What are cranial nerves? |
Your cranial nerves are pairs of nerves that connect your brain to different parts of your head, neck, and trunk. There are 12 of them, each named for their function or structure.
Each nerve also has a corresponding Roman numeral between I and XII. This is based off their location from front to back. For example, your olfactory nerve is closest to the front of your head, so it’s designated as I.
Their functions are usually categorized as being either sensory or motor. Sensory nerves are involved with your senses, such as smell, hearing, and touch. Motor nerves control the movement and function of muscles or glands.
What is the acronym for this?
|Cranial Nerve:||Major Functions:|
|III Oculomotor||eyelid and eyeball movement|
|IV Trochlear|| innervates superior oblique |
turns eye downward and laterally
|V Trigeminal||chewing face & mouth touch & pain|
|VI Abducens||turns eye laterally|
|VII Facial||controls most facial expressions secretion of tears & saliva taste|
|VIII Vestibulocochlear(auditory)||hearing equillibrium sensation|
|IX Glossopharyngeal||taste senses carotid blood pressure|
|X Vagus||senses aortic blood pressure slows heart rate stimulates digestive organs taste|
|XI Spinal Accessory|| controls trapezius & sternocleidomastoid |
controls swallowing movements
|XII Hypoglossal||controls tongue movements|
Which cranial nerve is the largest? |
CN V (Trigeminal)
Which cranial nerve is the only one that exits the "posterior" side of the brainstem?
CN IV (Trochlear)
How many cranial nerves are responsible for eye movements?
Three: CN III (Oculomotor), IV (Trochlear), and VI (Abducens).
What does "abducens" refer to?
The abducens nerve carries motor impulses to the lateral rectus eye muscle which moves the eye laterally causing abduction of the eye.
Which cranial nerves carry gustatory (taste) information?
CN VII (Facial), CN IX (Glossopharyngeal) and CN X (Vagus).
Which cranial nerve is the longest?
CN X (Vagus) which reaches from the medulla to the digestive and urinary organs.
What two cranial nerves carry sensory information about blood pressure to the brain?
CN IX (Glossopharyngeal) and CN X (Vagus).
Which cranial nerve is responsible for pupillary constriction?
CN III (Oculomotor).
The cranial nerves are composed of twelve pairs of nerves that emanate from the nervous tissue of the brain. In order reach their targets they must ultimately exit/enter the cranium through openings in the skull. Hence, their name is derived from their association with the cranium. The function of the cranial nerves is for the most part similar to the spinal nerves, the nerves that are associated with the spinal cord. The motor components of the cranial nerves are derived from cells that are located in the brain. These cells send their axons (bundles of axons outside the brain = a nerve) out of the cranium where they will ultimately control muscle (e.g., eye movements) , glandular tissue (e.g., salivary glands) or specialized muscle (e.g., heart or stomach). The sensory components of cranial nerves originate from collections of cells that are located outside the brain. These collections of nerve cells bodies are called sensory ganglia. They are essentially the same functionally and anatomically as the dorsal root ganglia which are associated with the spinal cord. In general, sensory ganglia of the cranial nerves send out a branch that divides into two branches: a branch that enters the brain and one that is connected to a sensory organ. Examples of sensory organs are pressure or pain sensors in the skin and more specialized ones such as taste receptors of the tongue. Electrical impulses are transmitted from the sensory organ through the ganglia and into the brain via the sensory branch that enter the brain. There are two exceptions to this rule that should be noted when the special senses of smell and vision are discussed. In summary, the motor components of cranial nerves transmit nerve impulses from the brain to target tissue outside of the brain. Sensory components transmit nerve impulses from sensory organs to the brain.
Cranium CN I
CN I. Olfactory Nerve
The olfactory nerve is actually a collection of sensory nerve rootlets that extend down from the olfactory bulb and pass through the many openings of the cribriform plate in the ethmoid bone. These specialized sensory receptive parts of the olfactory nerve are then located in the olfactory mucosa of the upper parts of the nasal cavity. During breathing air molecules attach to the olfactory mucosa and stimulate the olfactory receptors of cranial nerve I and electrical activity is transduced into the olfactory bulb. Olfactory bulb cells then transmit electrical activity to other parts of the central nervous system via the olfactory tract.
Cranium CN II
CN II. Optic Nerve
The optic nerve originates from the bipolar cells of the retina which are connected to the specialized receptors in the retina (rod and cone cells). Light strikes the rod and cone cells and electrical impulses are transduced and transmitted to the bipolar cells. The bipolar cells in turn transmit electrical activity to the central nervous system through the optic nerve. The optic nerve exits the back of the eye in the orbit and enters the optic canal and exits into the cranium. It enters the central nervous system at the optic chiasm (crossing) where the nerve fibers become the optic tract just prior to entering the brain.
