Their central processes enter the brainstem, join the

spinal tract of the trigeminal and terminate in the spinal nucleus of the trigeminal (Fig. 15.18A).

The cell bodies of the SVE branchiomotor neurons are located in the nucleus ambiguus. The fibers of these neurons innervate all of the laryngeal and pharyngeal muscles with the exception of the stylopharyngeus and the tensor veli palatini muscles (Fig. 15.18B). The vagus nerve has a very extensive GVE distribution. It supplies parasympathetic innervation to the laryngeal mucous glands and all of the thoracic and most of the abdominal organs. The dorsal motor nucleus of the vagus houses the nerve cell bodies of preganglionic parasympathetic neurons

whose fibers accompany the other vagal fibers upon their exit from the brainstem. These fibers run in the main trunk of the vagus into the thorax where they leave the main trunk and join the autonomic plexuses scattered throughout the thoracic and abdominal cavities. The preganglionic fibers terminate and synapse in the terminal parasympathetic ganglia or ganglia near or within the viscera. Parasympathetic innervation decreases the heart rate (calms the heart), reduces adrenal gland secretion, activates peristalsis, and stimulates glandular activity of various organs (Fig. 15.18C). deep surface of the sternocleidomastoid muscle providing it with motor innervation. It continues its inferior course to the posterior triangle of the neck and then proceeds to the deep aspect of the upper part of the trapezius muscle to supply it with motor innervation. In view of its origin, many neuroanatomists no longer consider the accessory nerve to be a true cranial nerve, but instead a unique type of spinal nerve.

Additionally, there are differences of opinion relating to the classification of the functional components of the spinal accessory nerve. Some authors consider that this nerve carries branchiomotor SVE fibers since neurons of the spinal accessory nucleus develop in a manner characteristic of SVE, not GSE, neurons; whereas others believe that they are somatomotor, that is GSE.

Recent literature supports that GSA proprioceptive fibers

are carried by the spinal accessory nerve from the upper cervical spinal cord levels to the structures it innervates, but questions the branchial arch.

 

CLINICAL CONSIDERATIONS

Unilateral damage of the vagus nerve near its emergence from the brainstem results in a number of deficiencies on the ipsilateral side. Damage to the SVE branchiomotor fibers will cause flaccid paralysis or weakness of: (i) the pharyngeal muscles and levator veli palatini of the soft palate, resulting in dysphagia (difficulty swallowing); (ii) the laryngeal muscles, resulting in dysphonia (hoarseness) and dyspnea (difficulty breathing); and (iii) loss of the gag reflex (efferent limb). Damage to the GVA fibers will cause loss of general sensation from the soft palate, pharynx, larynx, esophagus, and trachea. Damage to the GVE fibers will cause cardiac arrhythmias. A bilateral lesion of the vagus nerve is incompatible with life, due to the interruption of parasympathetic innervation to the heart.

 

 

SPINAL ACCESSORY NERVE (CN XI)

The spinal accessory nerve supplies motor innervation to the sternocleidomastoid, trapezius, and

many of the intrinsic laryngeal muscles

The spinal accessory nerve

(Fig. 15.19) supplies motor innervation to the sternocleidomastoid, trapezius, and many of the intrinsic laryngeal muscles. In the early literature this nerve was described as consisting of two distinct parts: a cranial (bulbar) and a spinal root. It is now understood that the “cranial root” of the accessory nerve is composed of aberrant vagal fibers arising from the nucleus ambiguus in the medulla. These vagal fibers collectively form a distinct root as they emerge from the brainstem. On the other hand, the spinal accessory nerve derives its fibers from the spinal accessory nucleus residing in the posterolateral aspect of the ventral horns of cervical spinal cord levels C2–C5 (or C6). This nucleus is continuous superiorly with the nucleus ambiguus of the medulla.

