Cranial Nerve I: Olfactory Nerve
The true olfactory nerves are short connections that project from the olfactory mucosa within the nose and the olfactory bulb within the cranial cavity (Fig 8–2; see also Chapter 19). There are 9 to 15 of these nerves on each side of the brain. The olfactory bulb lies just above the cribriform plate and below the frontal lobe (nestled within the olfactory sulcus). Axons from the olfactory bulb run within the olfactory stalk, synapse in the anterior olfactory nucleus, and terminate in the primary olfactory cortex (pyriform cortex) as well as the entorhinal cortex and amygdala.
Lateral view of the olfactory bulb, tract, mucous membrane, and nerves.
Cranial Nerve II: Optic Nerve
The optic nerve contains myelinated axons that arise from the ganglion cells in the retina. As noted above, axons within the optic nerve are myelinated by oligodendrocytes. The optic nerve passes through the optic papilla to the orbit, where it is contained within meningeal sheaths. The nerve changes its name to optic tract when the fibers have passed through the optic chiasm (Fig 8–3). Optic tract axons project to the superior colliculus and to the lateral geniculate nucleus within the thalamus, which relays visual information to the cortex (see Chapter 15).
Horizontal section through the head at the level of the orbits.
Cranial Nerve III: Oculomotor Nerve
Cranial nerves III, IV, and VI work together to control eye movements and are therefore discussed together. In addition, cranial nerve III controls pupillary constriction.
The oculomotor nerve (cranial nerve III) contains axons that arise in the oculomotor nucleus (which innervates all of the oculomotor muscles except the superior oblique and lateral rectus) and the nearby Edinger–Westphal nucleus (which sends preganglionic parasympathetic axons to the ciliary ganglion). The oculomotor nerve leaves the brain on the medial side of the cerebral peduncle, behind the posterior cerebral artery and in front of the superior cerebellar artery. It then passes anteriorly, parallel to the internal carotid artery in the lateral wall of the cavernous sinus, leaving the cranial cavity by way of the superior orbital fissure.
The somatic efferent portion of the nerve innervates the levator palpebrae superioris muscle; the superior, medial, and inferior rectus muscles; and the inferior oblique muscle (Fig 8–4). The visceral efferent portion innervates two smooth intraocular muscles: the ciliary and the constrictor pupillae.
The oculomotor, trochlear, and abducens nerves; ocular muscles.
Anosmia (absence of the sense of smell) can result from disorders (eg, viral infections, such as the common cold) involving the nasal mucosa. The tiny olfactory nerves and bulbs can be injured as a result of head trauma. The location of the olfactory bulb and stalk, below the frontal lobe, predisposes them to compression from frontal lobe tumors and olfactory groove meningiomas.
Cranial Nerve IV: Trochlear Nerve
The trochlear nerve is the only crossed cranial nerve. It originates from the trochlear nucleus, which is a group of specialized motor neurons located just caudal to (and actually constituting a subnucleus of) the oculomotor nucleus within the lower midbrain. Trochlear nerve axons arise from these neurons, cross within the midbrain, and then emerge contralaterally on the dorsal surface of the brain stem. The trochlear nerve then curves ventrally between the posterior cerebral and superior cerebellar arteries (lateral to the oculomotor nerve). It continues anteriorly in the lateral wall of the cavernous sinus and enters the orbit via the superior orbital fissure. It innervates the superior oblique muscle (see Fig 8–4).
Note: Because nerves III, IV, and VI are generally grouped together for discussion, nerve V is discussed after nerve VI.
Cranial Nerve VI: Abducens Nerve
The abducens nerve arises from neurons of the abducens nucleus located within the dorsomedial tegmentum within the caudal pons. These axons project through the body of the pons and leave it as the abducens nerve. This nerve emerges from the pontomedullary fissure, passes through the cavernous sinus close to the internal carotid, and exits from the cranial cavity via the superior orbital fissure. Its long intracranial course makes it vulnerable to pathologic processes in the posterior and middle cranial fossae. The nerve innervates the lateral rectus muscle (see Fig 8–4).
A few sensory (proprioceptive) fibers from the muscles of the eye are present in nerves III, IV, and VI and in some other nerves that innervate striated muscles. The central termination of these fibers is in the mesencephalic nucleus of V (see Chapter 7 and Fig 7–8).
