the regular or extrafusal fibers that make up the bulk of the muscle. Individual intrafusal fibers are much narrower than extrafusal fibers and do not run the length of the muscle. They are also too weak to contribute significantly to muscle tension or to cause changes in the overall length of the muscle directly by their contraction.

Morphologically, two types of intrafusal muscle fibers are found within muscle spindles: nuclear bag and nuclear chain fibers (see Fig. 9.2 B ). These names are derived from the arrangement of nuclei in the fibers. (Muscle fibers are formed by the fusion of many individual myoblasts during development; thus mature muscle cells are multinucleate.) Nuclear bag fibers are larger than nuclear chain fibers, and their nuclei are bunched together like a bag of oranges in the central, or equatorial, region of the fiber. In nuclear chain fibers, the nuclei are arranged in a row. Functionally, nuclear bag fibers are divided into two types: bag1 and bag2. As detailed later, bag2 fibers are functionally similar to chain fibers.

The neural innervation of an intrafusal fiber differs significantly from that of an extrafusal fiber, which is innervated by a single motor neuron. Intrafusal fibers are receive both sensory and motor innervation. The sensory innervation typically includes a single group Ia afferent fiber and a variable number of group II afferent fibers (see Fig. 9.2 B ). Group Ia fibers belong to the class of sensory nerve fibers with the largest diameters and conduct at 80 to 120 m/second; group II fibers are intermediate in size and conduct at 35 to 75 m/second. A group Ia afferent fiber forms a spiral-shaped termination, referred to as a primary ending, on each of the intrafusal muscle fibers in the spindle. Primary endings are found on both types of nuclear bag fibers and on nuclear chain fibers. The group II afferent fiber forms a secondary type ending on nuclear chain and bag2 fibers, but not on bag1 fibers. The primary and secondary endings have mechanosensitive channels that are sensitive to the level of tension on the intrafusal muscle fiber.

The motor supply to a muscle spindle consists of two types of γ motor axons (see Fig. 9.2 B ). Dynamic γ motor axons end on nuclear bag1 fibers, and static γ motor axons end on nuclear chain and bag2 fibers.

Muscle Spindles Detect Changes in Muscle Length

Muscle spindles respond to changes in muscle length because they lie in parallel with the extrafusal fibers, and therefore are stretched or shortened along with the extrafusal fibers. Because intrafusal fibers, like all muscle fibers, display spring-like properties, a change in their length changes the tension that they are under, and this change is sensed by mechanoreceptors of the group Ia and group II spindle afferent fibers. The nonselective cation channel Piezo2 has been identified as the principal transduction channel that allows spindle sensory afferent fibers to sense changes in mechanical stress that occur when a muscle changes length.

Fig. 9.3 shows the changes in activity of the afferent fibers of a muscle spindle when the muscle is stretched. It is clear that group Ia and group II fibers respond differently to stretch. Group Ia fibers are sensitive both to the amount of muscle stretch and to its rate, whereas group II fibers respond chiefly to the amount of stretch. Thus, when a muscle is stretched to a new, longer length, group II firing increases in proportion to the amount of stretch (see Fig. 9.3 , left ), and when the muscle is allowed to shorten, its firing rate decreases proportionately (see Fig. 9.3 , right ). Group Ia fibers show this same static-type response, and thus under steady-state conditions (i.e., constant muscle length), their firing rate reflects the amount of muscle stretch, similar to that of group II fibers.

