Chapter 11: Cranial Nerve Motor Nuclei and Brain Stem Motor Functions

Striking parallels exist between the functional and anatomical organization of the spinal and cranial somatic sensory systems. In fact, the principles governing the organization of one are nearly identical to those of the other. A similar comparison can be made between motor control of cranial structures and that of the limbs and trunk: Cranial muscles are innervated by motor neurons found in the cranial nerve motor nuclei, whereas limb and axial muscles are innervated by motor neurons in the motor nuclei of the ventral horn. A similar parallel exists with the control of body organs. Control of the glands and smooth muscle of the head, as well as the pupil, is mediated by parasympathetic preganglionic neurons located in cranial nerve autonomic nuclei. Abdominal visceral organs are controlled by parasympathetic neurons in the sacral cord.

This chapter examines in detail the cranial nerve motor nuclei innervating facial, jaw, and tongue muscles, as well as the muscles for swallowing. It also examines the cortical control of these nuclei, which is accomplished by the corticobulbar tract. This pathway is the cranial equivalent of the corticospinal tract, and the two pathways share numerous organizational principles. Knowing the patterns of corticobulbar connections with the cranial motor nuclei has important diagnostic value because it helps clinicians to understand the cranial motor signs produced by brain stem damage. This knowledge also helps clinicians to plan the proper therapy for the patient to avert potentially life-threatening sequelae. The autonomic and extraocular motor nuclei of the brain stem are also examined to achieve greater knowledge of regional anatomy. Such knowledge is essential for localizing central nervous system damage after trauma.

There Are Three Columns of Cranial Nerve Motor Nuclei

As we saw in Chapter 6, the cranial nerve sensory and motor nuclei are organized into columns that course rostrocaudally throughout the brain stem (Figure 11–2). The sensory columns are located laterally and the motor columns, medially. The sensory nuclei derive from a portion of the developing neural ectoderm, the alar plate, of the brain stem and the motor nuclei, from the basal plate (Figure 11–3). The two collections of developing neurons undergo migration and further subdivision to give rise to the various columns of sensory and motor nuclei.

The cranial nerve motor nuclei are organized into three columns (Figure 11–2): somatic skeletal, branchiomeric, and autonomic. Nuclei in the somatic skeletal motor column contain motor neurons that innervate striated muscle derived from the occipital somites (see Figure 6-4): the extraocular and tongue muscles. This column is close to the midline. Nuclei of the branchiomeric motor column contain motor neurons innervating striated muscle derived from the branchial arches (ie, branchiomeric or visceral, opposed to somatic, origin): facial, jaw, palatal, pharyngeal, and laryngeal muscles. This column is lateral to the somatic skeletal motor column (Figure 11–2) and is displaced ventrally from the ventricular floor (Figure 11–2, bottom inset). Nuclei of the autonomic motor column contain the parasympathetic preganglionic neurons that regulate the functions of cranial exocrine glands, smooth muscle, and many body organs. The autonomic motor column is lateral to the somatic skeletal motor column (Figure 11–2). Sometimes these three columns are termed general somatic motor, special visceral motor, and general visceral motor columns, respectively (see Box 6–1).

Neurons in the Somatic Skeletal Motor Column Innervate Tongue and Extraocular Muscles

Four nuclei comprise the somatic skeletal motor column (Figure 11–2). Three of these nuclei contain motor neurons that innervate the extraocular muscles: the oculomotor nucleus, the trochlear nucleus, and the abducens nucleus. The oculomotor nucleus is located in the rostral midbrain and innervates the medial rectus, inferior rectus, superior rectus, and inferior oblique muscles, which move the eyes (see Figure 12–4), as well as the levator palpebrae superioris muscle, an eyelid elevator. The motor axons course within the oculomotor (III) nerve. Motor neurons in the trochlear nucleus course in the trochlear (IV) nerve and innervate the superior oblique muscle. The abducens nucleus contains the motor neurons that project their axons to the periphery through the abducens (VI) nerve and innervate the lateral rectus muscle. The neuroanatomy of eye muscle control is the focus of Chapter 12. The hypoglossal nucleus is the fourth member of the somatic skeletal motor column (Figure 11–2). The axons of motor neurons in the hypoglossal nucleus course in the hypoglossal (XII) nerve and innervate intrinsic tongue muscles, including the genioglossus, hypoglossus, and styloglossus.

