Cranial+Nerves+VII-XII

=**Cranial Nerves VII-XII**=


 * 1. Know the major modalities and anatomical pathways of the cranial nerves.**

__Facial VII__ Facial nerve has a branchial motor component that starts at the motor nucleus if VII and descends through the geniculate ganglion and out the stylomastoid foramen where it branches off to innervate stapedius, stylohyoid, posterior belly of the digastric, muscles of facial expression including platysma, buccinators, and occipitalis. The branchial motor axons characterisitically loop around the CN VI nucleus on their way out. The visceral motor component descends through the geniculate ganglion where it gives off a branch that follows CN V1 to innervate the lacrimal gland, and another branch to innervate the submandicular and sublingual glands, and the mucous membranes of the nose, and hard and soft palates. A small general sensory component innervates the skin of the external ear. Lastly, the chorda tympani innervates the anterior 2/3 of the tongue.

__Vestibulocochlear VIII__ Primary sensory neurons extend from the sensory receptors in the cochlea and vestibular apparatus to cell bodies in the spiral (cochlear) ganglion and vestibular ganglion (semicircular canals). CN VIII projects centrally to the cochlear and vestibular nuclei.

High frequencies are generated by neurons at the base of the cochlea and project to synapse in the dorsal cochlear nuclei; low frequencies are generated by neurons near the apex of the cochlea and projects to synapse in the ventral cochlear nuclei

Cochlear neurons project mostly to the contralateral lateral lemniscus to the superior olivary nucleus. Fibers from the ventral cochlea form the trapezoid body before joining the lateral lemniscus. The lateral lemniscus projects to the inferior colliculus which project to the medial geniculate of the thalamus. The medial geniculate projects to the primary auditory cortex ont eh superior temporal gyrus, maintaining the tonotopic map at every level.

The vestibular nuclei projects to the cerebellum through the inferior cerebellar peduncle with reciprocal connections to medial and inferior vestibular nuclei to coordinate balance during movement. Lateral (Deiter’s) nucleus projects to the spinal cord via the vestibulospinal tract tin influence tone of antigravity muscles. The vestibular nuclei also project to the medial lateral feniculus to influence CN III, IV, and VI which allows coordination between eye movements and the body.

__Glossopharyngeal IX__ CN IX has a branchial motor component to stylopharyngeous, visceral motor to otic ganglion and parotid gland, visceral sensory from carotid body and sinus, general sensory from posterior 1/3 of tongue, and taste from the posterior 1/3 of the tongue.

It emerges from the medulla between the inferior olive and inferior cerebellar peduncle (rostral rootlets). It gives off the tympanic nerve in the jugular fossa before exiting the skull at the jugular foramen. The superior and inferior CN IX ganglia are at the jugular foramen and contain cell bodies for general, visceral, and special sensation. The carotid nerves, lingual, and pharyngeal branches join at the inferior ganglion.

Stylopharyngeus is used to elevate the pharynx during swallowing, speech, and gag reflex and is innerated by premotor corticobulbar fibers. Inferior salivatory nucleus sends visceral motor fibers through CN IX. Lastly, the tympanic nerve forms a middle ear plexus that innerates the mucus membrane of the middle ear, auditory tube, and mastoid air cells; it also forms the lesser petrosal nerve which goes back into the cranium at the middle fossa and out through the foramen ovale to the otic ganglion where it synapses with postsynaptic fibers that join V3 and travels to innervate the parotid gland.

__Vagus X__ Vagus runs from the brainstem to the splenic flexure of the colon and has a branchial motor, visceral motor, visceral sensory, and general sensory components.

The branchial motor component innervates stratedmuscle of the pharynx, palatoglossus, and larynx (except stylopharyngeous by CN IX, and tensor veli palatine by CN V3). Fibers from the nucleus ambiguous axons exit the medulla between the olive and pyramind with caudal rootlets traveling briefly with CN XI. These axons exist the jugular foramen with CN IX and XI. It gives off a pharyngeal branch, superior laryngeal branch (off of the inferior vagal ganglion), and recurrent laryngeal branch. The superior laryngeal nerve supplies the inferior constrictor, cricothryoid muscle, pharyngeal plexus, and superior cardiac nerves. The recurrent laryngeal branch hooks under the subclavian artery on the right side and the aortic arch on the left side; it supplies the intrinsic muscles of the larynx, except the cricothyroid muscle.