While muscle length is changing, group Ia firing reflects the rate of stretch or shortening that the muscle is undergoing. Its activity overshoots during muscle stretch and undershoots (and possibly ceases) during muscle shortening. These are called dynamic responses. This dynamic sensitivity also means that the activity of group Ia fibers is much more sensitive to transient and oscillatory stretches, such as shown in the middle diagrams of Fig. 9.3 . In particular, the tap profile is what occurs when a reflex hammer is used to hit the muscle tendon leading to a brief stretching of the attached muscle. The change in muscle length is too brief for significant changes in group II firing to occur, but because the magnitude of the rate of change (slopes of the tap profile) is so high with this stimulus, large dynamic responses are elicited in the group Ia fibers. Thus, the functionality of reflex arcs involving group Ia afferent fibers is being assessed when a reflex hammer is used to tap on tendons. More importantly, the behavior of this reponse provides information about the source of potential motor dysfunction (e.g., CNS or PNS; see section later in this chapter, “Motor Deficits Caused by Lesions of Descending Motor Pathways” ).

γ Motor Neurons Adjust the Sensitivity of the Spindle

Up to this point, we have described only how muscle spindles behave when there are no changes in γ motor neuron activity. The efferent innervation of muscle spindles is extremely important, however, because it determines the sensitivity of muscle spindles to stretch. For example, in Fig. 9.4 A, the activity of a muscle spindle afferent fiber is shown during a steady stretch. If only the extrafusal muscle fibers were to contract (this can be done experimentally by selective stimulation of α motor neurons; see Fig. 9.4 B ), the muscle spindle would be unloaded by the resultant shortening of the muscle. If this happens, the muscle spindle afferent fiber may stop discharging and become insensitive to further decreases in muscle length. However, the unloading of the spindle can be prevented if α and γ motor neurons are stimulated simultaneously. Such combined stimulation causes the intrafusal muscle fibers of the spindle to shorten along with the extrafusal muscle fibers, maintaining the baseline tension on the equatorial portion of the intrafusal fibers (see Fig. 9.4 C ).

Note that only the two polar regions of the intrafusal muscle contract; the equatorial region, where the nuclei are located, does not contract because it has little contractile protein. Nevertheless, when the polar regions contract, the equatorial region elongates and regains its sensitivity. Conversely, when a muscle relaxes (α motor neuron activity drops) and thus elongates (if its ends are being pulled), a concurrent decrease in γ motor neuron activity allows the intrafusal fibers to relax (and thus elongate) as well, and thereby prevent the tension on the central portion of the intrafusal fiber from reaching a level at which firing of the afferent fibers is saturated. Thus, the γ motor neuron system allows the muscle spindle to operate over a wide range of muscle lengths while retaining high sensitivity to small changes in length.

For voluntary movements, descending motor commands from the brain typically activate α and γ motor neurons simultaneously, presumably to maintain spindle sensitivity, as just described. This has two important functions: First, by maintaining the muscle spindle’s sensitivity as the muscle changes length, the spindle remains capable of sensing, and signaling to the CNS, any disturbances to the ongoing movement that cause an unexpected stretch of the muscle, and this in turn allows the CNS to initiate both reflex (see next section) and voluntary corrections. Second, if the spindle were to become unloaded during the movement, this would oppose the intended movement by decreasing the excitatory drive, via the group Ia reflex arc (see next section), to the α motor neurons driving the agonist muscles.

As mentioned earlier, there are two types of γ motor neurons: dynamic and static (see Fig. 9.2 ). This allows the CNS to have very precise control over the sensitivity of the muscle spindle. Dynamic γ motor axons end on nuclear bag1 fibers, and static γ motor axons synapse on nuclear chain and bag2 fibers. When a dynamic γ motor neuron is activated, the response of the group Ia afferent fiber is enhanced, but the activity of the group II afferent fibers is unchanged; when a static γ motor neuron discharges, the responsiveness of the group II afferent fibers and the static responsiveness of the group Ia afferent fibers are increased. The effects of stimulating the static and dynamic fibers on a group Ia afferent fiber’s response to stretch are illustrated in Fig. 9.5 . Descending pathways can preferentially influence dynamic or static γ motor neurons and thereby alter the nature of reflex activity in the spinal cord and also, presumably, the functioning of the muscle spindle during voluntary movements.