B. Action of the External Eye Muscles
The actions of eye muscles operating singly and in tandem are shown in Tables 8–3 and 8–4 (Fig 8–5). The levator palpebrae superioris muscle has no action on the eyeball but lifts the upper eyelid when contracted. Closing the eyelids is performed by contraction of the orbicular muscle of the eye; this muscle is innervated by nerve VII.
TABLE 8–3Functions of the Ocular Muscles. ||Download (.pdf) TABLE 8–3 Functions of the Ocular Muscles.
|Muscle ||Primary Action ||Secondary Action |
|Lateral rectus ||Abduction ||None |
|Medial rectus ||Adduction ||None |
|Superior rectus ||Elevation ||Adduction, intorsion |
|Inferior rectus ||Depression ||Adduction, extorsion |
|Superior oblique ||Depression ||Intorsion, abduction |
|Inferior oblique ||Elevation ||Extorsion, abduction |
TABLE 8–4Yoke Muscle Combinations. ||Download (.pdf) TABLE 8–4 Yoke Muscle Combinations.
|Cardinal Direction of Gaze ||Yoke Muscles |
|Eyes up, right ||Right superior rectus and left inferior oblique |
|Eyes right ||Right lateral rectus and left medial rectus |
|Eyes down, right ||Right inferior rectus and left superior oblique |
|Eyes down, left ||Right superior oblique and left inferior rectus |
|Eyes left ||Right medial rectus and left lateral rectus |
|Eyes up, left ||Right inferior oblique and left superior rectus |
Diagram of eye muscle action.
C. Control of Ocular Muscle Movements
The oculomotor system activates the various extraocular muscles in a highly coordinated manner. When the eyes scan the environment, they do so in short, rapid movements called saccades. When a target moves, a different form of ocular movement—smooth pursuit—is used to keep the image in sharp focus. When the head or body moves unexpectedly (eg, when one is jolted), reflex movements of the head and eye muscles compensate and maintain fixation on the visual target. This compensatory function is achieved by the vestibulo-ocular reflex (see Chapter 17).
The six individual muscles that move one eye normally act together with the muscles of the other eye in controlled movement. Both eyes move in the same direction to follow an object in space, but they move by simultaneously contracting and relaxing different muscles; this is called a conjugate gaze movement. Fixating on a single point is called vergence, which requires a different set of muscles, including the intraocular muscles. Each of the extraocular muscles is brought into play in conjugate gaze movements or vergence.
1. Gaze and vergence centers
Conjugate gaze and vergence are controlled from three areas in the brain stem. There are two lateral gaze centers in the paramedian pontine reticular formation near the left and right abducens nuclei and a vergence center in the pretectum just above the superior colliculi. Each of these three areas can be activated during head movement by the vestibular system via the medial longitudinal fasciculus (see Chapter 17). Activation of the lateral gaze center on the right produces conjugate gaze to the right and vice versa. Regions in the contralateral frontal lobe (the eye field area) influence voluntary eye movements via polysynaptic connections to the lateral gaze centers, whereas regions in the occipital lobe influence visual pursuit and also have connections with the vergence center (Fig 8–6).
Brain circuitry controlling right conjugate gaze. The command for voluntary conjugate movements in right lateral gaze originates in the frontal eye fields in the left frontal lobe. This command excites a lateral gaze control center, adjacent to the abducens nucleus, within the paramedian pontine reticular formation on the right side. This, in turn, activates the abducens nucleus on the right, turning the right eye to the right, and projects via the median longitudinal fasciculus to the oculomotor nucleus on the left, which turns the left eye to the right. (Reproduced, with permission, from Aminoff ML, Greenberg DA, Simon RP: Clinical Neurology. 6th ed. McGraw-Hill, 2005.)
Activity in each of the lateral gaze centers (located in the paramedian pontine reticular formation on each side, adjacent to the abducens nuclei) controls eye movements to the ipsilateral side. Thus, the lateral gaze center on the right is connected, via excitatory projections, to the right abducens nucleus that activates the lateral rectus muscle responsible for abduction of the right eye. The right-sided lateral gaze center also sends projections, via the medial longitudinal fasciculus, to the contralateral (left-sided) oculomotor nucleus, where they form excitatory synapses on oculomotor neurons innervating the medial rectus muscle. (This muscle is responsible for movement of the left eye across the midline to the right.) As a result of this arrangement, activation of the right-sided lateral gaze center results in movement of both eyes to the right (see Fig 8–6).