The Branchiomeric Motor Column Innervates Skeletal Muscles That Develop From the Branchial Arches

Three cranial nerve nuclei constitute this nuclear column: the facial motor nucleus, the trigeminal motor nucleus, and the nucleus ambiguus. The facial motor nucleus contains the motor neurons that innervate the muscles of facial expression. These axons course in the facial (VII) nerve. The axons of motor neurons of the trigeminal motor nucleus course in the trigeminal (V) nerve and innervate principally the muscles of mastication: masseter, temporalis, and external and internal pterygoid muscles. The nucleus ambiguus contains motor neurons that innervate striated muscles of the pharynx and larynx. This nucleus and its efferent projections through cranial nerves are organized rostrocaudally. A small number of motor neurons in the most rostral portion of the nucleus ambiguus course in the glossopharyngeal (IX) nerve and innervate one pharyngeal muscle, the stylopharyngeus. Most motor neurons in the nucleus send their axons through the vagus (X) nerve to innervate the pharynx and larynx. Because the pharyngeal muscles are innervated by the vagus nerve, a lesion of the nucleus ambiguus produces difficulty in swallowing. The vagus nerve is the efferent component of the gag reflex. In this reflex, mechanical stimulation of the pharynx, using a cotton swab for example, produces reflex contraction of the pharyngeal muscles. The glossopharyngeal nerve contains the afferent fibers that innervate mechanoreceptors of the pharynx that comprise the afferent limb of the gag reflex (see Chapter 6). The most caudal portion of the nucleus ambiguus contains laryngeal motor neurons whose axons course in a portion of the accessory (XI) nerve. This cranial nerve consists of distinct cranial and spinal roots, and only axons in the cranial root have their cell bodies in the nucleus ambiguus. These axons are probably displaced vagal fibers. They join the vagus nerve as they exit from the cranium and innervate the same structures as the vagus; accordingly, they are sometimes considered to be part of the vagus nerve.

Cell bodies of axons in the spinal root of the spinal accessory nerve are located in the spinal accessory nucleus (Figure 11–2). This nucleus is a part of the ventral horn of the upper cervical spinal cord—from the pyramidal decussation to about the fourth or fifth cervical segments—not the branchiomeric motor column. Axons in the spinal root of the spinal accessory nerve innervate the sternocleidomastoid muscle and the upper part of the trapezius muscle, which develop from the somites and not the branchial arches.

The Autonomic Motor Column Contains Parasympathetic Preganglionic Neurons

The autonomic motor column contains neurons that regulate the function of various body organs, smooth muscles, and exocrine glands. These neurons are part of the parasympathetic nervous system, a division of the autonomic nervous system (see Chapters 1 and 15). In contrast to the innervation of skeletal muscle, which is mediated by a single motor neuron (Figure 11–4A), the innervation of smooth muscle and glands is accomplished by two separate neurons: preganglionic and postganglionic neurons (Figure 11–4B). Parasympathetic preganglionic neurons are located in the various nuclei that comprise the autonomic motor column; these neurons are also found in the sacral spinal cord (see Chapter 15). Parasympathetic postganglionic neurons are located in peripheral autonomic ganglia.

The autonomic motor column, which is lateral to the somatic skeletal motor column (Figure 11–2), contains four nuclei. The Edinger-Westphal nucleus is located in the midbrain and in the pretectal region, dorsal to the oculomotor nucleus (Figure 11–4B1). It participates in pupillary constriction and lens accommodation. The parasympathetic neurons in the nucleus send their axons into the oculomotor (III) nerve to synapse on postganglionic neurons in the ciliary ganglion. These neurons innervate the ciliary muscle and the constrictor muscles of the iris.