The Phasic (or Ia) Stretch Reflex

The reflex arc responsible for the phasic stretch reflex is depicted in Fig. 9.6 ; the rectus femoris muscle serves as an example. A rapid stretch of the rectus femoris muscle strongly activates the group Ia fibers of the muscle spindles, which then convey this signal into the spinal cord. In the spinal cord, each group Ia afferent fiber branches many times to form excitatory synapses directly (monosynaptically) on virtually all α motor neurons that supply the same (also known as the homonymous ) muscle and with many α motor neurons that innervate synergists, such as the vastus intermedius muscle in this case, which also acts to extend the leg at the knee. If the excitation is powerful enough, the motor neurons discharge and cause a contraction of the muscle. Note that the group Ia fibers do not contact the γ motor neurons, possibly to avoid a positive-feedback loop situation. This selective targeting of α motor neurons is exceptional in that most other reflex and descending pathways target both α and γ motor neurons.

Other branches of group Ia fibers end on a variety of interneurons; however, one type, the reciprocal Ia inhibitory interneuron (the black neuron in Fig. 9.6 ), is particularly important with regard to the stretch reflex. These interneurons are identifiable because they are the only inhibitory interneurons that receive input from both the group Ia afferent fibers and Renshaw cells (see Fig. 9.12 ). They end on α motor neurons that innervate the antagonist muscles—in this case, the hamstring muscles, including the semitendinosus muscle—which act to flex the knee. Other branches of the group Ia afferent fibers synapse with yet other neurons that originate ascending pathways that provide various parts of the brain (particularly the cerebellum and cerebral cortex) with information about the state of the muscle.

The organization of the stretch reflex arc guarantees that one set of α motor neurons is activated and the opposing set is inhibited. This arrangement is known as reciprocal innervation. Although many reflexes involve such reciprocal innervation, this type of innervation is not the only possible organization of a motor control system; descending motor pathways can override such patterns.

The stretch reflex is quite powerful, in large part because of its monosynaptic nature. The power of this reflex also derives from the optimal convergence and divergence that exist in this pathway, which is not apparent from the circuit diagrams, such as Fig. 9.6 , that are typically used to illustrate reflex pathways. That is, each group Ia fiber contacts virtually all homonymous α motor neurons, and each such α motor neuron receives input from every spindle in that muscle. Although its monosynaptic nature makes the group Ia reflex rapid and powerful, it also means that there is relatively little opportunity for direct control of activity flow through its reflex arc. The CNS overcomes this problem by controlling muscle spindle sensitivity via the γ motor neuron system, as described previously.

Inverse Myotatic or Group Ib Reflex

The inverse myotatic reflex acts to oppose changes in the level of force in the muscle. Just as the stretch reflex can be thought of as a feedback system to regulate muscle length, the inverse myotatic, or group Ib, reflex can be thought of as a feedback system to help maintain force levels in a muscle. With the upper part of the leg as an example, the group Ib reflex arc is depicted in Fig. 9.7 .

The arc starts with the Golgi tendon organ receptor, which senses the tension in the muscle. Golgi tendon organs are located at the junction of the tendon and the muscle fibers and thus lie in series with the muscle fibers, in contrast to the parallel arrangement of the muscle spindles (see Fig. 9.2 ). Golgi tendon organs have a diameter of about 100 µm and a length of about 1 mm. A Golgi tendon organ is innervated by the terminals of group Ib afferent fibers. These terminals wrap about bundles of collagen fibers in the tendon of a muscle (or in tendinous inscriptions within the muscle).

Because of their in-series relationship to the muscle, Golgi tendon organs can be activated either by muscle stretch or by muscle contraction. In both cases, the actual stimulus sensed by the Golgi tendon organ is the force that develops in the tendon to which it is linked. For stretch, the response is due to the spring-like nature of the muscle, with the force on the muscle (“spring”) being proportional to how much it is stretched (based on Hooke’s law).

