Tongue Deviation Lesion

Cranial Nerves

I. THE OLFACTORY NERVE, the first cranial nerve (CN I) [Figure 13-1], mediates olfaction (smell). It is the only sensory system that has no precortical relay in the thalamus. The olfactory nerve is a special visceral afferent (SVA) nerve. It consists of unmyelinated axons of bipolar neurons that are located in the nasal mucosa, the olfactory epithelium. It enters the skull through the cribriform plate of the ethmoid bone (see appendix).

A. Olfactory pathway

1. Olfactory receptor cells are first-order neurons that project to the mitral cells of the olfactory bulb.

2. Mitral cells are the principal cells of the olfactory bulb. They are excitatory and glutaminergic. They project through the olfactory tract and lateral olfactory stria to the primary olfactory cortex and amygdala.

Olfactory Trigone

Olfactory trigone Anterior perforated substance Interpeduncular fossa

Crus cerebri (cerebral peduncle)

Pons

Middle cerebellar peduncle

CN VIII

Pyramid Cervical nerve I

(VOlfactory bulb (CN I) ^ Optic chasm —Olfactory tract

Infundibulum Tuber cinereum Mamillary body

Optic tract

CN III CN IV

CN V (motor root) CN V (sensory root) CN VI CN VII

CN VII (intermediate) CN VIII CN IX CN X CN XI

Pyramidal decussation

Figure 13-1. The base of the brain with attached cranial nerves (CN). (Reprinted with permission from Truex RC, Kellner CE: Detailed Atlas of the Head and Neck. New York, Oxford University Press, 1958, p. 34.)

3. The primary olfactory cortex (Brodmann's area 34) consists of the piriform cortex that overlies the uncus.

B. Lésions of the olfactory pathway result from trauma (e.g., skull fracture) and, often, from olfactory groove meningiomas. These lesions cause ipsilateral anosmia (localizing value). Lesions that involve the parahippocampal uncus may cause olfactory hallucinations [uncinate fits (seizures) with déjà vu].

C. Foster Kennedy syndrome (FKS) consists of ipsilateral anosmia, ipsilateral optic atrophy, and contralateral papilledema. It is usually caused by an anterior fossa meningioma.

II. THE OPTIC NERVE (CN II) is a special somatic afferent (SSA) nerve that subserves vision and pupillary light reflexes (afferent limb) [see Chapter 19]. It is not a true peripheral nerve, but is a tract of the diencephalon. A transected optic nerve cannot regenerate.

III. THE OCULOMOTOR NERVE (CN III) is a general somatic efferent (GSE), general visceral efferent (GVE) nerve.

A. General characteristics. The oculomotor nerve moves the eye, constricts the pupil, accommodates, and converges. It exits the brain stem from the interpeduncular fossa of the midbrain, passes through the cavernous sinus, and enters the orbit through the superior orbital fissure.

1. The GSE component arises from the oculomotor nucleus of the rostral midbrain.

It innervates four extraocular muscles and the levator palpebrae muscle. (Remember the mnemonic SIN: superior muscles are intorters of the globe.)

a. The medial rectus muscle adducts the eye. With its opposite partner, it converges the eyes.

b. The superior rectus muscle elevates, in torts, and adducts the eye.

C. The inferior rectus muscle depresses, extorts, and adducts the eye.

d. The inferior oblique muscle elevates, extorts, and abducts the eye.

e. The levator palpebrae muscle elevates the upper eyelid.

2. The GVE component consists of preganglionic parasympathetic fibers.

a. The Edinger-Westphal nucleus projects preganglionic parasympathetic fibers to the ciliary ganglion of the orbit through CN 111.

b. The ciliary ganglion projects postganglionic parasympathetic fibers to the sphincter muscle of the iris (miosis) and the ciliary muscle (accommodation).