The visceral motor component innervates the smooth muscle of the pharynx, larynx, and thoracic and abdominal visceral. Visceral motor CN X fibers originate in the dorsal motor nucleus of the vagus on the floor of the 4th ventricle. Preganglionic fibers synapse in parasympathetic ganglia located in end organs. These fibers act on cardiac fibers to slow the heart and reduce cardiac output, pulmonary fibers to cause bronchoconstriction, esophageal fibers to activate esophageal smooth muscle, and gastric nerves from the esophageal plexus to promote peristalsis (with myenteric and submucusal plexuses).

The visceral sensory component innervates the larynx, trachea, esophagus, thoracic and abdominal viscera, and stretch and chemoreceptors in the aortic arch. Sensory information from the epiglottis and larynx above the vocal folds are carried by the internal laryngeal nerve; sensory information from below the vocal folds is carried by the recurrent laryngeal nerve. Cell bodies in the inferior vagal ganglion receive sensory inputs and project fibers to synapse in the solitary nucleus. From there, fibers project to the hypothalamus, etc.

The general sensory component innervates the skin on the back of the ear, external acoustic meatus, part of the external surface of the tympanic membrane, and the pharynx. Sensory cell bodies are found in the superior vagal ganglion which sends fibers down into the spinal trigeminal tract where they synapse on second order fibers projecting to the ventral posterior thalamus through the trigeminothalamic tract.

__Accessory XI__ CN XI has cell bodies in the lateral spinal cord anterior gray matter and is in the same cell column as the nucleus ambiguous; hence, CN XI is a branchial motor nerve rather than somatic motor. Fibers exit the lateral cord at C1-C5 posterior to the ventral cervical roots and ascend through foramen magnum to join CN IX and CN X before exiting the jugular foramen. CN XI then passes behind the styloid process and innervates sternocleidomastoid and trapezius.

Sternocleidomastoid turns the head away from the side of the muscle.

__Hypoglossal XII__ CN XII sends somatic motor innervation to all the intrinsic tongue muscles (genioglossus, styloglossus, and hyoglossus) except palatoglossus, which is innervated by CN X. Together, the intrinsic tongue muscles act to protrude the tongue. Corticobulbar fibers as well as sensory input from the solitary nucleus (for suck, swallow, and chew reflexes) give input the contralateral CN XII nucleus.

The CN XII nucleus in the medulla is located between the dorsal medial nucleus of CN X and the midline. CN XII emerges at the ventrolateral sulcus between the olive and the pyramind to exist the cranium through the hypoglossal foramen. CN XII passes medial to CN IX, X and XI and inbetween the internal carotid artery and internal jugular vein. It loops anteriorly above the hyoid bone and divides to supply the intrinsic tongue muscles.


 * 2. Describe how to exam each cranial nerve.**

__Facial VII__ Test facial expression plus taste on the anterior tongue.

__Vestibulocochlear VIII__ Test audition by rubbing fingers next to each ear. Weber test is with a tuning fork on the apex of the head. Rinne test is with a tuning fork to the mastoid process until not audible and then quickly move in front of the ear to test air vs. bone conduction. If conduction is better through bone for the affected ear and the Weber test sounds louder in the affected ear, then there is conductive loss in the affected ear. If conduction is better through air in the affected ear and the Weber sounds louder in the unaffected ear, then there is sensory-motor hearing loss. If conduction is better through bone at the affected ear and the Weber sounds louder in the unaffected ear, then it may be a combination of sensory-motor and conductive loss.

Test vestibular function with the caloric test. Cold water put in the ear of a person in a coma will cause nystagmus toward the cold; however, in an awake person, it will elicit a saccade towards the opposite direction away from the cold. Basically, for a person in a coma, use COWS (cold to opposite, warm to same). Alternatively, in a person in a coma, you can turn the head and watch the eye movements which should keep the eyes in the same position (doll’s eyes); this doesn’t work in an awake person.

__Glossopharyngeal IX__ Test swallowing and the gag reflex with a pharyngeal swab. Gag doesn’t occur during swallowing because the swallowing sequence triggers inhibitory signals in the brainstem centers that control gag reflexes and suppresses it.

__Vagus X__ Test swallowing and the gag reflex with a pharyngeal swab. Also test hoarseness of voice which may suggest lesion of the recurrent laryngeal nerve. Can also test elevation of the soft palate with phonation; failure to elevate on one side draws uvula to the opposite side of lesion.