To distinguish between the responsiveness of the muscle spindles and Golgi tendon organs, the firing patterns of group Ia and group Ib fibers can be compared when a muscle is stretched and then held at a longer length ( Fig. 9.8 ). The firing rate of the group Ia fibers maintains its increase until the stretch is reversed. In contrast, the group Ib fiber shows an initial large increase in firing, reflecting the increased tension on the muscle caused by the stretch, but then shows a gradual return toward its initial firing rate as the tension on the muscle is lowered because of cross-bridge recycling and the resultant lengthening of the sarcomeres. Therefore, Golgi tendon organs signal force, whereas spindles signal muscle length. Further evidence of this distinction is that group Ib firing is correlated with force level during isometric contraction even though muscle length and therefore group Ia activity are unchanged.

The group Ib afferent fibers branch as they enter the spinal cord and end on interneurons. There are no monosynaptic connections to α motor neurons. Rather, the group Ib afferent fibers synapse onto two classes of interneurons: interneurons that inhibit α motor neurons that supply the homonymous muscle (in this case the rectus femoris muscle) and excitatory interneurons that activate α motor neurons to the antagonist (the semitendinosus muscle). Because there are two synapses in series in the CNS, this is a disynaptic reflex arc. Because of these connections, group Ib fiber activity should have the opposite action of the group Ia stretch reflex during passive stretch of the muscle, which explains the group Ib reflex’s other name, the inverse myotatic reflex.

Functionally, however, the two reflex arcs can act synergistically, as the following example shows. Recall that the Golgi tendon organs monitor force levels across the tendon that they supply. If during maintained posture (such as standing at attention) knee extensors (such as the rectus femoris muscle) begin to fatigue, the force pulling on the patellar tendon declines. The decline in force reduces the activity of Golgi tendon organs in this tendon. Because the group Ib reflex normally inhibits the α motor neurons to the rectus femoris muscle, reduced activity of the Golgi tendon organs enhances the excitability of (i.e., disinhibits) the α motor neurons and thereby helps reverse the decrease in force caused by the fatigue. Simultaneously, bending of the knee stretches the knee extensors and activates the afferent fibers from the muscle spindles, which then excite the same α motor neurons. The coordinated action of afferent fibers from both the muscle spindle and Golgi tendon organ help oppose the decrease in contraction of the rectus femoris muscle due to fatigue and thereby work together to maintain the standing posture.

Flexion Reflexes and Locomotion

The flexion reflex starts with activation of one or more of a variety of sensory receptors, including nociceptors, whose signals can be carried to the spinal cord via a variety of afferent fibers, including group II and group III fibers, collectively called the flexion reflex afferent (FRA) fibers. In flexion reflexes, afferent volleys (1) cause excitatory interneurons to activate the α motor neurons that supply the flexor muscles in the ipsilateral limb and (2) cause inhibitory interneurons to inhibit the α motor neurons that supply the antagonistic extensor muscles ( Fig. 9.9 ). This pattern of activity causes one or more joints in the stimulated limb to flex. In addition, commissural interneurons evoke the opposite pattern of activity in the contralateral side of the spinal cord (see Fig. 9.9 ), which results in extension of the opposite limb, the crossed extension reflex. For lower limbs in humans (or for both forelimbs and hind limbs in quadrupeds), the crossed extension part of the reflex helps in maintaining balance by enabling the contralateral limb to be able to support the additional load that is transferred to it when the flexed limb is lifted.

Because flexion typically brings the affected limb in closer to the body and away from a painful stimulus, flexion reflexes are a type of withdrawal reflex. In Fig. 9.9 , the neural circuit of the flexion reflex is shown for neurons that affect only the knee joint. Actually, however, considerable divergence of the primary afferent and interneuronal pathways occurs in the flexion reflex. In fact, all the major joints of a limb (e.g., hip, knee, and ankle) may be involved in a strong flexor withdrawal reflex. Details of the flexor withdrawal reflex vary, depending on the nature and location of the stimulus.