B. Clinical correlation

1. Oculomotor paralysis (palsy) is seen with transtentorial herniation (e.g., tumor, subdural or epidural hematoma).

a. Denervation of the levator palpebrae muscle causes ptosis (i.e., drooping of the upper eyelid).

b. Denervation of the extraocular muscles causes the affected eye to look "down and out" as a result of the unopposed action of the lateral rectus and superior oblique muscles. The superior oblique and lateral rectus muscles are innervated by CN IV and CN VI, respectively. Oculomotor palsy results in diplopia (double vision) when the patient looks in the direction of the paretic muscle.

C. Interruption of parasympathetic innervation (internal ophthalmoplegia) results in a dilated, fixed pupil and paralysis of accommodation (cycloplegia).

2. Other conditions associated with CN III impairment a. Transtentorial (uncal) herniation. Increased supratentorial pressure (e.g., from a tumor) forces the hippocampal uncus through the tentorial notch and compresses or stretches the oculomotor nerve.

(1) Pupilloconstrictor fibers are affected first, resulting in a dilated, fixed pupil.

(2) Somatic efferent fibers are affected later, resulting in external strabis~ mus (exotropia).

b. Aneurysms of the carotid and posterior communicating arteries often compress CN III within the cavernous sinus or interpeduncular cistern. They usu* ally affect the peripheral pupilloconstrictor fibers first (e.g., uncal herniation). C. Diabetes mellitus (diabetic oculomotor palsy) often affects the oculomotor nerve. It damages the central fibers and spares the pupilloconstrictor fibers.

IV. THE TROCHLEAR NERVE (CN IV) is a GSE nerve.

A. General characteristics. The trochlear nerve is a pure motor nerve that innervates the superior oblique muscle. This muscle depresses, intorts, and abducts the eye. (See Figure 17-4G.)

1. It arises from the contralateral trochlear nucleus of the caudal midbrain.

2. It decussates beneath the superior medullary velum of the midbrain and exits the brain stem on its dorsal surface, caudal to the inferior colliculus.

3. It encircles the midbrain within the subarachnoid space, passes through the cavernous sinus, and enters the orbit through the superior orbital fissure.

B. Clinical correlation. CN IV paralysis results in the following conditions:

1. Extorsion of the eye and weakness of downward gaze

2. Vertical diplopia, which increases when looking down

3. Head tilting to compensate for extorsion (may be misdiagnosed as idiopathic torticollis)

4. Head trauma. Because of its course around the midbrain, the trochlear nerve is particularly vulnerable to head trauma. The trochlear decussation underlies the superior medullary velum. Trauma at this site often results in bilateral fourth-nerve palsies. Pressure against the free border of the tentorium (herniation) may injure the nerve.

V. THE TRIGEMINAL NERVE (CN V) is a special visceral efferent (SVE), general somatic afferent (GSA) nerve (see Chapter 10).

A. General characteristics. The trigeminal nerve is the nerve of pharyngeal (brachial) arch 1 (mandibular). It has three divisions: ophthalmic (CN V-l), maxillary (CN V-2), and mandibular (CN V-3) [see Chapter 10].

1. The SVE component arises from the motor trigeminal nucleus that is found in the lateral midpontine tegmentum. It innervates the muscles of mastication (i.e., temporalis, masseter, lateral, and medial pterygoids), the tensores tympani and veli palatini, the myelohyoid muscle, and the anterior belly of the digastric muscle.

2. The GSA component provides sensory innervation to the face, mucous membranes of the nasal and oral cavities and frontal sinus, hard palate, and deep structures of the head (proprioception from muscles and the temporomandibular joint). It innervates the dura of the anterior and middle cranial fossae (supratentorial dura).

B. Clinical correlation. Lesions result in the following neurologic deficits:

1. Loss of general sensation (hemianesthesia) from the face and mucous membranes of the oral and nasal cavities

2. Loss of the corneal reflex (afferent limb, CN V-l) [Figure 13-2]

Corneal Reflex Arc

Principal sensory nucleus (CN V)

Genu CN VII

Tertiary neuron

CN VII

Facial nucleus

Decussating corneal reflex fiber

Trigeminothalamic pain fiber

Primary neuron V-1

CN VII

Secondary neuron Spinal trigeminal nucleus Spinal trigeminal tract

Figure 13-2. The corneal reflex pathway showing the three neurons and decussation. This reflex is consensual, like the pupillary light reflex. Second-order pain neurons arc found in the caudal division of the spinal trigeminal nucleus. Second-order corneal reflex neurons are found at more rostral levels.