Parasympathetic preganglionic neurons are also located in nuclei of the caudal pons and medulla (Figure 11–4B2). Neurons of the superior and inferior salivatory nuclei are located in the pons and medulla. They are somewhat dispersed, not forming a discrete cell column. The axons of neurons of the superior salivatory nucleus course in the intermediate nerve. They synapse in two peripheral ganglia: (1) the pterygopalatine ganglion, where postganglionic neurons innervate the lacrimal glands and glands of the nasal mucosa, and (2) the submandibular ganglion, from which postganglionic parasympathetic neurons innervate the submandibular and sublingual salivary glands. The intermediate nerve is sometimes considered to be the sensory branch of the facial nerve because it contains afferent fibers, which are the axons of pseudounipolar neurons of the geniculate ganglion (see Chapters 6 and 9). The inferior salivatory nucleus contains parasympathetic preganglionic neurons whose axons course in the glossopharyngeal nerve and synapse on postganglionic neurons in the otic ganglion (Figure 11–4B2). Parasympathetic postganglionic neurons in the otic ganglion innervate the parotid gland, which secretes saliva.

The dorsal motor nucleus of the vagus nerve forms a column of parasympathetic preganglionic neurons beneath the floor of the fourth ventricle in the medulla (Figure 11–4B3). These neurons synapse in extracranial parasympathetic ganglia, called terminal ganglia (Figure 11–4B3). These ganglia are located in the viscera of the thoracic and abdominal cavities, including the gastrointestinal tract proximal to the splenic flexure of the colon. The functions of the vagal parasympathetic neurons include regulating heart rate (ie, slowing), gastric motility (ie, increasing), and bronchial muscle control (ie, contracting to constrict airway). (The colon distal to the splenic flexure is innervated by parasympathetic preganglionic neurons of the sacral spinal cord [see Chapter 15].)

The remaining sections of this chapter will focus on the cortical control of cranial motor nuclei and their regional anatomy in the pons and medulla.

The Cranial Motor Nuclei Are Controlled by the Cerebral Cortex and Diencephalon

Nuclei within the somatic skeletal and branchiomeric motor columns that innervate facial, tongue, jaw, laryngeal, and pharyngeal muscles are controlled by the cortical motor areas: the primary motor cortex, the supplementary motor area, the premotor cortex, and the cingulate motor area. These are the same cortical regions that control limb and trunk muscles (see Chapter 10). However, the cranial motor representations project to the various brain stem motor nuclei through the corticobulbar tract, one of the three components of the corticospinal system (Chapter 10). Nuclei that innervate extraocular muscles are controlled by different cortical areas and not by the corticobulbar tract and will be considered in Chapter 12. The nuclei comprising the autonomic motor column are influenced by projections from the cerebral cortex and hypothalamus. The autonomic nervous system and hypothalamus are considered in Chapter 15.

Of all the cortical motor areas, the primary motor cortex contributes the greatest number of axons to the corticobulbar tract. The cell bodies of these primary motor cortex axons are located within layer V of the cranial representation, which is the lateral precentral gyrus close to the lateral sulcus (see Figure 10–8). Their descending axons course within the internal capsule, along with but rostral to the corticospinal fibers. Corticobulbar neurons project to the pons and medulla. Their axons terminate either bilaterally or contralaterally, depending on the particular nucleus (see below). Muscles innervated by motor nuclei that receive a bilateral projection from the corticobulbar tract do not become weak after a unilateral lesion of the motor cortex, the internal capsule, or some other portion of its descending pathway. The projection from the intact side is sufficient for near-normal control of force production. This is not the case, however, for muscles receiving only a contralateral projection. In these instances, weakness reveals the unilateral damage. This relationship between the laterality of cortical control and the laterality of motor signs after unilateral damage is similar to that of the corticospinal system.