The interneurons subserving flexion reflexes also appear to be part of the central pattern generator (CPG) for generating locomotion, demonstrating how reflex circuits are used for multiple purposes. A CPG is a set of neurons and circuits capable of generating the rhythmic activity that underlies motor acts, even in the absence of sensory input. For example, activation of the FRA interneurons leads to a pattern of flexor excitation and extensor inhibition on one side, and the converse pattern on the opposite side; alternating activation of FRA interneurons on each side of the spinal cord leads to a stepping pattern. That is, walking motion could result from alternately activating the FRA interneurons on each side. Note that such a rhythmic activity pattern in the FRA circuits need not be dependent on activity from the FRA fibers themselves (e.g., they could be activated by descending pathways from the brain).

To show that these circuits are actually involved in generating the locomotion rhythm, spinal cord preparations were made that showed spontaneous locomotion (i.e., if the brainstem is transected and weight is supported, the spinal cord circuits can generate activity that causes the limbs to perform a normal locomotion sequence). In one such preparation, the electromyographic signals from the flexors and extensors of a limb were recorded, and the FRA fibers then stimulated to demonstrate the effect on locomotion rhythm ( Fig. 9.10 ). Before any stimulus, a spontaneous alternating pattern of flexor and extensor electromyographic (EMG) activity exists. If the FRA fibers were not involved in the locomotion circuit, or at least were not a critical part of the circuits responsible for generating the rhythm (see Fig. 9.10 B ), the stimulus would be expected to produce only a transient response (i.e., a single burst in the flexor EMG record and brief inhibition of activity in the extensor EMG record) but to have no long-term effect on ongoing EMG pattern. Such a transient response is observed (see Fig. 9.10 A; EMG records just after the stimulus). However, the stimulus also causes a permanent, approximately 180-degree phase shift in locomotor rhythm, as can be shown by comparing the times of contractions before and after the stimulus. The dashed vertical lines indicate the times at which a flexor EMG response would be expected if the stimulus had produced no phase shift from the EMG activity pattern. Before the stimulus, each vertical line is aligned with the onset of a flexor EMG burst, whereas after the stimulus, each vertical line occurs at the end of the flexor burst. Therefore, the stimulus affected the locomotor CPG itself, and the FRA interneurons are a critical part of this CPG (see Fig. 9.10 C ).

A second important point illustrated by this experiment is that the locomotion CPG (and CPGs in general) can be influenced by strong afferent fiber activity. The afferent fiber’s influence ensures that the pattern generator adapts to changes in the terrain as locomotion proceeds. Such changes may occur rapidly during running, and locomotion must then be adjusted to ensure proper coordination.

Lateral Corticospinal and Corticobulbar Tracts

The corticospinal and corticobulbar tracts originate from a wide region of the cerebral cortex. This region includes the primary motor, premotor, supplementary, and cingulate motor areas of the frontal lobe and the somatosensory cortex of the parietal lobe. The cells of origin of these tracts include both large and small pyramidal neurons of layer V of the cortex, including the giant pyramidal cells of Betz. Although Betz cells are a defining feature of the primary motor cortex, they represent a small minority (<5%) of the neurons that contribute to these tracts, in part because they are found only in the primary motor cortex, and even there they represent a minority of the neurons contributing to the tracts. These tracts leave the cortex and enter the internal capsule, then traverse the midbrain in the cerebral peduncle, pass through the basilar pons, and emerge to form the pyramids on the ventral surface of the medulla (see Fig. 9.13 A ). The corticobulbar axons leave the tract as it descends in the brainstem and terminate in the motor nuclei of the various cranial nerves. The corticospinal fibers continue caudally, and in the most caudal region of the medulla, about 85% of them cross to the opposite side. They then descend in the contralateral lateral funiculus as the lateral corticospinal tract. The lateral corticospinal axons terminate at all spinal cord levels, primarily on interneurons, but also on motor neurons. The remaining uncrossed axons continue caudally in the ventral funiculus on the same side as the ventral corticospinal tract, which belongs to the medial system. Many of these fibers ultimately decussate (cross) at the spinal cord level at which they terminate.