3. Flaccid paralysis of the muscles of mastication

4. Deviation of the jaw to the weak side as a result of the unopposed action of the opposite lateral pterygoid muscle

5. Paralysis of the tensor tympani muscle, which leads to hypoacusis (partial deafness to low-pitched sounds)

6. Trigeminal neuralgia (tic douloureux), which is characterized by recurrent paroxysms of sharp, stabbing pain in one or more branches of the nerve (see Chapter 10)

VI. THE ABDUCENT NERVE (CN VI)

A. General characteristics. The abducent nerve is a pure GSE nerve that innervates the lateral rectus muscle, which abducts the eye.

1. It arises from the abducent nucleus chat is found in the dorsomedial tegmentum of the caudal pons.

2. Exiting intraaxial fibers pass through the corticospinal tract. A lesion results in al* ternating abducent hemiparesis.

3. It passes through the pontine cistern and cavernous sinus and enters the orbit through the superior orbital fissure.

B. Clinical correlation. CN VI paralysis is the most common isolated palsy that results from the long peripheral course of the nerve. It is seen in patients with meningitis, subarachnoid hemorrhage, late-stage syphilis, and trauma. Abducent nerve paralysis results in the following defects:

1. Convergent (medial) strabismus (esotropia) with inability to abduct the eye

2. Horizontal diplopia with maximum separation of the double images when looking toward the paretic lateral rectus muscle

A. General characteristics. The facial nerve is a GSA, general visceral afferent (GVA), SVA, GVE, and SVE nerve (Figures 13-3 and 13-4). It mediates facial movements, taste, salivation, lacrimation, and general sensation from the external ear. It is the nerve of the pharyngeal (brachial) arch 2 (hyoid). It includes the facial nerve proper (motor division), which contains the SVE fibers that innervate the muscles of facial (mimetic) expression. CN VII includes the intermediate nerve, which contains GSA, SVA, and GVE fibers. All first-order sensory neurons arc found in the geniculate ganglion within the temporal bone.

1. Anatomy. The facial nerve exits the brain stem in the cerebellopontine angle. It enters the internal auditory meatus and the facial canal. It then exits the facial canal and skull through the stylomastoid foramen.

2. The GSA component has cell bodies located in the geniculate ganglion. It innervates the posterior surface of the external ear through the posterior auricular branch of CN VII. It projects centrally to the spinal trigeminal tract and nucleus.

3. The GVA component has no clinical significance. The cell bodies are located in the geniculate ganglion. Fibers innervate the soft palate and the adjacent pharyngeal wall.

4. The SVA component (taste) has cell bodies located in the geniculate ganglion. It vjuuiiiaiiuiuuini yicii IV_J

Figure 13-3. The functional components of the facial nerve (cranial nerve (CN) VII).

VII. THE FACIAL NERVE (CN VII)

CN II

CN II

Internal Capsule Stroke

vjuuiiiaiiuiuuini yicii IV_J

Figure 13-3. The functional components of the facial nerve (cranial nerve (CN) VII).

Face area of motor cortex

Orbicularis oculi

Buccinator

Orbicularis oris

Platysma

Muscles of facial expression: Frontalis-

UMN lesion of corticobulbar tract-Cdi*

(e.g., stroke of internal capsule)

Pontine Stroke Muscle Innervation

Facial nucleus of pons

Upper face division

Lower face division

Figure 13-4. Corticobulbar innervation of the facial nerve [cranial nerve (CN) VIIJ nucleus. An upper motor neuron (UMN) lesion (e.g., stroke involving the internal capsule) results in contralateral weakness of the lower face, with sparing of the upper face. A lower motor neuron (LMN) lesion (e.g., Bell's palsy) results in paralysis of the facial muscles in both the upper and lower face.

