Spinal Accessory Nerve (Cranial Nerve XI)
Component: SVE. Our understanding of the nature of this nerve has been clouded by several controversies. Early anatomists believed that the spinal accessory nerve had two components: a cranial portion and a spinal portion. Later studies revealed that the cranial portion represents aberrant fibers of the vagus nerve. A second issue concerns the embryological origin of the nerve—namely, whether the fibers should be classified as SVE or GSE. Most authors believe that SVE is more appropriate because the developmental features of this nerve resemble more closely those of other SVE neurons than they do GSE neurons. The important point to remember is that this nerve is a purely somatic motor nerve and contains no other components.
The spinal accessory nerve arises from ventral horn cells of the first five to six cervical segments. Fibers from these cells are initially directed laterally, exit the spinal cord, ascend for a short distance within the vertebral canal into the skull, and then exit the skull through the jugular foramen. The root fibers then innervate the trapezius and sternomastoid muscles (Fig. 14-5).
The basic functions of the sternomastoid and trapezius muscles are to cause contralateral turning and lifting of the head.
Clinical Disorders. Lesions of the sternomastoid muscle may produce difficulty in movement of the head to the opposite side, whereas lesions of the trapezius muscle result in a lowering of the shoulder on the affected side. The scapula will appear to be lower on the affected side with its medial border situated more laterally than normal. However, reports of the effects of such lesions have not been entirely consistent because some authors have reported difficulty in movement of the head to the ipsilateral rather than the contralateral side.
FIGURE 14-5 Diagram illustrates the origin and distribution of the spinal accessory nerve (cranial nerve XI). Note that the cell bodies of origin are within the spinal cord, and the nerve fibers innervate the trapezius and sternomastoid muscles. Also shown in this illustration is the upper motor neuron for this nerve. The cell bodies of origin for this nerve receive a projection from the cortex that is crossed.
Patients are tested for spinal accessory nerve damage involving the sternomastoid by being asked to raise their head from a pillow if they are lying on their back, or, if the patients are standing, they are asked to press their head forward against resistance. The muscles on both sides are then compared. As mentioned earlier, damage to fibers innervating the trapezoid muscle is evident by sagging of the shoulder and outward and downward rotation of the scapula. Damage could also be determined by asking the patient to shrug one shoulder and to compare the resistance on each side of the body.
Supranuclear paralysis also can occur with CN XI. Corticospinal fibers that innervate spinal accessory neurons are contralateral in origin. Therefore, the part of the body affected will be on the side contralateral to the cortical lesion. Such lesions would produce a paresis or paralysis of the sternomastoid and trapezius muscles.
Vagus Nerve (Cranial Nerve X)
Components: SVE, GVE, GVA, SVA, GSA. Because it contains both sensory and motor neurons, by definition CN X is a mixed nerve. Its complexity is due to the fact that it contains two types of motor components: (1) a somatic motor component that is classified as SVE because it innervates muscles derived from the fourth and fifth branchial arches; and (2) a GVE component whose axons innervate wide areas of the body viscera. There are three kinds of sensory components: (1) a small GSA component conveying somesthetic impulses from the back of the ear; (2) a GVA component that conveys, in part, signals concerning changes in blood pressure to the brain; and (3) SVA components conveying taste impulses and changes in blood oxygen levels to the brain.
SVE Component: Origin, Distribution, and Function. The SVE component of the vagus nerve originates from the nucleus ambiguus. Axons from the nucleus ambiguus pass in a ven-trolateral direction to the lateral margin of the brain and exit the skull through the jugular foramen. Peripherally, there are several branches of the SVE component of the vagus nerve. One branch, the pharyngeal nerve, constitutes the main motor branch that innervates the pharynx and soft palate. A second branch, the superior laryngeal nerve, descends near the pharynx and breaks into further branches to supply the inferior constrictor muscle, crico-thyroid muscle, and superior cardiac nerve. The third branch, the recurrent laryngeal nerve, supplies the muscles of the larynx (Fig. 14-6).
The SVE component allows the muscles of the pharynx and intrinsic muscles of the larynx to contract. Normal contractions play an important role in speech. GVE Component. Fibers classified as GVE arise from the dorsal motor nucleus, which is located near the floor of the fourth ventricle and which extends somewhat more caudally beyond the fourth ventricle into the region of the closed medulla. Axons arising from the dorsal motor nucleus pass laterally, exiting the brain and joining the vagus nerve as preganglionic parasympathetic fibers. Preganglionic parasympathetic fibers of the vagus nerve innervate many structures within the body viscera. These include the trachea, lungs, heart, kidney, esophagus, stomach and intestines, pancreas, spleen, and liver.