Bilateral Corticobulbar Tract Projections Innervate the Hypoglossal Nucleus, Trigeminal Nucleus, and Nucleus Ambiguus

The corticobulbar projection from the primary motor cortex to the hypoglossal nucleus is most commonly a bilateral one (Figure 11–5). Unilateral lesion of this projection, for example in the internal capsule, does not produce weakness of tongue muscles in the majority of people. In some individuals, however, contralateral tongue weakness does occur, suggesting a predominantly crossed (ie, unilateral) corticobulbar projection to the hypoglossal nucleus in these individuals. By contrast, a lesion of the hypoglossal nucleus or nerve consistently produces ipsilateral tongue paralysis. In the case of nucleus or nerve damage, when patients are asked to protrude their tongue, it deviates to the side of the lesion.

Because the primary motor cortex projects bilaterally to the trigeminal motor nuclei (Figure 11–5), unilateral cortical or descending pathway lesions do not produce weakness of the target muscles. Bilateral control by the primary motor cortex may reflect the fact that jaw muscles on both sides of the mouth are typically activated in tandem during most motor acts, for example, chewing or talking. This is similar to the bilateral control of axial muscles, for maintaining posture, by the medial descending spinal cord pathways (see Chapter 10).

The motor cortex also exerts bilateral control of motor neurons in the nucleus ambiguus (Figure 11–5), leading to the redundancy in their control, as discussed earlier. Whereas a unilateral lesion of the corticobulbar tract may not produce laryngeal and pharyngeal signs, brain stem lesions that damage the nucleus ambiguus and surrounding regions produce ipsilateral paralysis of pharyngeal and laryngeal muscles. Such damage results in hoarseness and swallowing impairments. Importantly, this also impairs the airway protective reflex, the automatic closure of the larynx during swallowing to prevent food and fluids from entering the trachea. When this reflex is impaired, small amounts of food or fluids can slip into the trachea, which can lead to aspiration pneumonia.

Unlike the nucleus ambiguus, which is under bilateral cortical control, the spinal accessory nucleus receives a predominantly ipsilateral cortical projection. This ipsilateral projection targets primarily the motor neurons of the sternocleidomastoid muscle, which turns the head to the opposite side. Interestingly, whereas the cortical projection is ipsilateral, the motor actions of the muscle produce a movement directed to the contralateral side.

Cortical Projections to the Facial Motor Nucleus Have a Complex Pattern

A facial nerve or nucleus lesion produces facial muscle paralysis over the entire ipsilateral face; this is a common occurrence in Bell's palsy, a viral infection of facial motor neurons. A unilateral lesion of the primary motor cortex, the internal capsule, or the descending cortical fibers produces differential effects on the voluntary control of upper and lower facial muscles. After the lesion, upper facial muscles retain voluntary control. A patient with such a lesion can furrow his or her brow symmetrically. In contrast, lower facial muscles contralateral to the side of the lesion become weak. A patient with such damage would smile asymmetrically when asked to smile by his or her physician. Surprisingly, if the patient were provoked to smile, for example by hearing a particularly humorous joke, he or she could do so symmetrically, implying no facial weakness.

Knowledge of three features of the origin of corticobulbar neurons and the pattern of their connections helps to explain these peculiar effects. First, the primary motor cortex has dense contralateral projections to lower facial muscle motor neurons and sparse bilateral projections to upper facial motor neurons (Figure 11–6A). Thus, a lesion would be expected to weaken only the contralateral lower facial muscles. Second, motor neurons innervating upper facial muscles receive bilateral control by several premotor areas, especially the premotor cortex and cingulate motor region (Figure 11–6B). Third, the descending axons of these premotor regions are separated from those of the primary motor cortex; they are located farther rostrally in the corona radiata and internal capsule. They are typically spared with local cortical or internal capsule injury because they receive a different arterial supply (see Figure 3–6). As for the patient who is able to smile symmetrically after hearing a funny joke, that observation is also thought to be related to the intact premotor connections, especially those from the cingulate motor areas, which receive their major inputs from brain regions regulating emotions.

The rest of this chapter focuses on the spatial relations between the cranial nerve motor nuclei innervating striated muscle, the corticobulbar tract, and key brain stem structures. In addition, this chapter further explains the three-dimensional organization of the brain stem.