Face area of motor cortex

Orbicularis oculi

Buccinator

Orbicularis oris

Platysma

Muscles of facial expression: Frontalis-

UMN lesion of corticobulbar tract-Cdi*

(e.g., stroke of internal capsule)

Facial nucleus of pons

Upper face division

Lower face division

Figure 13-4. Corticobulbar innervation of the facial nerve [cranial nerve (CN) VIIJ nucleus. An upper motor neuron (UMN) lesion (e.g., stroke involving the internal capsule) results in contralateral weakness of the lower face, with sparing of the upper face. A lower motor neuron (LMN) lesion (e.g., Bell's palsy) results in paralysis of the facial muscles in both the upper and lower face.

projects centrally to the solitary tract and nucleus. It innervates the taste buds from the anterior two-thirds of the tongue through:

a. The intermediate nerve b. The chorda tympani, which is located in the tympanic cavity medial to the tympanic membrane and malleus. It contains the SVA and GVE (parasympathetic) fibers.

C. The lingual nerve (a branch of CN V-3)

d. The central gustatory pathway (see Figure 13-3). Taste fibers from CN VII, CN IX, and CN X project through the solitary tract to the solitary nucleus. The solitary nucleus projects through the central tegmental tract to the ventral posteromedial nucleus (VPM) of the thalamus. The VPM projects to the gustatory cortex of the parietal lobe (parietal operculum).

5. The GVE component is a parasympathetic component that innervates the lacrimal, submandibular, and sublingual glands. It contains preganglionic parasympathetic neurons that are located in the superior salivatory nucleus of the caudal pons.

a. Lacrimal pathway (see Figure 13-3). The superior salivatory nucleus projects through the intermediate and greater petrosal nerves to the pterygopalatine (sphenopalatine) ganglion. The pterygopalatine ganglion projects to the lacrimal gland of the orbit.

b. Submandibular pathway (see Figure 13-3). The superior salivatory nucleus projects through the intermediate nerve and chorda tympani to the submandibular ganglion. The submandibular ganglion projects to and innervates the submandibular and sublingual glands.

6. The SVE component arises from the facial nucleus, loops around the abducent nucleus of the caudal pons, and exits the brain stem in the cerebellopontine angle. It enters the internal auditory meatus, traverses the facial canal, sends a branch to the stapedius muscle of the middle ear, and exits the skull through the stylomastoid foramen. It innervates the muscles of facial expression, the stylohyoid muscle, the posterior belly of the digastric muscle, and the stapedius muscle.

B. Clinical correlation. Lesions (see Figure 14-2) cause the following conditions:

1. Flaccid paralysis of the muscles of facial expression (upper and lower face)

2. Loss of the corneal reflex (efferent limb), which may lead to corneal ulceration

3. Loss of taste (ageusia = gustatory anesthesia) from the anterior two-thirds of the tongue, which may result from damage to the chorda tympani

4. Hyperacusis (increased acuity to sounds) as a result of stapedius paralysis

5. Bell's palsy (peripheral facial paralysis), which is caused by trauma or infection and involves the upper and lower face

6. Crocodile tears syndrome (lacrimation during eating), which is a result of aberrant regeneration after trauma

7. Supranuclear (central) facial palsy, which results in contralateral weakness of the lower face, with sparing of the upper face (see Figure 1 3-4)

8. Bilateral facial nerve palsies, which occur in Gui Ilain-Barre syndrome (see Chapter 14)

9. Möbius* syndrome, which consists of congenital facial diplegia (CN VII) and convergent strabismus (CN VI)

VIII. THE VESTIBULOCOCHLEAR NERVE (CN VIII) is an SSA nerve. It has two functional divisions: the vestibular nerve, which maintains equilibrium and balance, and the cochlear nerve, which mediates hearing (see Chapters 1 1 and 12). It exits the brain stem at the cerebellopontine angle and enters the internal auditory meatus. It is confined to the temporal bone.