This arrangement also provides an anatomic basis for reflexes involving eye movements, such as the vestibulo-ocular reflex. Sudden rotation of the head to the left results in movement of endolymph within the semicircular canals, whose neurons project to the vestibular nuclei (see Fig 8–6). These nuclei, in turn, send excitatory projections via the medial longitudinal fasciculus to the right-sided lateral gaze center (and also send inhibitory projections to the left-sided lateral gaze center). Increased activity in the right-sided lateral gaze center triggers eye movements to the right, stabilizing the image on the retina.
2. Control of pupillary size
The diameter of the pupil is affected by parasympathetic efferent fibers in the oculomotor nerve and sympathetic fibers from the superior cervical ganglion (Fig 8–7). Constriction (miosis) of the pupil is caused by the stimulation of parasympathetic fibers, whereas dilation (mydriasis) is caused by sympathetic activation. Both pupils are normally affected simultaneously by one or more of such causes as emotion, pain, drugs, and changes in light intensity and accommodation.
The pupillary light reflex is a constriction of both eyes in response to a bright light. Even if the light hits only one eye, both pupils usually constrict; this is a consensual response. The pathways for the reflex include optic nerve fibers (or their collaterals) to the pretectum, a nuclear area between thalamus and midbrain (Fig 8–8). Short fibers go from the pretectum to both Edinger–Westphal nuclei (the visceral components of the oculomotor nuclei) by way of the posterior commissure and to both ciliary ganglia by way of the oculomotor nerves. Postganglionic parasympathetic fibers to the constrictor muscles are activated, and the sympathetic nerves of the dilator muscle are inhibited.
The path of the pupillary light reflex.
The accommodation reflex involves pathways from the visual cortex in the occipital lobe to the pretectum. From here, fibers to all nuclei of nerves III, IV, and VI cause vergence of the extraocular muscles as well as parasympathetic activation of the constrictor and ciliary muscles within each eye.
D. Clinical Correlations for Nerves III, IV, and VI and Their Connections
Clinical findings include strabismus, diplopia, and ptosis. Strabismus (squint) is the deviation of one or both eyes. In internal strabismus, the visual axes cross each other; in external strabismus, the visual axes diverge from each other. Diplopia (double vision) is a subjective phenomenon reported to be present when the patient is, usually, looking with both eyes; it is caused by misalignment of the visual axes. Ptosis (lid drop) is caused by weakness or paralysis of the levator palpebrae superioris muscle; it is seen with lesions of nerve III and sometimes in patients with myasthenia gravis.
2. Classification of ophthalmoplegias
Lesions that cause ophthalmoplegia (paralysis) of nerves III, IV, and VI may be central or peripheral (Table 8–5).
TABLE 8–5Paralyses of Individual Eye Muscles.* ||Download (.pdf) TABLE 8–5 Paralyses of Individual Eye Muscles.*
|Muscle ||Nerve ||Deviation of Eyeball ||Diplopia Present When Looking* ||Direction of Image |
|Medial rectus ||III ||Outward (external squint) ||Toward nose ||Vertical |
|Superior rectus ||III ||Downward and inward ||Upward and outward ||Oblique |
|Inferior rectus ||III ||Upward and inward ||Downward and outward ||Oblique |
|Inferior oblique ||III ||Downward and outward ||Upward and inward ||Oblique |
|Superior oblique ||IV ||Upward and outward ||Downward and inward ||Oblique |
|Lateral rectus ||VI ||Inward (internal squint) ||Toward temple ||Vertical |
a. Oculomotor (nerve III) paralysis—External ophthalmoplegia is characterized by divergent strabismus, diplopia, and ptosis. The eye deviates downward and outward. Internal ophthalmoplegia is characterized by a dilated pupil and loss of light and accommodation reflexes. There may be paralysis of individual muscles of nerve III, as shown in Table 8–5.
Isolated involvement of nerve III (often with a dilated pupil) occurs as an early sign in uncal herniation because of expanding hemispheric mass lesions that compress the nerve against the tentorium. Nerve III crosses the internal carotid, where it joins the posterior communicating artery; aneurysms of the posterior communicating artery thus can compress the nerve. Isolated nerve III palsy also occurs in diabetes, presumably because of ischemic damage, and when caused by diabetes, often spares the pupil (Fig 8–9).