Lesion of the Genu of the Internal Capsule Interrupts the Corticobulbar Tract

Similar to the corticospinal projection, neurons that form the corticobulbar tract originate from multiple cortical sites: the primary motor cortex, the supplementary motor area, the premotor cortex, and the cingulate motor area (see Figure 10–7). The corticobulbar projection descends in the genu and the posterior limb of the internal capsule, rostral to the corticospinal projection (Figure 11–7A, B). The various parts of the internal capsule are supplied by different cerebral artery branches (see Figure 3–6). The superficial portion is supplied by deep branches of the middle cerebral artery. The inferior part of the posterior limb is supplied by the anterior choroidal artery, and the inferior parts of the genu and anterior limbs are supplied primarily by deep branches of the anterior cerebral artery. In the midbrain, the descending cortical fibers, including the corticobulbar and corticospinal tracts, are together within the basis pedunculi (Figure 11–7C).

The Trigeminal Motor Nucleus Is Medial to the Main Trigeminal Sensory Nucleus

As the corticobulbar tract descends further, the projection becomes fragmented into innumerable small fascicles in the isthmus of the pons (Figure 11–8A). Farther caudally in the pons (Figure 11–8B), the fascicles coalesce to form a discrete bundle of descending cortical axons. This is at the level of the most rostral component of the branchiomeric motor column, the trigeminal motor nucleus (Figures 11–2 and 11–8B). The trigeminal motor nucleus is located lateral to the main trigeminal sensory nucleus (see Chapter 6). The trigeminal root fibers are located nearby (Figure 11–8B). The trigeminal motor nucleus is innervated bilaterally by the corticobulbar tract.

The Fibers of the Facial Nerve Have a Complex Trajectory Through the Pons

The pontine section shown in Figure 11–9A cuts through portions of the facial nerve. The axons leave the facial nucleus, where the motor neurons are located, and follow a path toward the floor of the fourth ventricle (Figure 11–9B). These fibers of the facial nerve are not seen in Figure 11–9A because they do not course in discrete and straight fascicles.

As the facial nerve fibers approach the ventricular floor, they first ascend close to the midline. Next, the fibers sweep around the medial, dorsal, and rostral aspects of the abducens nucleus, which contains motor neurons innervating the lateral rectus muscle, which abducts the eye (ie, looking away from the nose). This component is termed the genu of the facial nerve and, with the abducens nucleus, forms the facial colliculus, a surface landmark on the pontine floor of the fourth ventricle (Figure 11–9, inset). The facial nerve fibers then run ventrally and caudally to exit the pons at the pontomedullary junction. In addition to the axons of branchiomeric motor neurons, the facial nerve also contains visceral motor axons from the superior salivatory nucleus that innervate the pterygopalatine and submandibular ganglia. The pterygopalatine ganglion innervates lacrimal glands and the nasal mucosa. The submandibular ganglion innervates submandibular and sublingual salivary glands.

The vascular supply to the pons is derived by separate paramedian, short circumferential, and long circumferential branches of the basilar artery (see Figure 3–3B2). At the level of the pons in Figure 11–9, the anterior inferior cerebellar artery (AICA) is the long circumferential branch. The more rostral pontine levels (Figure 11–8) also receive their blood supply from branches of the basilar artery.

The Glossopharyngeal Nerve Enters and Exits From the Rostral Medulla

The myelin-stained section through the rostral medulla is through the glossopharyngeal nerve root (Figure 11–10A). The motor axons of the glossopharyngeal nerve originate from neurons in two nuclei: Motor neurons innervating striated muscle (stylopharyngeus muscle) are located in the rostral portion of the nucleus ambiguus; autonomic motor neurons (parasympathetic preganglionic neurons) are located in the inferior salivatory nucleus. The parasympathetic preganglionic neurons innervate the otic ganglion, which, in turn, innervates the parotid gland for salivation.