A. Vestibular nerve (see Figure 12-1)

1. General characteristics a. It is associated functionally with the cerebellum (flocculonodular lobe) and ocular motor nuclei.

b. It regulates compensatory eye movements.

C. Its first-order sensory bipolar neurons are located in the vestibular ganglion in the fundus of the internal auditory meatus.

d. It projects its peripheral processes to the hair cells of the cristae of the semicircular ducts and the hair cells of the utricle and saccule.

e. It projects its central processes to the four vestibular nuclei of the brain stem and the flocculonodular lobe of the cerebellum.

f. It conducts efferent fibers to the hair cells from the brain stem.

2. Clinical correlation. Lesions result in disequilibrium, vertigo, and nystagmus. B. Cochlear nerve (see Figure 11-1)

1. General characteristics a. Its first-order sensory bipolar neurons are located in the spiral (cochlear) ganglion of the modiolus of the cochlea, within the temporal bone.

b. It projects its peripheral processes to the hair cells of the organ of Corti.

C. It projects its central processes to the dorsal and ventral cochlear nuclei of the brain stem.

d. It conducts efferent fibers to the hair cells from the brain stem.

2. Clinical correlation. Destructive lesions cause hearing loss (sensorineural deafness). Irritative lesions can cause tinnitus (ear ringing). An acoustic neuroma (schwannoma) is a Schwann cell tumor of the cochlear nerve that causes deafness (see Chapter 14).

IX. THE GLOSSOPHARYNGEAL NERVE (CN IX) is a GSA, GVA, SVA, SVE, and GVE nerve (Figure 13-5).

A. General characteristics. The glossopharyngeal nerve is primarily a sensory nerve. Along with CN X, CN XI, and CN XII, it mediates taste, salivation, and swallowing. It mediates input from the carotid sinus, which contains baroreceptors that monitor arterial blood pressure. It also mediates input from the carotid body, which contains chemoreceptors that monitor the CO? and 02 concentration of the blood.

1. Anatomy. CN IX is the nerve of pharyngeal (branchial) arch 3. It exits the brain stem (medulla) from the postolivary sulcus with CN X and CN XI. It exits the skull through the jugular foramen with CN X and CN XI.

2. The GSA component innervates part of the external ear and the external auditory meatus through the auricular branch of the vagus nerve. It has cell bodies in the superior ganglion. It projects its central processes to the spinal trigeminal tract and nucleus.

3. The GVA component innervates structures that are derived from the endoderm (e.g., pharynx). It innervates the mucous membranes of the posterior one-third of the tongue, tonsil, upper pharynx, tympanic cavity, and auditory tube. It also in^ nervates the carotid sinus (baroreceptors) and carotid body (chemoreceptors) through the sinus nerve. It has cell bodies in the inferior (petrosal) ganglion. It is the afferent limb of the gag reflex and the carotid sinus reflex.

4. The SVA component innervates the taste buds of the posterior one-third of the tongue. It has cell bodies in the inferior (petrosal) ganglion. It projects its central processes to the solitary tract and nucleus (for a discussion of the central pathway, see VII A 4 d).

5. The SVE component innervates only the stylopharyngeus muscle. It arises from the nucleus ambiguus of the lateral medulla.

6. The GVE component is a parasympathetic component that innervates the parotid gland. Preganglionic parasympathetic neurons are located in the inferior salivatory nucleus of the medulla. They project through the tympanic and lesser petrosal

Uvula Deviates Left

Figure 13-5. Innervation of the palatal arches and uvula. Sensory innervation is mediated by the glossopharyngeal nerve [cranial nerve (CN) IX). Motor innervation of the palatal arches and uvula is mediated by the vagus nerve (CN X). (A) A normal palate and uvula in a person who is saying "Ah." (B) A patient with an upper motor neuron (UMN) lesion (left) and a lower motor neuron (LMN) lesion (right). When this patient says "Ah," the palatal arches sag. The uvula deviates toward the intact (left) side.