Left-sided oculomotor (third nerve) palsy in a patient with diabetes. There is failure of adduction of the left eye, ptosis of the left eyelid, and normal pupillary function. (Reproduced, with permission, from Riordan-Eva P, Witcher JP: Vaughan & Asbury's General Ophthalmology. 17th ed. McGraw-Hill, 2008.)
b. Trochlear (nerve IV) paralysis—This rare condition is characterized by slight convergent strabismus and diplopia on looking downward. The patient cannot look downward and inward and hence has difficulty in descending stairs. The head is tilted as a compensatory adjustment; this may be the first indication of a trochlear lesion.
c. Abducens (nerve VI) paralysis—This eye palsy is the most common owing to the long course of nerve VI. There is weakness of eye abduction. Features of abducens paralysis include convergent strabismus and diplopia.
d. Internuclear ophthalmoplegia—Lesions of the medial longitudinal fasciculus (rostral to the abducens nuclei) interfere with conjugate movements of the eyes. A unilateral lesion of the median longitudinal fasciculus on the left, for example, produces a syndrome in which, when the patient attempts to look to the right, the left eye fails to adduct. This is because ascending influences, from the right-sided lateral gaze center, can no longer reach the left-sided oculomotor nucleus (see Fig 8–6). There is usually nystagmus (rapid, jerking movements) in the abducting eye (ie, the eye looking right). The impaired adduction of the left eye is not due to weakness of the medial rectus (because the muscle can be activated during convergence) but rather reflects disconnection of the oculomotor nucleus from the contralateral lateral gaze center. This syndrome is called internuclear ophthalmoplegia. Unilateral internuclear ophthalmoplegia is often seen as a result of ischemic disease of the brain stem; bilateral internuclear ophthalmoplegia can be seen in patients with multiple sclerosis.
Cranial Nerve V: Trigeminal Nerve
The trigeminal nerve, shown in Figure 8–10, contains a large sensory root, which carries sensation from the skin and mucosa of most of the head and face, and a smaller motor root, which innervates most of the chewing muscles (masseter, temporalis, pterygoids, mylohyoid), and the tensor tympani muscle of the middle ear.
The trigeminal nerve and its branches.
The efferent fibers of the nerve (the minor portion) originate in the motor nucleus of V in the pons; this cell group receives bilateral input from the corticobulbar tracts and reflex connections from the spinal tract of nerve V and controls the muscles involved in chewing.
The sensory root (the main portion of the nerve) arises from cells in the semilunar ganglion (also known as the gasserian, or trigeminal, ganglion) in a pocket of dura (Meckel's cavity) lateral to the cavernous sinus. It passes posteriorly between the superior petrosal sinus in the tentorium and the skull base and enters the pons.
Fibers of the ophthalmic division enter the cranial cavity through the superior orbital fissure. Fibers of the maxillary division pass through the foramen rotundum. Sensory fibers of the mandibular division, joined by the motor fibers involved in mastication, course through the foramen ovale.
Trigeminal nerve fibers carrying light touch project to the main (principal) trigeminal nucleus (see Fig 7–8). After synapsing, this pathway passes from the nerve's main sensory nucleus via crossed fibers in the ventral trigeminothalamic tract and via uncrossed fibers in the dorsal trigeminothalamic tract to the ventral posteromedial (VPM) nuclei of the thalamus and higher centers. Pain and temperature fibers in the trigeminal nerve enter the brain stem, turn caudally, and descend for a short distance within the spinal tract of V. These fibers then synapse with secondary neurons in the spinal nucleus of V. From there, the pathway passes to the thalamus via the ventral trigeminothalamic tract. Proprioceptive fibers in the trigeminal nerve project to the mesencephalic trigeminal nucleus (mesencephalic nucleus of V), where their cell bodies are located. Collaterals project to the motor nucleus of V. The reflex connections pass to the cerebellum and the motor nuclei of cranial nerves V, VII, and IX.
The sensory distribution of the divisions of the face is shown in Figure 8–11 and Table 8–6.
Sensory distribution of nerve V.