From a clinical perspective, the glossopharyngeal nerve can be considered a sensory nerve because a unilateral lesion does not produce frank motor dysfunction (either somatic or visceral motor) on clinical examination. Recall that the glossopharyngeal nerve also contains gustatory and viscerosensory afferent fibers that terminate in the solitary nucleus as well as somatic sensory afferents that terminate in the trigeminal spinal nucleus (see Figure 11–10B).

A Level Through the Mid-medulla Reveals the Locations of Six Cranial Nerve Nuclei

The three cranial nerve motor nuclei in the mid-medulla—the hypoglossal nucleus, the dorsal motor nucleus of vagus, and the nucleus ambiguus—are medial to the three sensory nuclei at this level—the solitary, vestibular, and spinal trigeminal nuclei (Figure 11–10B). The cranial nerve sensory and motor nuclei are roughly separated by the sulcus limitans (Figure 11–10B). The hypoglossal and vagal nuclei are immediately beneath the floor of the fourth ventricle, whereas the nucleus ambiguus is deeper within the medulla (Figure 11–10B; see also Figure 11–13). The precise location of the nucleus ambiguus cannot be determined in myelin-stained sections; its approximate location is indicated in Figure 11–10B.

Infarction in the territory of different arterial branches interrupts the function of specific cranial nerve nuclei and brain stem pathways

In the medulla, different cranial nerve nuclei receive their arterial supply from specific branches of the vertebral-basilar system (Figure 11–12). The medial portion of the medulla is supplied by branches of the main portion of the vertebral artery. This region contains the hypoglossal nucleus, the medial lemniscus, and the pyramid. Infarction of this region of the medulla produces three deficits. First, tongue muscles are paralyzed on the side of the lesion because the hypoglossal motor neurons and axons are destroyed. Second, tactile sensation, vibration sense, and limb proprioception sense on the side opposite the lesion are impaired because the medial lemniscus is affected. Third, muscles of the limb on the side opposite the lesion are weak because corticospinal axons in the pyramid are affected.

The dorsolateral portion of the medulla is supplied by the posterior inferior cerebellar artery (PICA) (Figure 11–12). Six key sensory and motor signs—which comprise the lateral medullary, or Wallenberg, syndrome—can be produced when the territory of this artery becomes infarcted. We considered several sensory signs of this syndrome in Chapter 6, and we will consider this syndrome further in Chapter 15. Among the sensory and motor signs, three are associated with damage to different cranial nerve nuclei:

• Difficulty in swallowing and hoarseness result from lesions of the nucleus ambiguus. An associated change, the loss of the gag reflex, is due either to lesions of the nucleus ambiguus (the efferent limb of the reflex) or to loss of pharyngeal sensation (cranial nerve IX) (the afferent limb).

• Vertigo (an illusion of a whirling movement; sometimes described as dizziness) and nystagmus (involuntary rhythmical oscillation of the eyes) are produced by vestibular nuclear lesions (see Chapter 12).

• Loss of pain and temperature senses on the ipsilateral face is due to lesions of the spinal trigeminal nucleus and tract.

The remaining signs result from damage to ascending or descending pathways that course through the dorsolateral medulla:

• Reduced pain and temperature senses on the contralateral limbs and trunk reflect lesion of the anterolateral system.

• Ipsilateral limb ataxia (jerky or uncoordinated movements) is due to lesions of the inferior cerebellar peduncle, which brings sensory information to the cerebellum (see Chapter 13).

• Horner syndrome results from damage to descending axons from the hypothalamus that regulate the functions of the sympathetic nervous system. (The precise location of these axons in the dorsolateral medulla is not known.) Horner syndrome consists of pupillary constriction due to unopposed actions of parasympathetic pupillary constrictors; pseudoptosis due to weakness of the tarsal muscle, a smooth muscle that assists the action of the levator palpebrae muscle (ptosis is drooping of the upper eyelid due to levator palpebrae muscle weakness); reddening of facial skin due to loss of sympathetic vasoconstrictor activity and resulting vasodilation; and impaired sweating due to loss of sympathetic control of the sweat glands (see Chapter 15).