 

Delicate rootlets emerging from the surface of the lateral funiculus of the spinal cord (interposed between the dorsal and ventral spinal roots) converge and assemble to form the spinal accessory nerve. This nerve trunk ascends, enters the cranial vault through the foramen magnum, and proceeds on the lateral aspect of the medulla to join the aberrant vagal fibers as they emerge from the medulla. The two groups of fibers accompany one another for a short distance but then

diverge to go their separate ways. The aberrant vagal fibers join the main trunk of the vagus nerve and follow those fibers of the vagus that are destined to supply most of the intrinsic

laryngeal muscles. The spinal accessory nerve exits the cranial vault via the jugular foramen. It courses inferiorly to the deep surface of the sternocleidomastoid muscle providing it with motor innervation. It continues its inferior course to the posterior triangle of the neck and then proceeds to the deep aspect of the upper part of the trapezius muscle to supply it with motor innervation. In view of its origin, many neuroanatomists no longer consider the accessory nerve to be a true cranial nerve, but instead a unique type of spinal nerve. Additionally, there are differences of opinion relating to the classification of the functional components of the spinal accessory nerve. Some authors consider that this nerve carries branchiomotor SVE fibers since neurons of the spinal accessory nucleus develop in a manner characteristic of SVE, not GSE, neurons; whereas others believe that they are somatomotor, that is GSE. Recent literature supports that GSA proprioceptive fibers are carried by the spinal accessory nerve from the upper cervical spinal cord levels to the structures it innervates, but questions the branchial arch origins of the trapezius and sternocleidomastoid muscles.

 

CLINICAL CONSIDERATIONS

 

A unilateral lesion confined to the spinal accessory nucleus or the nerve proximal to its muscular distribution results in an ipsilateral flaccid paralysis and subsequent atrophy of the sternocleidomastoid and upper part of the trapezius muscles. An individual with such a lesion is unable to turn his or her head away from the lesion. Normally, unilateral contraction of the sternocleidomastoid muscle draws the mastoid process inferiorly, bending the head sideways (approximating the ear to the shoulder), which is accompanied by an upward turning of the chin towards the opposite side. If the upper part of the trapezius is paralyzed, the upper border of the scapula is rotated laterally and inferiorly with its inferior angle pointing towards the spine. This results in slight drooping of the ipsilateral shoulder, accompanied by a weakening of the shoulder when attempting to raise it.

 

 

HYPOGLOSSAL NERVE (CN XII)

The hypoglossal nerve provides motor innervation to the muscles of the tongue

 

The hypoglossal nerve

(Fig. 15.20) provides motor innervation to the muscles of the tongue. The cell bodies of

the GSE lower motoneurons of the hypoglossal nerve reside in the hypoglossal nucleus, a cell column in the medulla. This nucleus, located ventral to the floor of the fourth ventricle near the midline, forms a triangular elevation—the hypoglossal trigone —in the floor of the midline of the ventricle. The nerve cell bodies of the hypoglossal nucleus give rise to axons that course ventrally to arise as a series of tiny rootlets on the ventral surface of the medulla in the sulcus separating the pyramid and the olive. These rootlets collect to form the hypoglossal nerve, which exits the cranial vault through the hypoglossal foramen. The nerve then courses to the submandibular region to serve the ipsilateral side of the tongue. The hypoglossal nerve innervates the intrinsic muscles (transverse, longitudinals, and vertical) and all the extrinsic muscles of the tongue (styloglossus, hyoglossus, and genioglossus) with the exception of the

palatoglossus. Recent studies indicate that GSA fibers terminating in muscle spindles of the tongue musculature transmit roprioceptive sensation to the trigeminal system involved in reflex activity of mastication. Some investigators believe that the cell bodies of these GSA pseudounipolar neurons are located in the mesencephalic nucleus of the trigeminal nerve, whereas others maintain that they are dispersed along the hypoglossal nerve.

 

CLINICAL CONSIDERATIONS

A unilateral lesion of the hypoglossal nerve will cause the tongue to deviate toward the side of the lesion (impaired side). A lesion in the hypoglossal nucleus or nerve results in flaccid paralysis and subsequent atrophy of the ipsilateral tongue musculature. Hemiparalysis of the tongue causes creasing (wrinkling) of the dorsal surfaceof the tongue ipsilateral to the lesion. Normally, the simultaneouscontraction of the paired genioglossi muscles causes the tongue to protrudestraightforward. During examination of the patient it is important toremember that a unilateral lesion of the hypoglossal nerve will cause thetongue to deviate towards the side of the lesion (impaired side) since thefunctional genioglossus on the intact side is unopposed by the paralyzed,inactive genioglossus on the lesion side.