TABLE 8–6Distribution of the Trigeminal Nerve. ||Download (.pdf) TABLE 8–6 Distribution of the Trigeminal Nerve.
|Ophthalmic division |
| Area of skin labeled in Figure 8–12 |
| Cornea, conjunctiva, and intraocular structures (the sclera is |
| innervated by fibers of the anterior branches of the ciliary plexus) |
| Mucosa of paranasal sinuses (frontal, sphenoid, and ethmoid) |
| Mucosa of upper and anterior nasal septum and lateral wall of nasal cavity |
| Lacrimal duct |
|Maxillary division |
| Area of skin labeled in Figure 8–12 |
| Mucosa of maxillary sinus |
| Mucosa of posterior part of nasal septum and lower part of nasal cavity |
| Upper teeth and gum |
| Hard palate |
| Soft palate and tonsil (via sphenopalatine ganglion, greater petrosal nerve, and nervus intermedius) |
|Mandibular division |
| Area of skin labeled in Figure 8–12 |
| Mucosa of the cheek, lower jaw, floor of the mouth, tongue |
| Proprioception from jaw muscles |
| Lower teeth and gum |
| Mastoid cells |
| Muscles of mastication |
The afferent axons for the corneal reflex (in which corneal stimulation evokes a protective blink response) are carried in the ophthalmic branch of nerve V and synapse in the spinal tract and nucleus of V. From there, impulses are relayed to the facial (VII) nuclei, where motor neurons that project to the orbicularis oculi muscles are activated. (The efferent limb of the corneal reflex is thus carried by nerve VII.) The jaw jerk reflex is a monosynaptic (stretch) reflex for the masseter muscle. Rapid stretch of the muscle (elicited gently with a reflex hammer) evokes afferent impulses in Ia sensory axons in the mandibular division of nerve V, which send collaterals to the mesencephalic nucleus of V, which sends excitatory projections to the motor nucleus of V. Both afferent and efferent limbs of the jaw jerk reflex thus run in nerve V.
Symptoms and signs of nerve V involvement include loss of sensation of one or more sensory modalities of the nerve; impaired hearing from paralysis of the tensor tympani muscle; paralysis of the muscles of mastication, with deviation of the mandible to the affected side; loss of reflexes (cornea, jaw jerk, sneeze); trismus (lockjaw); and, in some disorders, tonic spasm of the muscles of mastication.
Because the spinal tract of V is located near the lateral spinothalamic tract in the medulla and lower pons, laterally placed lesions at these levels produce a crossed picture of pain and temperature insensibility on the ipsilateral face and on the contralateral side of the body below the face. This occurs, for example, in Wallenberg's syndrome, in which there is damage to the lateral medulla, usually because of occlusion of the posterior inferior cerebellar artery.
Trigeminal neuralgia is characterized by attacks of severe pain in the distribution of one or more branches of the trigeminal nerve. Although the cause is not always clear, it is known that it can be caused by pressure from a small vessel on the root entry zone of the nerve. Trigeminal neuralgia is also seen in some patients with multiple sclerosis. Pain may follow even gentle stimulation of a trigger zone on the lip, face, or tongue that is sensitive to cold or pressure. Involvement is usually unilateral. Carbamazepine can be helpful in trigeminal neuralgia.
Cranial Nerve VII: Facial Nerve
The facial nerve consists of the facial nerve proper and the nervus intermedius (Fig 8–12). Both parts pass through the internal auditory meatus, where the geniculate ganglion for the taste component lies. The facial nerve proper contains axons that arise in the facial (VII) nucleus. The nerve exits through the stylomastoid foramen; it innervates the muscles of facial expression, the platysma muscle, and the stapedius muscle in the inner ear.
The nervus intermedius sends parasympathetic preganglionic fibers to the pterygopalatine ganglion to innervate the lacrimal gland and, via the chorda tympani nerve to the submaxillary and sublingual ganglia in the mouth, to innervate the salivary glands.
The visceral afferent component of the nervus intermedius, with cell bodies in the geniculate ganglion, carries taste sensation from the anterior two-thirds of the tongue via the chorda tympani to the solitary tract and nucleus. The somatic afferent fibers from the skin of the external ear are carried in the facial nerve to the brain stem. These fibers connect there to the trigeminal nuclei and are, in fact, part of the trigeminal sensory system.