The Spinal Accessory Nucleus Is Located at the Junction of the Spinal Cord and Medulla

The pyramidal decussation marks the boundary between the spinal cord and medulla (Figure 11–13B). The spinal accessory nerve contains axons of motor neurons whose cell bodies are located in the spinal accessory nucleus (Figure 11–13B). Recall that these motor neurons innervate the sternocleidomastoid muscle and the upper part of the trapezius muscle. Comparison of this section with the one through the cervical enlargement (eg, see Figure AII–5) reveals the similarity in location of the spinal accessory nucleus, on the one hand, and the ventral horn motor nuclei, on the other.

There are three separate columns of cranial nerve motor nuclei (Figure 11–2), from medial to lateral: somatic skeletal motor, branchiomeric motor, and autonomic.

Somatic Skeletal Motor Nuclei

The somatic skeletal motor column is the most medial motor column. It comprises four nuclei, each of which contains motor neurons that innervate striated muscle derived from the occipital somites. The oculomotor nucleus (1) (Figure 11–2) contains motor neurons whose axons course in the oculomotor (III) nerve and innervate the following extraocular muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique. The oculomotor nucleus also innervates the levator palpebrae superioris muscle. The trochlear nucleus (2), via the trochlear (IV) nerve, innervates the contralateral superior oblique muscle. The abducens nucleus (3), via the abducens (VI) nerve, innervates the lateral rectus muscle. The hypoglossal nucleus (4) gives rise to axons that course in the hypoglossal (XII) nerve and innervate tongue muscles (Figures 11–2, 11–5, 11–10, and 11–12). The hypoglossal nucleus is the only nucleus of this column that receives a projection from the primary motor cortex.

Branchiomeric Motor Nuclei

The branchiomeric motor column is displaced ventrally from the floor of the fourth ventricle (Figures 11–2 and 11–3). It contains three nuclei, each of which innervates striated muscles derived from the branchial arches. The trigeminal motor nucleus (1) (Figures 11–5 and 11–8B) innervates the muscles of mastication via the trigeminal (V) nerve. This nucleus receives a bilateral projection from the motor cortex. The facial nucleus (2) (Figures 11–2 and 11–9) innervates the muscles of facial expression. The axons of facial motor neurons course in the facial (VII) nerve. Facial motor neurons that innervate lower face muscles receive a contralateral projection from the primary motor cortex. Motor neurons innervating upper facial muscles receive weak bilateral projections from the primary motor cortex but dense projections from premotor areas (Figure 11–6). The nucleus ambiguus (3) innervates the muscles of the pharynx and larynx predominantly via the vagus (X) nerve and to a lesser extent via the glossopharyngeal (IX) nerve and the cranial root of the spinal accessory (XI) nerve (Figure 11–5). The spinal accessory nucleus (spinal root) is in line with the nucleus ambiguus but is not part of the branchiomeric motor column. It innervates the sternocleidomastoid and trapezius muscles via the spinal accessory (XI) nerve (Figures 11–2 and 11–13B).

Autonomic Nuclei

The autonomic motor column contains four nuclei (Figure 11–2). Each nucleus contains parasympathetic preganglionic neurons (Figures 11–4 and 11–7). The Edinger-Westphal nucleus (1) is located in the midbrain. Its axons project via the oculomotor nerve to the ciliary ganglion, where postganglionic neurons innervate the constrictor muscles of the iris and the ciliary muscle (see Chapter 12). Axons from the superior salivatory nucleus (2) course in the intermediate nerve (a branch of the facial nerve). Via synapses in the pterygopalatine and submandibular ganglia, this nucleus influences the lacrimal gland and glands of the nasal mucosa. The inferior salivatory nucleus (3), via the glossopharyngeal nerve, synapses on postganglionic neurons in the otic ganglion. From there, postganglionic neurons innervate the parotid gland. Axons from the dorsal motor nucleus of the vagus (4) (Figures 11–10 and 11–13) course in the periphery in the vagus nerve and innervate terminal ganglia in most of the thoracic and abdominal viscera (proximal to the splenic flexure of the colon).