Figure 13-5. Innervation of the palatal arches and uvula. Sensory innervation is mediated by the glossopharyngeal nerve [cranial nerve (CN) IX). Motor innervation of the palatal arches and uvula is mediated by the vagus nerve (CN X). (A) A normal palate and uvula in a person who is saying "Ah." (B) A patient with an upper motor neuron (UMN) lesion (left) and a lower motor neuron (LMN) lesion (right). When this patient says "Ah," the palatal arches sag. The uvula deviates toward the intact (left) side.

nerves to the otic ganglion. Postganglionic fibers from the otic ganglion project to the parotid gland through the auriculotemporal nerve (CN V-3).

B. Clinical correlation. Lesions cause the following conditions:

1. Loss of the gag (pharyngeal) reflex (interruption of the afferent limb)

2. Hypersensitive carotid sinus reflex (syncope)

3. Loss of general sensation in the pharynx, tonsils, fauces, and back of the tongue

4. Loss of taste from the posterior one-third of the tongue

5. Glossopharyngeal neuralgia, which is characterized by severe stabbing pain in the root of the tongue

X. THE VAGAL NERVE (CN X) is a GSA, GVA, SVA, SVE, and GVE nerve (see Figure 13-5).

A. General characteristics. The vagal nerve mediates phonation, swallowing (with CN

IX, CN XI, and CN XII), elevation of the palate, taste, and cutaneous sensation from the ear. It innervates the viscera of the neck, thorax, and abdomen.

1. Anatomy. The vagal nerve is the nerve of pharyngeal (brachial) arches 4 and 6. Pharyngeal arch 5 is either absent or rudimentary. It exits the brain stem (medulla) from the postolivary sulcus. It exits the skull through the jugular foramen with CN IX and CN XI.

2. The GSA component innervates the infra tentorial dura, external ear, external auditory meatus, and tympanic membrane. It has cell bodies in the superior (jugular) ganglion, and it projects its central processes to the spinal trigeminal tract and nucleus.

3. The GVA component innervates the mucous membranes of the pharynx, larynx, esophagus, trachea, and thoracic and abdominal viscera (to the left colic flexure). It has cell bodies in the inferior (nodose) ganglion. It projects its central processes to the solitary tract and nucleus.

4. The SVA component innervates the taste buds in the epiglottic region. It has cell bodies in the inferior (nodose) ganglion. It projects its central processes to the solitary tract and nucleus. For a discussion of the central pathway, see VII A 4 d.

5. The SVE component innervates the pharyngeal (brachial) arch muscles of the larynx and pharynx, the striated muscle of the upper esophagus, the muscle of the uvula, and the levator veli palatini and palatoglossus muscles. It receives SVE input from the cranial division of the spinal accessory nerve (CN XI). It arises from the nucleus ambiguus in the lateral medulla. The SVE component provides the efferent limb of the gag reflex.

6. The GVE component innervates the viscera of the neck and the thoracic (heart) and abdominal cavities as far as the left colic flexure. Preganglionic parasympathetic neurons that are located in the dorsal motor nucleus of the medulla project to the terminal (intramural) ganglia of the visceral organs (see Figure 18-2 and Table 18-1).

B. Clinical correlation. Lesions and reflexes cause the following conditions:

1. Ipsilateral paralysis of the soft palate, pharynx, and larynx that leads to dyspho-nia (hoarseness), dyspnea, dysarthria, and dysphagia

2. Loss of the gag (palatal) reflex (efferent limb)

3. Anesthesia of the pharynx and larynx that leads to unilateral loss of the cough reflex

4. Aortic aneurysms and tumors of the neck and thorax that frequently compress the vagal nerve

5. Complete laryngeal paralysis, which can be rapidly fatal if it is bilateral (asphyxia)

6. Parasympathetic (vegetative) disturbances, including bradycardia (irritative lesion), tachycardia (destructive lesion), and dilation of the stomach

7. The oculocardiac reflex, in which pressure on the eye slows the heart rate (affer-ent limb of CN V-l and efferent limb of CN X)

8. The carotid sinus reflex, in which pressure on the carotid sinus slows the heart rate (bradycardia) [efferent limb of CN X]

XL THE ACCESSORY NERVE (CN XI), or spinal accessory nerve, is an SVE nerve (Fig-ure 13-6).

