The Cranial Nerves (Organization of the Central Nervous System) Part 3

Cranial Nerves of the Pons and Midbrain

Facial Nerve (Cranial Nerve VII)

Components:SVE,GVE,SVA,GSA. The facial nerve is also a mixed nerve. It contains two types of motor components and two types of sensory components. Because this is the nerve of the second branchial arch and innervates muscles derived from the mesenchyme of this arch, it is classified as SVE. The GVE components serve as preganglionic parasympathetic neurons that are associated with a number of different processes, such as salivation, lacrima-tion, and secretion of mucous membranes within the nasal cavity. The SVA component is associated with the transmission of signals from the tongue to the brain, and the GSA component conveys somesthetic inputs to the brain from the region of the back of the ear and external auditory meatus.

SVE Component. The motor nucleus of the facial nerve is found in the ventrolateral aspect of the tegmentum of the lower pons. Its axons take an aberrant course to exit the brainstem. They initially ascend in a dorsomedial direction to the region of the floor of the fourth ventricle. They then pass laterally over the abducens nucleus (CN VI) and descend in a ventrolateral trajectory, exiting the brainstem at the level of the caudal border of the pons (Fig. 14-8). Upon exiting the brain, fibers of the facial nerve enter the internal acoustic meatus and petrous portion of the temporal bone. The fibers then continue along and through the facial canal and, ultimately, exit the skull through the sty-lomastoid foramen. SVE fibers divide into a number of branches and supply the muscles of facial expression (i.e., buccinator muscle [region of the cheek] and frontalis and orbicularis oris muscles [upper part of face]) as well as the auricular, posterior belly of the digastric, stylohyoid, platysma, and stapedius muscles.


 Diagram illustrates: (1) the special visceral afferent pathway for taste inputs to the brain from the anterior two thirds of the tongue via the facial (VII) nerve; and (2) general visceral efferent pathway to the lac-rimal, pterygopalatine, nasal, palatine, and salivary glands from cranial nerve (CN) VII. Not shown is the distribution of fibers to the muscles of facial expression contained in the motor root for the special visceral efferent component of CN VII. Sup. = superior; fasc. = fasciculus; N = nerve.

FIGURE 14-8 Diagram illustrates: (1) the special visceral afferent pathway for taste inputs to the brain from the anterior two thirds of the tongue via the facial (VII) nerve; and (2) general visceral efferent pathway to the lac-rimal, pterygopalatine, nasal, palatine, and salivary glands from cranial nerve (CN) VII. Not shown is the distribution of fibers to the muscles of facial expression contained in the motor root for the special visceral efferent component of CN VII. Sup. = superior; fasc. = fasciculus; N = nerve.

The major function of the SVE component is to control the muscles of facial expression. Several other actions include reflex closing of the eyelids upon touching the cornea,and reflex contraction of the stapedius muscle following a loud noise.

GVE Component. The GVE component of the facial nerve arises from the superior salivatory nucleus located in the reticular formation of the lower pons (Fig. 14-8). Pregan-glionic neurons exit the brain in the intermediate nerve, which emerges between the facial and auditory-vestibular nerves. The nerve breaks into two divisions. One branch joins the chorda tympani and then the lingual nerve and, ultimately, synapses in the submandibular ganglion. Post-ganglionic parasympathetic fibers arise from the sub-mandibular ganglion and supply the submandibular and sublingual glands. Other preganglionic fibers in the intermediate nerve join the major petrosal nerve and terminate in the pterygopalatine ganglion. From this ganglion, post-ganglionic parasympathetic fibers arise and supply the lac-rimal, nasal, and palatine glands.

Activation of the GVE components induces salivation from the submandibular and sublingual glands and secretion from the lacrimal and mucous glands of the nasal and oral cavities. Lesions of the intermediate nerve commonly produce disturbances in secretion of saliva and lacrimal secretion.