CN III. Oculomotor Nerve
The oculomotor nerve originates from motor neurons in the oculomotor (somatomotor) and Edinger-Westphal (visceral motor) nuclei in the brainstem. Nerve cell bodies in this region give rise to axons that exit the ventral surface of the brainstem as the oculomotor nerve. The nerve passes through the two layers of the dura mater including the lateral wall of the cavernous sinus and then enters the superior orbital fissure to access the orbit. The somatomotor component of the nerve divides into a superior and inferior division. The superior division supplies the levator palpebrae superioris and superior rectus muscles. The inferior division supplies the medial rectus, inferior rectus and inferior oblique muscles. The visceromotor or parasympathetic component of the oculomotor nerve travels with inferior division. In the orbit the inferior division sends branches that enter the ciliary ganglion where they form functional contacts (synapses) with the ganglion cells. The ganglion cells send nerve fibers into the back of the eye where they travel to ultimately innervate the ciliary muscle and the constrictor pupillae muscle.
CN IV. Trochlear Nerve
The trochlear nerve is purely a motor nerve and is the only cranial nerve to exit the brain dorsally. The trochlear nerve supplies one muscle: the superior oblique. The cell bodies that originate the fourth cranial nerve are located in ventral part of the brainstem in the trochlear nucleus. The trochlear nucleus gives rise to nerves that cross (decussate) to the other side of the brainstem just prior to exiting the brainstem. Thus, each superior oblique muscle is supplied by nerve fibers from the trochlear nucleus of the opposite side. The trochlear nerve fibers curve forward and enter the dura mater at the angle between the free and attached border of the tentorium cerebelli. The nerve travels in the lateral wall of the cavernous sinus and then enters the orbit via the superior orbital fissure. The nerve travels medially and diagonally across the levator palpebrae superioris and superior rectus muscle to innervate the superior oblique muscle.
CN V. Trigeminal Nerve
The trigeminal nerve as the name indicates is composed of three large branches. They are the ophthalmic (V1, sensory), maxillary (V2, sensory) and mandibular (V3, motor and sensory) branches. The large sensory root and smaller motor root leave the brainstem at the midlateral surface of pons. The sensory root terminates in the largest of the cranial nerve nuclei which extends from the pons all the way down into the second cervical level of the spinal cord. The sensory root joins the trigeminal or semilunar ganglion between the layers of the dura mater in a depression on the floor of the middle crania fossa. This depression is the location of the so called Meckle's cave. The motor root originates from cells located in the masticator motor nucleus of trigeminal nerve located in the midpons of the brainstem. The motor root passes through the trigeminal ganglion and combines with the corresponding sensory root to become the mandibular nerve. It is distributed to the muscles of mastication, the mylohyoid muscle and the anterior belly of the digastric. The mandibular nerve also innervates the tensor veli palatini and tensor tympani muscles. The three sensory branches of the trigeminal nerve emanate from the ganglia to form the three branches of the trigeminal nerve. The ophthalmic and maxillary branches travel in the wall of the cavernous sinus just prior to leaving the cranium. The ophthalmic branch travels through the superior orbital fissure and passes through the orbit to reach the skin of the forehead and top of the head. The maxillary nerve enters the cranium through the foramen rotundum via the pterygopalatine fossa. Its sensory branches reach the pterygopalatine fossa via the inferior orbital fissure (face, cheek and upper teeth) and pterygopalatine canal (soft and hard palate, nasal cavity and pharynx). There are also meningeal sensory branches that enter the trigeminal ganglion within the cranium. The sensory part of the mandibular nerve is composed of branches that carry general sensory information from the mucous membranes of the mouth and cheek, anterior two-thirds of the tongue, lower teeth, skin of the lower jaw, side of the head and scalp and meninges of the anterior and middle cranial fossae.
CN VI. Abducens Nerve
The abducens nerve originates from neuronal cell bodies located in the ventral pons. These cells give rise to axons that course ventrally and exit the brain at the junction of the pons and the pyramid of the medulla. The nerve of each side then travels anteriorly where it pierces the dura lateral to the dorsum sellae. The nerve continues forward and bends over the ridge of the petrous part of the temporal bone and enters the cavernous sinus. The nerve passes lateral to the carotid artery prior to entering superior orbital fissure. The abducens nerve passes through the common tendonous ring of the four rectus muscles and then enters the deep surface of the lateral rectus muscle. The function of the abducens nerve is to contract the lateral rectus which results in abduction of the eye. The abducens nerve in humans is solely and somatomotor nerve.