The superior salivatory nucleus receives cortical impulses from the nucleus of the solitary tract via the dorsal longitudinal fasciculus and reflex connections. Visceral efferent axons run from the superior salivatory nucleus via nerve VII to the pterygopalatine and submandibular ganglia. They synapse there with postganglionic parasympathetic neurons that innervate the submandibular and sublingual salivary glands.
The taste fibers run through the chorda tympani and nervus intermedius to the solitary nucleus, which is connected with the cerebral cortex through the medial lemnisci and the VPM nucleus of the thalamus and with the salivatory nucleus and motor nucleus of VII by reflex neurons. The cortical taste area is located in the inferior central (face) region; it extends onto the opercular surface of the parietal lobe and adjacent insular cortex.
The facial nucleus receives crossed and uncrossed fibers by way of the corticobulbar (corticonuclear) tract (see Fig 7–9). The facial muscles below the forehead receive contralateral cortical innervation (crossed corticobulbar fibers only). Therefore, a lesion rostral to the facial nucleus—a central facial lesion—results in paralysis of the contralateral facial muscles except the frontalis and orbicularis oculi muscles. This can occur, for example, as a result of a stroke which damages part of the motor cortex in one cerebral hemisphere. Because the frontalis and orbicularis oculi muscles receive bilateral cortical innervation, they are not paralyzed by lesions involving one motor cortex or its corticobulbar pathways.
The complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper) paralyzes all ipsilateral face muscles; this is equivalent to a peripheral facial lesion. Peripheral facial paralysis (Bell's palsy) can occur as an idiopathic condition, but it is seen as a complication of diabetes and can occur as a result of tumors, sarcoidosis, AIDS, and Lyme disease. When an attempt is made to close the eyelids, the eyeball on the affected side may turn upward.
The symptoms and signs depend on the location of the lesion. A lesion in or outside the stylomastoid foramen results in flaccid paralysis (lower-motor-neuron type) of all the muscles of facial expression in the affected side; this can occur from a stab wound or from swelling of the parotid gland (eg, as seen in mumps). A lesion in the facial canal involving the chorda tympani nerve results in reduced salivation and loss of taste sensation from the ipsilateral anterior two-thirds of the tongue. A lesion higher up in the canal can paralyze the stapedius muscle. A lesion in the middle ear involves all components of nerve VII, whereas a tumor in the internal auditory canal (eg, a schwannoma) can cause dysfunction of nerves VII and VIII.
Cranial Nerve VIII: Vestibulocochlear Nerve
Cranial nerve VIII is a double nerve that arises from spiral and vestibular ganglia in the labyrinth of the inner ear (Fig 8–13). It passes into the cranial cavity via the internal acoustic meatus and enters the brain stem behind the posterior edge of the middle cerebellar peduncle in the pontocerebellar angle. The cochlear nerve is concerned with hearing; the vestibular nerve is part of the system of equilibrium (position sense). The functional anatomy of the auditory system (and its clinical correlations) is discussed in Chapter 16; the vestibular system is discussed in Chapter 17.
The vestibulocochlear nerve.
Cranial Nerve IX: Glossopharyngeal Nerve
Cranial nerve IX contains several types of fibers (Fig 8–14). Branchial efferent fibers from the ambiguus nucleus pass to the stylopharyngeal muscle.
The glossopharyngeal nerve. TP, tympanum plexus; FR, foramen rotundum; FO, foramen ovale.
Visceral efferent (parasympathetic preganglionic) fibers from the inferior salivatory nucleus pass through the tympanic plexus and lesser petrosal nerve to the otic ganglion, from which the postganglionic fibers pass to the parotid gland. The inferior salivatory nucleus receives cortical impulses via the dorsal longitudinal fasciculus and reflexes from the nucleus of the solitary tract.
Visceral afferent fibers arise from unipolar cells in the inferior (formerly petrosal) ganglia. Centrally, they terminate in the solitary tract and its nucleus, which in turn projects to the thalamus (VPM nucleus) and then to the cortex. Peripherally, the visceral afferent axons of nerve IX supply general sensation to the pharynx, soft palate, posterior third of the tongue, fauces, tonsils, auditory tube, and tympanic cavity. Through the sinus nerve, they supply special receptors in the carotid body and carotid sinus that are concerned with reflex control of respiration, blood pressure, and heart rate. Special visceral afferents supply the taste buds of the posterior third of the tongue and carry impulses via the superior ganglia to the gustatory nucleus of the brain stem. A few somatic afferent fibers enter by way of the glossopharyngeal nerve and end in the trigeminal nuclei.