SVA Component. SVA neurons convey taste sensation from the anterior two thirds of the tongue to the CNS. The cell bodies for these neurons lie in the geniculate ganglion, and the peripheral processes run in the lingual and chorda tympani nerves. Centrally, they pass into the brainstem through the intermediate nerve and terminate in the rostral half of the solitary nucleus. Taste information is transmitted from the solitary nucleus to the nucleus VPM of the thalamus and from the VPM to the taste-receiving regions of the lateral parts of the postcentral gyrus.

GSA Component. As indicated earlier, the facial nerve also contains a small GSA component, which conveys cutaneous sensation from the back of the ear and external auditory meatus.4 The cell bodies lie in the geniculate ganglion, and the central processes enter the CNS through the intermediate nerve. Once these fibers have entered the CNS, they then enter the spinal tract of the trigeminal nerve and synapse upon neurons of the spinal trigeminal nucleus. In this manner, cutaneous sensation originating from the facial nerve is transmitted to the cerebral cortex via the trigeminal system in a manner similar to that described earlier for GSA inputs from the vagus and glossopharyngeal nerves.

Clinical Disorders

Upper Motor Neurons. Corticobulbar fibers provide bilateral inputs to the dorsal half of the motor nucleus of the facial nerve. However, inputs to more ventral aspects of this nucleus, whose axons innervate facial muscles below the forehead, are from the contralateral cerebral cortex. Therefore, the muscles of the forehead (i.e., frontalis and orbicularis oculi) are generally not affected by a frontal cortical lesion. Individuals can typically wrinkle their foreheads and close their eyes with unilateral lesions of the cerebral cortex. On the other hand, as a result of supranuclear lesions, patients will not be able to raise the corners of their mouths or move their lips contralateral to the lesions. Thus, this distinction is characteristic of an upper motor neuron lesion with respect to the facial nerve and clearly different from a lower motor neuron lesion of this cranial nerve (described in the following section).

Lower Motor Neurons. A lower motor neuron paralysis may result from damage to the facial nerve, its peripheral branches, or the facial nucleus. The patient shows little or no facial expression. If muscle tone is lost, the affected side of the face may take on the appearance of an empty, smooth, mask-like expression. The angle of the mouth on the affected side may also droop, and, when attempting to display their teeth, patients cannot bring the angle of the mouth laterally. Speech may also be affected, and patients are unable to whistle. These patients also cannot close the affected eye, and the eye-blink reflex is lost. Moreover, lesions of the facial nerve can also produce hyperacusis, which is an increase in sensitivity to sounds on the side of the lesion, because of a paralysis of the stapedius muscle.

These effects are commonly due to an external blow to the face or overexposure to cold weather and affect peripheral branches of the facial nerve after the nerve exits the skull. These disorders are commonly referred to as Bell’s palsy.

The effects of damage to the facial nerve upon sensory systems include primarily loss of taste sensation from the anterior two thirds of the tongue and loss of general sensation from the back of the ear and external auditory meatus.

Trigeminal Nerve (Cranial Nerve V)

Components: GSA, SVE. The trigeminal nerve is very large and can be easily seen upon its emergence at the level of the middle of the pons near the position of emergence of the middle cerebellar peduncle. It contains a massive GSA component, which provides most of the somatosensory inputs from the region of the anterior two thirds of the head (i.e., pain, touch, pressure, temperature) to the CNS. The SVE component, which innervates skeletal muscle from the mesenchyme of the first branchial arch, is much smaller in size than the sensory branches but provides motor innervation of the muscles of mastication.