FIGURE 14-6 Diagram illustrates the origin, course, and distribution of all the components of the vagus nerve (cranial nerve [CN] X). The distribution of the autonomic component of the vagus nerve is also indicated in this diagram.
With respect to the origin of the GVE component, there appear to be phylogenetic variations. Most authors agree that, in humans, the GVE component of the vagus nerve arises from the dorsal motor nucleus. Nevertheless, a variety of studies conducted in other animals, such as rodents, have indicated that, in such less-developed species, the nucleus ambiguus contributes preganglionic para-sympathetic fibers that innervate the heart. Accordingly, the precise origin of the parasympathetic projection to the heart in humans remains somewhat controversial.
The main actions of the descending fibers of the vagus nerve are to cause bronchoconstriction; a speeding up of peristalsis; a slowing of the cardiac cycle; and increases in secretions of the bronchi, stomach, pancreas, and intestines.
GVA Component. GVA fibers that form afferent branches of the vagus nerve travel with GVE fibers. Therefore, these sensory fibers originate from the same regions of the viscera that receive GVE terminals. These include such regions as the plexus around the abdominal and thoracic viscera, mucosal linings of the larynx, pharynx, soft palate, and esophagus.
GVA fibers also arise from the aortic arch. Stretch receptors in the aortic arch serve as baroreceptors, sensing changes in blood pressure. GVA fibers from the aortic arch as well as other parts of the body viscera have their cell bodies located in the inferior (or nodose) ganglion. Central processes of these neurons then enter the medulla and synapse within the solitary nucleus.
Most sensory inputs into the CNS in association with GVA of the vagus do not reach conscious levels of awareness with the exception of some vague negative or positive feelings, such as those of thirst, hunger, and satiety. These sensory inputs do serve another purpose, such as to provide afferent sources for a variety of reflexes, which ultimately involve activation of the dorsal motor nucleus of the vagus nerve. Several of these reflexes include peristalsis of the stomach and intestines, vomiting, gastric and bronchial secretions (which produce coughing), and changes in the lumen of the lungs. One reflex of considerable importance is the baroreceptor reflex. In this reflex, increases in blood pressure within the aorta activate receptors in the aortic arch. Fibers arising from the aortic arch and whose cell bodies lie in the inferior ganglion transmit signals associated with these changes in aortic pressure to the solitary nucleus. The solitary nucleus, in turn, signals the dorsal motor nucleus of the vagus and the nucleus ambiguus, which then transmit signals to the heart. The result is a l owering of heart rate. However, decreases in blood pressure result in the opposite effects, which are mediated through the same pathway. Note that the glossopharyngeal nerve also contributes to this reflex by relaying visceral sensory signals to the same region of the brainstem from receptors located in the carotid sinus. In this manner, parts of the lower brainstem serve to produce homeostatic regulation of cardiovascular processes.
SVA Component. There are two functional components of SVA fibers. One component is associated with respiratory functions. Receptors that are situated in the aortic body are chemoreceptors that can detect changes in oxygen and carbon dioxide as well as in pH levels within the blood. Therefore, this sensory component of the vagus nerve is classified here as an SVA because the defining property of an SVA neuron is that its receptors are chemoreceptors.1 Similar to GVA neurons, SVA neurons arising from the aortic body have their cell bodies located in the inferior ganglion. Central processes of these neurons enter the lower medulla and synapse upon neurons of the reticular formation located near the solitary nucleus. See the discussion on the SVA component of the glossopharyngeal nerve concerning the functional significance of these SVA inputs.
The second group of SVA neurons is associated with taste. Small groups of taste buds located in the epiglottis and posterior wall of the pharynx serve as receptors for afferent fibers contained with the vagus nerve. Again, cell bodies for these fibers lie within the inferior ganglion, and central processes of this component of the vagus nerve enter the lower brainstem and synapse within the caudal aspect of the solitary nucleus.2 Fibers from the solitary nucleus mediating taste signals ascend to the ventral posteromedial nucleus (VPM) of the thalamus, which, in turn, transmits this information to the ventrolateral aspect (i.e., head region) of the postcentral gyrus.