__Accessory XI__ Test for sternocleidomastoid (turn head against resistance) and trapezius muscles (shoulder shrug).

__Hypoglossal XII__ Test deviation of tongue during protrusion. Weakness causes tongue deviation toward the side of a lower motor nucleus lesion and away from the side of a cortical or upper motor nucleus lesion. Atrophy of the weak side suggests a lower motor nucleus lesion.


 * 3. Localize cranial nerve or pathway lesion based on the functional deficits produced.**

__Facial VII__ Facial expression is initiated in the motor cortex through the corticobulbar tract via posterior limb of the internal capsule. However, cortical innervation is different for the upper and lower face. The upper face (frontalis, orbicularis oculi) receives bilateral VII input but the lower face only receives contralateral VII input. As a result, unilateral upper motor nucleus lesions (cortex and corticobulbar path) would cause //only// lower facial weakness with forehead and eye closure function intact. However, lower motor nucleus lesions (nuclear and peripheral) will cause weakness of the frontalis and eye closure as well as lower facial expression.

Common idioplathic nerve lesions are Bell’s palsy. Reflexes mediated by the branchial motor component of VII include the blink reflex to light (with CN II), to corneal stimulation (with CN V1), and to noise (CN VIII). Also, the stapedius reflex (with CN VIII) to tense the eardrum helps reduce loud noise. Lastly, the branchial motor VII also mediates sucking and snout reflexes to oral stimulation (infants, demented patients). Lesions of CN VII in the pons will likely be accompanied by ipsilateral CN VI lesion; if the lesion is peripheral, CN VIII may also be involved.

__Vestibulocochlear VIII__ Lesions of the VIII can cause hearing loss. However, because pathways are bilateral above the cochlear nuclei, a lesion above the CN VIII nerve rarely causes hearing loss. Nystagmus may be indicative of vestibular dysfunction. Lesions of the vestibulospinal tract cause balance problems, dizziness, and nausea.

__Glossopharyngeal IX__ Glossopharyngeal neuralgeia can occur through excessive firing of the CN IX nerve, resulting in excessive pain; the cause of this pain is unknown though carbazepine can reduce excessive nerve discharges. Fainting can result due to the carotid body and sinus stimulating the brain stem nuclei that regulate blood pressure, resulting in bradycardia (slow heart rate) and a drop in blood pressure.

__Vagus X__ Vagus nerve stimulation can be used to control seizures; devices for this purpose are typically installed on the left side to reduce vagus overstimulation and bradycardia because most cardiac innervation is from the right vagus nerve. How vagal stimulation prevents seizures is unknown.

In the dark ages, the vagus nerve can be cut to reduce gastric secretion for recurrent ulcers but it is now known that vagus activation isn’t really a major contributer to ulcer formation and, even if it was, we have better pharmacological approaches now.

Stimulation of vagal sensory afferents from the pharynx can cause cough; vagal-induced bronchoconstriction can cause shortness of breath. Both these symptoms are usually self-limiting.

Activation of the recurrent laryngeal nerve can cause relaxation of the vocal cords and hoarseness of voice; lesions of the recurrent laryngeal nerve can cause vocal cord paralysis. Lesion of the pharyngeal branch of CN X can result in the droop of the palate on the affected side.

__Accessory XI__ Lesions of CN XI can cause a weak head turn to the opposite side of the nerve (weak sternocleidomastoid) and ipsilateral shoulder drop (weak trapezius). CN XI is vulnerable to radical neck surgery (to remove head and neck tumors), pressure on the trapezius, etc. CN XI can also be affected by upper motor nucleus lesions of the opposite cortex, such as those caused by a stroke.

__Hypoglossal XII__ Lower motor nucleus lesions can cause weakening of the intrinsic tongue muscles on the affected side, resulting in tongue deviation toward the side of the lesion upon protrusion and atrophy of the weakened side. Upper motor nucleus lesions cause the tongue to deviate away from the side of the cortical lesion because of the decussation of the motor fibers as they descend from cortical areas to the intrinsic tongue muscles.

Because CN XII passes between the internal carotid artery and internal jugular vein, it is vulnerable to lesions involving these structures. For example, dissection of the internal carotid artery can disrupt the lining of the vessel, resulting in swelling of the artery and a transient interruption of flow that can involve CN XII as it passes. This transient stroke-like event can result in temporary right-sided weakness.