GSA: Origin, Distribution, and Function. The cell bodies of the GSA component of the trigeminal nerve are located in the trigeminal (also called the Gasserian or semilunar) ganglion. The ganglion itself is located on a cleft of the petrous bone lateral to the cavernous sinus. There are three principal divisions of the sensory components of the trigeminal nerve: ophthalmic, maxillary, and mandibular (Fig. 14-9A). Concerning the peripheral distribution of the ophthalmic division, nerve fibers supply the forehead, cornea, upper part of the eyelid, dorsal surface of the nose, and mucous membranes of the nasal and frontal sinuses. The central processes of this branch enter the skull through the superior orbital fissure. The peripheral distribution of the maxillary division includes the lateral surface of the nose; upper teeth; hard palate; upper cheek; and mucous membranes of the upper teeth, nose, and roof of the mouth. This division enters the skull through the foramen rotundum. The third division, called the mandibular division, supplies the lower jaw, lower teeth, chin, parts of the posterior cheek, temple, external ear, anterior two thirds of the tongue, and floor of the mouth. All branches of the trigeminal nerve innervate the dura. The mandibular division enters the skull through the foramen ovale.

(A) Distribution of the sensory (general somatic afferent) and motor (special visceral efferent) components of the trigeminal nerve, including the sensory arrangement of the sensory divisions of the trigeminal nerve.

FIGURE 14-9 (A) Distribution of the sensory (general somatic afferent) and motor (special visceral efferent) components of the trigeminal nerve, including the sensory arrangement of the sensory divisions of the trigeminal nerve.

(B) Organization and distribution of the central trigeminal pathways from the periphery to the cerebral cortex. Fibers conveying pain and thermal sensations are indicated in red; fibers conveying tactile and pressure sensations are indicated in blue; the motor root is indicated in black on the left side of figure, and the ascending lateral spinothalamic tract is shown in black on the right side of figure.

FIGURE 14-9 (B) Organization and distribution of the central trigeminal pathways from the periphery to the cerebral cortex. Fibers conveying pain and thermal sensations are indicated in red; fibers conveying tactile and pressure sensations are indicated in blue; the motor root is indicated in black on the left side of figure, and the ascending lateral spinothalamic tract is shown in black on the right side of figure.

As noted earlier, the central processes of each of the divisions of the trigeminal nerve enter the skull through different foramina. However, upon entry into the pons, these (first-order) fibers may take one of two primary directions: (1) they may synapse directly within the main sensory nucleus of CN V; or (2) the fibers may enter the tract of CN V and descend to different levels of the lower pons and medulla and then make a synapse within the spinal nucleus of CN V. Some trigeminal pain fibers associated with the posterior aspect of the face may even extend as far caudally as C2 of the spinal cord. From both the main sensory and spinal nucleus, second-order neurons arise, and their axons are distributed to the VPM of the contralateral thalamus. Fibers that arise from the spinal nucleus are distributed to the contralateral VPM via the ventral trigemi-nothalamic tract. Fibers that issue from the main sensory nucleus are distributed bilaterally to the VPM. Those fibers that pass ipsilaterally do so in the dorsal trigeminothalamic tract, whereas fibers passing contralaterally do so in the ventral trigeminothalamic tract. Collectively, it would certainly appear that the ventral trigeminothalamic tract is far more significant in transmitting sensory information from the trigeminal system to the thalamus. Third-order sensory fibers arising from the VPM then project to the ipsilateral face region of the postcentral gyrus (Fig. 14-9B).

Both experimental and clinical studies have revealed that the fibers mediating pain and temperature sensation are distributed to the caudal aspect of the spinal nucleus, whereas conscious proprioception, pressure, and tactile sensation are distributed through the main sensory nucleus and possibly parts of the spinal nucleus. Knowledge of the dissociation of pain fibers from other forms of somatosen-sory inputs has been applied clinically; for example, severing the sensory root fibers after they enter the spinal tract of CN V can alleviate intense forms of trigeminal neuralgia.