GSA Component. The vagus nerve also includes a very small GSA component. Receptors (for pain and temperature, pressure, and tactile stimuli) of this component lie in the skin of the back of the ear and external auditory canal. Central processes for this component have their cell bodies located in the superior (or jugular) ganglion of the vagus nerve and enter the lower medulla with the vagus nerve. However, after entering the CNS, these fibers terminate on neurons in the spinal trigeminal nucleus and, thus, from a functional perspective, become part of the trigeminal system in which these signals are transmitted to the cerebral cortex via projections to the VPM of the tha-lamus (see discussion of pathways of the trigeminal system, Fig. 14-6). Clinical Disorders
Damage to the SVE Component. Lesions of the nucleus ambiguus or of peripheral aspects of the vagus nerve cause paralysis of the laryngeal muscles and paresis of the pharynx. The uvula is often deviated toward the normal side, as is the pharynx. Such lesions frequently produce hoarseness and difficulty in swallowing. If the lesions are bilateral, both vocal cords remain in an abducted position, which results in aphonia (loss of voice) and, more importantly, asphyxia, which can be fatal because of constriction of the laryngeal muscles.
Damage to the GVE Component. Hyperactivity of the vagus nerve may result in increased stomach secretions and ulceration of the stomach. Unilateral lesions of the GVE component of the vagus nerve are generally not very noticeable, with the exception of an ipsilateral loss of the carotid sinus baroreflex.
Concerning supranuclear influences, both the dorsal motor nucleus and nucleus ambiguus receive inputs from the cerebral cortex bilaterally. Therefore, unilateral damage of these corticobulbar fibers is generally not noticeable.
Damage to the GVA Component. Lesions of the vagus nerve invariably affect both sensory and motor nerves. Therefore, it is difficult to state the precise effect of lesions limited only to sensory branches of the vagus nerve. However, it is reasonable to conclude that disruption of sensory fibers would certainly alter the cough reflex, vomiting, swallowing, mucous secretions of the gastrointestinal and respiratory tracts, and regulation of respiratory and cardiovascular functions. The presence of a tumor on part of the vagus nerve may have stimulation-like properties and, thus, cause reflex vomiting, coughing, increased secretions within the respiratory pathways, and even fainting.
Glossopharyngeal Nerve (Cranial Nerve IX)
Components:SVE,GVE,GVA,SVA,GSA. The glossopharyngeal nerve is highly similar to the vagus nerve both in its anatomical as well as functional relationships. It is also highly complex and contains the same number of components as the vagus nerve. It has two kinds of motor components. One component innervates the stylopharyngeus muscles, which are derived from mesenchyme (i.e., third branchial arch), and is, therefore, classified as SVE. Axons from this branch innervate the (stylopharyngeus) muscles of the pharynx. The second component, a GVE, is a preganglionic para-sympathetic neuron that is associated with the process of salivation. Of the three sensory components, the GVA division transmits information from carotid sinus barore-ceptors to the medulla, the SVA division transmits changes in blood gases and pH sensed by the carotid body and taste signals from the posterior tongue to the medulla, and the GSA component transmits somatosensory inputs from the back of the ear to the medulla (Fig. 14-7).
FIGURE 14-7 The diagram illustrates the origin and distribution of sensory, motor, and autonomic branches of the glossopharyngeal nerve. The diagram also illustrates the anatomical arrangement of the inferior and superior ganglia associated with the peripheral sensory fibers that enter the brain through the glossopharyngeal and vagus nerves (cranial nerve [CN] IX and X, respectively). Cross section of the medulla shown in the "face" illustrates the principal sensory and motor nuclei associated with the glossopharyngeal nerve.
SVE Component. The rostral half of the nucleus ambiguus contains the cell bodies of origin of the SVE component of the glossopharyngeal nerve in contrast to the caudal half of the nucleus ambiguus, which gives rise to vagal efferent fibers (Fig. 14-7). SVE fibers of the glossopharyn-geal nerve pass laterally from the nucleus ambiguus to exit the brain. They exit the skull through the jugular foramen and innervate the stylopharyngeus muscle. Upon contraction, this muscle elevates the upper part of the pharynx, which occurs during speech and swallowing. GVE Component. The GVE component of the glossopharyn-geal nerve arises from the inferior salivatory nucleus, which
is located within the reticular formation of the medulla (Fig. 14-7). These are preganglionic parasympathetic neurons that innervate the otic ganglion. The otic ganglion gives rise to short postganglionic parasympathetic neurons that innervate the parotid gland. Thus, the function of the GVE component is to stimulate the parotid gland to release saliva.