A. General characteristics. The accessory nerve mediates head and shoulder movement and innervates the laryngeal muscles. It has the following divisions:

1. The cranial division (accessory portion), which arises from the nucleus ambiguus of the medulla. It exits the medulla from the postolivary sulcus and joins the vagal nerve (CN X). It exits the skull through the jugular foramen with CN IX and CN X. It innervates the intrinsic muscles of the larynx through the inferior (recurrent) laryngeal nerve, with the exception of the cricothyroid muscle.

2. The spinal division (spinal portion), which arises from the ventral horn of cervical segments CI through C6. The spinal roots exit the spinal cord laterally between the ventral and dorsal spinal roots, ascend through the foramen magnum, and exit the skull through the jugular foramen. It innervates the sternocleidomastoid muscle with the cervical plexus (C-2) and the trapezius muscle with the cervical plexus (C-3 and C-4).

B. Clinical correlation. Lesions cause the following conditions:

Lesion Cervix

Figure 13-6. The cranial and spinal divisions of the accessory nerve [cranial nerve (CN) IX]. The cranial division hitchhikes a ride with the accessory nerve, then joins the vagal nerve to become the interior (recurrent) laryngeal nerve. The recurrent laryngeal nerve innervates the intrinsic muscles of the larynx, except for the cricothyroid muscle. The spinal division innervates the trapezoid and sternocleidomastoid muscles. Three nerves pass through the jugular foramen (glomus jugulare tumor).

Figure 13-6. The cranial and spinal divisions of the accessory nerve [cranial nerve (CN) IX]. The cranial division hitchhikes a ride with the accessory nerve, then joins the vagal nerve to become the interior (recurrent) laryngeal nerve. The recurrent laryngeal nerve innervates the intrinsic muscles of the larynx, except for the cricothyroid muscle. The spinal division innervates the trapezoid and sternocleidomastoid muscles. Three nerves pass through the jugular foramen (glomus jugulare tumor).

1. Paralysis of the sternocleidomastoid muscle that results in difficulty in turning the head to the contralateral side

2. Paralysis of the trapezius muscle that results in shoulder droop and inability to shrug the shoulder

3. Paralysis of the larynx if the cranial root is involved

Cerebral Arteries Innervation

Figure 13-7. Motor innervation of the tongue. Corticobulbar fibers project predominantly to die contralateral hypoglossal nucleus. An upper motor neuron (UMN) lesion causes deviation of the protruded tongue to the weak (contralateral) side. A lower motor neuron (LMN) lesion causes deviation of the protruded tongue to the weak (ipsilateral) side. (A) Normal tongue. (B) Tongue with UMN and LMN lesions.

Figure 13-7. Motor innervation of the tongue. Corticobulbar fibers project predominantly to die contralateral hypoglossal nucleus. An upper motor neuron (UMN) lesion causes deviation of the protruded tongue to the weak (contralateral) side. A lower motor neuron (LMN) lesion causes deviation of the protruded tongue to the weak (ipsilateral) side. (A) Normal tongue. (B) Tongue with UMN and LMN lesions.

XII. THE HYPOGLOSSAL NERVE (CN XII) is a GSE nerve (Figure 13-7).

A. General characteristics. The hypoglossal nerve mediates tongue movement. It arises from the hypoglossal nucleus of the medulla and exits the medulla in the preolivary sulcus. It exits the skull through the hypoglossal canal, and it innervates the intrinsic and extrinsic muscles of the tongue. Extrinsic muscles are the genioglossus, styloglossus, and hyoglossus.

B. Clinical correlation

1. Transection results in hemiparalysis of the tongue.

2. Protrusion causes the tongue to point toward the weak side because of the unopposed action of the opposite genioglossus muscle.

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  • Aman
    Is tongue deviation upper or lower motor neuron?
    3 years ago

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