The tongue receives its sensory innervation through multiple pathways: Three cranial nerves contain taste fibers (nerve VII for anterior one-third of tongue; nerve IX for posterior one-third of tongue; nerve X for epiglottis), and the general sensory afferent fibers are mediated by nerve V (Fig 8–15). The central pathway for taste sensation is shown in Figure 8–16.
Sensory innervation of the tongue.
Diagram of taste pathways.
The glossopharyngeal nerve is rarely involved alone by disease processes (eg, by neuralgia); it is generally involved with the vagus and accessory nerves because of its proximity to them. The pharyngeal (gag) reflex depends on nerve IX for its sensory component, whereas nerve X innervates the motor component. Stroking the affected side of the pharynx does not produce gagging if the nerve is injured. The carotid sinus reflex depends on nerve IX for its sensory component. Pressure over the sinus normally produces slowing of the heart rate and a fall in blood pressure.
Cranial Nerve X: Vagus Nerve
Branchial efferent fibers from the ambiguus nucleus contribute rootlets to the vagus nerve and the cranial component of the accessory nerve (XI). Those of the vagus nerve pass to the muscles of the soft palate and pharynx (Fig 8–17). Those of the accessory nerve join the vagus outside the skull and pass, via the recurrent laryngeal nerve, to the intrinsic muscles of the larynx.
The vagus nerve. J, jugular (superior) ganglion; N, nodose (inferior) ganglion.
Visceral efferent fibers from the dorsal motor nucleus of the vagus course to the thoracic and abdominal viscera. Their postganglionic fibers arise in the terminal ganglia within or near the viscera. They inhibit heart rate and adrenal secretion and stimulate gastrointestinal peristalsis and gastric, hepatic, and pancreatic glandular activity (see Chapter 20).
Somatic afferent fibers of unipolar cells in the superior (formerly called the jugular) ganglion send peripheral branches via the auricular branch of nerve X to the external auditory meatus and part of the earlobe. They also send peripheral branches via the recurrent meningeal branch to the dura of the posterior fossa. Central branches pass with nerve X to the brain stem and end in the spinal tract of the trigeminal nerve and its nucleus.
Visceral afferent fibers of unipolar cells in the inferior (formerly nodose) ganglion send peripheral branches to the pharynx, larynx, trachea, esophagus, and thoracic and abdominal viscera. They also send a few special afferent fibers to taste buds in the epiglottic region. Central branches run to the solitary tract and terminate in its nucleus. The visceral afferent fibers of the vagus nerve carry the sensations of abdominal distention and nausea and the impulses concerned with regulating the depth of respiration and controlling blood pressure. The ambiguus nucleus receives cortical connections from the corticobulbar tract and reflex connections from the extrapyramidal and tectobulbar tracts and the nucleus of the solitary tract.
Lesions of the vagus nerve may be intramedullary or peripheral. Vagus nerve lesions near the skull base often involve the glossopharyngeal and accessory nerves and sometimes the hypoglossal nerve as well. Complete bilateral transection of the vagus nerve is fatal.
Unilateral lesions of the vagus nerve, within the cranial vault or close to the base of the skull, produce widespread dysfunction of the palate, pharynx, and larynx. The soft palate is weak and may be flaccid so the voice has a nasal twang. Weakness or paralysis of the vocal cord may result in hoarseness. There can be difficulty in swallowing, and cardiac arrhythmias may be present.
Damage to the recurrent laryngeal nerve, which arises from the vagus, can occur as a result of invasion or compression by tumor or as a complication of thyroid surgery. It may be accompanied by hoarseness or hypophonia.
Cranial Nerve XI: Accessory Nerve
The accessory nerve consists of two separate components: the cranial component and the spinal component (Fig 8–18).
Schematic illustration of the accessory nerve, viewed from below.
In the cranial component, branchial efferent fibers (from the ambiguus nucleus to the intrinsic muscles of the larynx) join the accessory nerve inside the skull but are part of the vagus outside the skull.