GVA Component. Baroreceptors constitute the GVA component of the glossopharyngeal nerve and are located in the carotid sinus. Like those found in the aortic arch in association with the vagus nerve, these glossopharyngeal affer-ents respond to changes in blood pressure. The cell bodies for these sensory fibers lie in the inferior (or petrosal) ganglion, and the central processes enter the brainstem and synapse within the solitary nucleus.3
As noted earlier, the solitary nucleus synapses with the dorsal motor nucleus of the vagus nerve and nucleus ambiguus. In this manner, increases in blood pressure activate a reflex mechanism similar to that described earlier for the vagus nerve. Here, stretch receptors in the carotid sinus trigger impulses along the GVA component of the glossopharyngeal nerve, which then causes neurons in the solitary nucleus to discharge. Stimulation of the solitary nucleus causes activation of neurons in the dorsal motor nucleus of the vagus and nucleus ambiguus, thus resulting in a vagal slowing of the heart. This is called the carotid sinus baroreflex.
SVA Component. Similar to the vagus nerve, the glossopharyngeal nerve contains two functionally different types of SVA fibers. The receptors for one group of fibers are located in the carotid body. They are chemoreceptors and respond to changes in blood levels of carbon dioxide and oxygen and pH. Such changes are conveyed by first-order sensory affer-ents toward the brainstem. The cell bodies lie in the inferior ganglion and their central processes enter the brainstem and synapse in caudal parts of the solitary nucleus. When there is an increase in carbon dioxide levels within the blood, afferent fibers within the glossopharyngeal nerve discharge and ultimately activate reticulospinal neurons within the reticular formation. These fibers descend to the spinal cord and synapse upon ventral horn cells of the cervical cord (C3-C5) whose axons form the phrenic nerve, which innervates the muscles of the diaphragm. Thus, activation of SVA afferents of the glossopharyngeal nerve can cause reflex contraction of the diaphragm, which results in increased respiratory frequency and reduction in the levels of carbon dioxide within the blood. This reflex is called the carotid body (chemo) reflex and functions in concert with similar receptor mechanisms associated with the vagus nerve.
A second group of SVA fibers are associated with taste sensation from the posterior third of the tongue. Activation of taste receptors in this region of the tongue results in a discharge along the afferent limb of the glossopharyngeal nerve whose cell bodies lie in the inferior ganglion. These axons, which synapse within the solitary nucleus, cause activation of an ascending pathway to the VPM of the tha-lamus, which, in turn, activates neurons within the taste-receiving areas of the postcentral gyrus.
GSA Component. GSA afferents arise from the tympanic membrane and skin of the external ear, posterior third of the tongue, eustachian tube, tonsil, and upper part of the pharynx. These afferents have their cell bodies located in the superior ganglion and convey somatosensory information, including pain sensation, to the brainstem and, ultimately, to the cerebral cortex. Similar to the GSA afferents of the vagus nerve, glossopharyngeal GSA afferents synapse within the spinal nucleus of the trigeminal nerve, and, thus, these somatosensory inputs are conveyed to the thalamus and cortex via the trigeminothalamic pathways.
Clinical Disorders. Damage to the glossopharyngeal nerve can result in a variety of symptoms. Concerning sensory functions, damage to this nerve bilaterally may result in loss of taste and, perhaps, somesthetic sensation from the posterior third of the tongue. Glossopharyngeal neuralgia (i.e., severe pain in the region of the distribution of this nerve) may also occur in patients after chewing or swallowing.
With respect to motor functions, damage to this nerve would result in a weakness of the muscles of the pharynx and would impair reflexes dependent upon these muscles, such as the gag, uvular, and palatal reflexes. In fact, glos-sopharyngeal function may be tested by determining whether the gag reflex can be elicited in response to stroking of the pharynx wall. Damage to this nerve would also affect its GVE component, resulting in a loss of secretion from the parotid gland. Because the descending corticobulbar fibers provide bilateral innervation to the motor neurons in the brainstem, unilateral lesions of the cerebral cortex have little effect upon reflex functions of the glossopharyngeal nerve.
Vestibulocochlear Nerve (Cranial Nerve VIII)
This nerve, which enters the brainstem at the level of the cerebellopontine angle of the upper medulla, is classified as SSA because the receptors are highly specialized, in that they convey auditory and vestibular signals to the CNS.