The receptors for some of the fibers contained within the mandibular branch are muscle spindles. These fibers mediate unconscious proprioceptive signals to the brain and terminate in the mesencephalic nucleus of CN V, which represents part of the first-order sensory neuron. For this reason, the unusual feature is that the mesencephalic nucleus, which appears to be similar in appearance to cells of the Gasserian ganglion, does not lie outside the CNS but, instead, is situated within it. Although the mesen-cephalic nucleus is functionally similar to the dorsal root ganglion, it represents an anomaly in that it is the only sensory structure whose first-order cell bodies lie within the CNS and not in the periphery. Similar to neurons of the dorsal root ganglion, there is a second limb of the axon emanating from the mesencephalic nucleus, which transmits signals away from it to the motor nucleus of CN V. This provides the basis for a monosynaptic reflex that is sometimes referred to as the jaw-jerk reflex. This is a stretch reflex because it occurs after stimulation of muscle spindles in the masseter muscle of the lower jaw. Afferent impulses (1a fibers) cause a discharge of neurons in the motor nucleus, which is then followed by a jaw-closing response. Other fibers from the mesencephalic nucleus project to the cerebellum, thus providing the cerebellum with information concerning the status of muscles of the lower jaw.

From this discussion, it is reasonable to conclude that fibers of the trigeminal system share parallel relationships with several of the sensory pathways of the spinal cord. For example, the pathways that mediate pain and temperature sensation from the head to the thalamus via the ventral trigeminothalamic tract can be likened to the lateral spi-nothalamic tract, the pathways that mediate conscious proprioception and tactile inputs to the thalamus via the dorsal trigeminothalamic tract can be likened to the medial lemniscus, and the pathway involving inputs to the mesencephalic nucleus and its projection to the cerebellum shares similarities with the posterior spinocerebel-lar tract. In this manner, the same kinds of sensory inputs that reach the brain from the body region can also reach the brain from the region of the head by virtue of specific ascending pathways within the trigeminal complex.

SVE: Origin, Distribution, and Function. The motor trigeminal nucleus is located just medial to the main sensory nucleus of CN V and is separated from it by root fibers of the trigeminal nerve (Fig. 14-9B). Axons of the motor nucleus pass in a ventrolateral direction and exit the brain at the approximate level of entry of the sensory fibers. Motor fibers exit the skull through the foramen ovale and supply the muscles of mastication (i.e., masseter, pterygoid, tempora-lis, and mylohyoid muscles). The main functions of these muscles are to produce chewing and biting responses (see earlier description of jaw-jerk reflex). The motor nucleus receives bilateral inputs from the cerebral cortex. Therefore, motor deficits following a unilateral upper motor neuron lesion are generally not observed.

Clinical Disorders. Because the trigeminal nerve contains both motor and sensory components, dysfunctions of either component may result from lesions of this nerve. If there is a paralysis or paresis affecting the muscles of mastication, they will become flaccid after showing spasticity. Moreover, if the patient is asked to open his or her mouth, and the pterygoid muscles are affected, then the jaw will deviate to the affected side.

Concerning the sensory components, applying pain, tactile, or temperature stimuli to the area in question can test for damage to any of the sensory branches. Failure to recognize any of these stimuli would indicate a sensory loss to the affected area. If sensory loss includes the ophthalmic branch, then it is likely that the corneal reflex (i.e., blinking in response to touching the cornea, which involves reflex connections between sensory afferent fibers in the ophthalmic nerve that make synaptic connections with motor fibers of CN VII) will be lost. Severe pain can result from irritation of the trigeminal nerve by such factors as inflammation, tumor, or vascular lesion. This is called trigeminal neuralgia (sometimes called tic douloureux) and is often localized to a portion of one side of the face (usually associated with a specific branch of the trigeminal nerve that is subject to such irritation). Neurologic pain may also occur in association with the viral disease, herpes zoster (shingles), affecting mainly the ophthalmic division of the trigeminal nerve, called ophthalmic zoster.

Sensory loss does not only result from peripheral nerve damage. It may result from damage to the CNS as well. For example, a lesion resulting from an occlusion of the posterior inferior cerebellar artery involves the lateral aspect of the medulla; the ensuing disorder is Wallenberg’s syndrome. This will produce (in addition to some problems with eating) damage to both the lateral spinothalamic tract as well as to the spinal trigeminal tract and nucleus. Accordingly, there will be a loss of pain and temperature sensation on the ipsilateral side of the face and contralat-eral side of the body.

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