In the spinal component, the branchial efferent fibers from the lateral part of the anterior horns of the first five or six cervical cord segments ascend as the spinal root of the accessory nerve through the foramen magnum and leave the cranial cavity through the jugular foramen. These fibers supply the sternocleidomastoid muscle and partly supply the trapezius muscle. The central connections of the spinal component are those of the typical lower motor neuron: voluntary impulses via the corticospinal tracts, postural impulses via the basal ganglia, and reflexes via the vestibulospinal and tectospinal tracts.
A 24-year-old medical student noticed while shaving one morning that he was unable to move the left side of his face. He worried that a serious problem, possibly a stroke, might have occurred. He had had influenza-like symptoms the week before this sudden attack.
Neurologic examination showed that the patient could not wrinkle his forehead on the left side or show his teeth or purse his lips on that side. Taste sensation was abnormal in the left anterior two-thirds of the tongue, and he had trouble closing his left eye. A test of tear secretion showed that secretion on the right side was normal, but the left lacrimal gland produced little fluid. Loud noises caused discomfort in the patient, who was in good health otherwise, and there were no additional signs or symptoms.
What is the differential diagnosis? What is the most likely diagnosis?
A 56-year-old mailman complained of attacks of severe stabbing pains in the right side of the face, which started about 6 months earlier. The pain would occur several times a day, lasting only a few seconds. The patient was unable to shave, because touching his right cheek would trigger an excruciating pain (he now had a full beard). On windy days the attacks seemed to occur more frequently. Sometimes drinking or eating would trigger the pain. The patient had lost weight recently. A dentist had not found any tooth-related problems.
The neurologic examination was almost entirely normal. However, when the patient's face was tested for touch and pain sensibility, a pain attack was set off each time his right cheek was touched.
What is the most likely diagnosis? Would a radiologic examination be useful?
Cases are discussed further in Chapter 25. Tests designed to determine the function of cranial nerves are described in Appendix A.
Interruption of the spinal component leads to paralysis of the sternocleidomastoid muscle, causing the inability to rotate the head to the contralateral side, and paralysis of the upper portion of the trapezius muscle, which is characterized by a wing-like scapula and the inability to shrug the ipsilateral shoulder.
Cranial Nerve XII: Hypoglossal Nerve
Somatic efferent fibers from the hypoglossal nucleus in the ventromedian portion of the gray matter of the medulla emerge between the pyramid and the olive to form the hypoglossal nerve (Fig 8–19). The nerve leaves the skull through the hypoglossal canal and passes to the muscles of the tongue. A few proprioceptive fibers from the tongue course in the hypoglossal nerve and end in the trigeminal nuclei of the brain stem. The hypoglossal nerve distributes motor branches to the geniohyoid and infrahyoid muscles with fibers derived from communicating branches of the first cervical nerve. A sensory recurrent meningeal branch of nerve XII innervates the dura of the posterior fossa of the skull.
Central connections of the hypoglossal nucleus include the corticobulbar (corticonuclear) motor system (with crossed fibers, as shown in Fig 7–9), as well as reflex neurons from the sensory nuclei of the trigeminal nerve and the nucleus of the solitary tract (not shown).
Peripheral lesions that affect the hypoglossal nerve usually come from mechanical causes. Nuclear and supranuclear lesions can have many causes (eg, tumors, bleeding, demyelination).
Lesions of the medulla produce characteristic symptoms that are related to the involvement of the nuclei of the last four cranial nerves that lie within the medulla and the motor and sensory pathways through it. Extramedullary lesions of the posterior fossa may involve the roots of the last four cranial nerves between their emergence from the medulla and their exit from the skull.
BOX 8–1 Essentials for the Clinical Neuroanatomist After reading and digesting this chapter, you should know and understand:
Overall location of cranial nerves (Fig 8-1)
Motor and sensory roles of each cranial nerve (Table 8-1)
Location of cell bodies for each cranial nerve (Table 8-1 and diagrams for each cranial nerve)
Ganglia related to each cranial nerve (Table 8-2)
Anatomic course of each cranial nerve
Eye muscle actions (Table 8-3 and Fig 8-5)
The clinical presentation of damage to each cranial nerve, including gaze palsies, internuclear ophthalmoplegia, upper versus lower facial nerve lesions