The lateral corticospinal tract is a relatively minor tract in lower mammals but is quantitatively and functionally very important in primates, particularly in humans, in which it contains more than 1 million axons. This number still represents a relatively small proportion of the outflow from the cortex because there are approximately 20 million axons in the cerebral peduncles. Nevertheless, the corticospinal pathway is critical for the fine independent control of finger movement, inasmuch as isolated lesions of the corticospinal tract typically lead to a permanent loss of this ability, even though other movement abilities are often recovered with such lesions. Indeed, in primates, corticospinal synapses directly onto motor neurons are particularly prevalent for the motor neurons controlling finger muscles and are probably the basis of the ability to make independent, finely controlled finger movements.

The corticobulbar tract, the name for the tract that projects from the cortex to the brainstem cranial nerve motor nuclei, has subdivisions that are comparable with the lateral and ventral corticospinal tracts. For example, part of the corticobulbar tract ends contralaterally in the portion of the facial nucleus that supplies muscles of the lower part of the face and in the hypoglossal nucleus. This component of the corticobulbar tract is organized like the lateral corticospinal tract. The remainder of the corticobulbar tract ends bilaterally, including bilateral innervation of both sides of the upper face (forehead). This particular arrangement of input to the lower and upper face can have important clinical implications if, for example, only lower face muscles on one side are disrupted versus disruption of both upper and lower face muscles on one side.

Rubrospinal Tract

The rubrospinal tract, which plays a more prominent role in nonprimates than primates, originates in the magnocellular portion of the red nucleus, which is located in the midbrain tegmentum. These fibers decussate in the midbrain, descend through the pons and medulla, and then take up a position just ventral to the lateral corticospinal tract in the spinal cord. They preferentially affect motor neurons controlling distal musculature, as do the corticospinal fibers. Red nucleus neurons receive input from the cerebellum and from the motor cortex, which allows for integration of activity from these two motor systems.

Pontine and Medullary Reticulospinal Tracts

Neurons in the medial area of the rectiular formation of the pons give rise to the pontine reticulospinal tract. The tract descends in the ventral funiculus and ends on the ipsilateral medial group of interneurons. Its function is to excite motor neurons controlling the proximal extensor muscles that support posture.

The medullary reticulospinal tracts arise from neurons of the medial medulla, particularly those of the gigantocellularis reticular nucleus. The tracts descend bilaterally in the ventral lateral funiculus, and they end mainly on interneurons associated with cell groups of medial motor neurons. The function of the pathway is mainly inhibitory.

Lateral and Medial Vestibulospinal Tracts

The lateral vestibulospinal tract originates in the lateral vestibular nucleus (also known as Deiter’s nucleus ), is located around the medulla and pons junction. This tract descends ipsilaterally through the ventral funiculus of the spinal cord and ends on interneurons associated with the medial motor neuron groups. The lateral vestibulospinal tract excites motor neurons that supply extensor muscles of the proximal part of the limb that are important for postural control. In addition, this pathway inhibits flexor motor neurons by exciting the reciprocal group Ia interneurons that receive group Ia input from extensor muscles, which in turn inhibit flexor motor neurons. The excitatory input to the lateral vestibular nucleus is from both the semicircular canals and the otolith organs, whereas the inhibitory input is from the Purkinje neurons of the anterior vermis region of the cerebellar cortex. An important function of the lateral vestibulospinal tract is to assist in postural adjustments after angular and linear accelerations of the head.

The medial vestibulospinal tract originates from the medial vestibular nucleus. This tract descends in the ventral funiculus of the spinal cord to the cervical and midthoracic levels, and it ends on the medial group of interneurons. Sensory input to the medial vestibular nucleus from the labyrinth is chiefly from the semicircular canals. This pathway thus mediates adjustments in head position in response to angular acceleration of the head.