What is sixth nerve palsy? Sixth nerve palsy is a disorder that affects eye movement. It’s caused by damage to the sixth cranial nerve. The primary function of the sixth cranial nerve is to send signals to your lateral rectus muscle. This small muscle is located on the outer side in your eye. It is responsible for turning your eye away from your nose. When the lateral rectus muscle weakens, your eye crosses inward toward your nose. Symptoms of sixth nerve palsy Because each eye has its own lateral rectus muscle and sixth cranial nerve, sixth nerve palsy can affect one or both eyes. Your symptoms and the severity of the condition depend on whether both eyes are affected. Double vision is the most common symptom of sixth nerve palsy. You may notice this vision impairment when both eyes are open or when you’re looking at something in the distance. Sometimes, double vision occurs when looking in the direction of the damaged eye. It’s also possible to have sixth nerve palsy without double vision. Another symptom of this condition is poor eye alignment or strabismus, also called crossed eyes. This is when your eyes don’t look in the same direction at the same time. Double vision and strabismus are typical with sixth nerve palsy. But you may have other symptoms. The sixth cranial nerve travels from the brainstem to the lateral rectus muscle. This means neurologic disorders may cause sixth nerve palsy. When sixth nerve palsy occurs without other symptoms, it’s known as isolated sixth nerve palsy. The addition of other symptoms may suggest involvement of more than just the sixth nerve. What causes sixth nerve palsy? There are several causes of sixth nerve palsy. The condition can be congenital and affect a person from birth. This is sometimes due to injury of the sixth cranial nerve during labor or delivery. But sometimes the cause of congenital sixth nerve palsy is unknown. Various circumstances and illnesses can also cause the disorder. This includes a head injury or skull fracture that damages the sixth cranial nerve. The disorder may also develop as the result of inflammation in the sixth cranial nerve. Other conditions that can cause sixth cranial nerve damage or inflammation include: stroke infection Lyme disease brain tumor meningitis diabetic neuropathy multiple sclerosis brain aneurysm The most common cause of sixth nerve palsy in children is trauma, like from an accident involving a head injury. In adults, the most common cause is a stroke. Risk factors for sixth nerve palsy Anyone can develop sixth nerve palsy, and there’s no particular group of people at higher risk for this disorder. But you can take steps to protect yourself. Since trauma is a common cause, you should use caution and protect your head from injuries when playing sports or riding a bicycle. Likewise, since stroke is a common cause of sixth nerve palsy in adults, you can take precautions to reduce your risk of stroke. These measures include: controlling high blood pressure increasing physical activity losing weight maintaining a healthy diet How to diagnose sixth nerve palsy? If you have double vision or if your eyes aren’t aligning properly, see your doctor. To diagnose sixth nerve palsy, your doctor will ask questions about your medical history and do a complete physical examination. Because sixth nerve palsy has various possible causes, your doctor may order a series of tests. Treating the underlying problem may gradually correct the disorder. These tests include: brain scan to check for a brain tumor, skull fracture, brain injury, or increased pressure in the brain blood test or a lumbar puncture to diagnose or rule out meningitis neurological tests to check for abnormalities in your nervous system How to treat sixth nerve palsy? In some cases, treatment is unnecessary and sixth nerve palsy improves in time, such as when the disorder is caused by a viral infection that has to run its course. Other times, the disorder only improves once the underlying cause has been treated. Treatment depends on your diagnosis. Your doctor may prescribe antibiotics if your sixth nerve palsy is caused by a bacterial infection. Prescription-strength corticosteroids can treat sixth nerve palsy caused by inflammation. If you have a brain tumor, symptoms of sixth nerve palsy may not improve until you have surgery, chemotherapy, or other treatments to remove the tumor or kill cancer cells. You may never recover from sixth nerve palsy caused by trauma. Your doctor may monitor your condition over a six-month period. If double vision or strabismus hasn’t improved or worsens, options include wearing an eye patch over the affected eye long-term to alleviate double vision. Your doctor may also recommend prism glasses to provide single binocular vision and align your eyes. Some medical procedures are also effective. These include Botulinum toxin injections (Botox) where your doctor paralyzes the muscles on one side of your eye to correct poor alignment. Eye surgery is another option. If successful, surgery can stop an affected eye from pulling inward toward the nose. Complications and outlook for sixth nerve palsy? Sixth nerve palsy doesn’t cause complications. But you may have complications from underlying conditions. This is why it’s important to understand the cause of your disorder. The long-term outlook for this condition depends on the cause. With treatment, symptoms of sixth nerve palsy usually go away within the first six months of onset. Even though symptoms may not completely go away after a trauma, you may notice some vision improvement as your body heals.
CN VII. Facial Nerve
The facial nerve is mixed nerve containing both sensory and motor components. The nerve emanates from the brain stem at the ventral part of the pontomedullary junction. The nerve enters the internal auditory meatus where the sensory part of the nerve forms the geniculate ganglion. In the internal auditory meatus is where the greater petrosal nerve branches from the facial nerve. The facial nerve continues in the facial canal where the chorda tympani branches from it the facial nerve leaves the skull via the styolomastoid foramen. The chorda tympani passes through the petrotympanic fissure before entering the infratemporal fossae. The main body of the facial nerve is somatomotor and supplies the muscles of facial expression. The somatomotor component originates from neurons in the facial motor nucleus located in the ventral pons. The visceral motor or autonomic (parasympathetic) part of the facial nerve is carried by the greater petrosal nerve. The greater petrosal nerve leaves the internal auditory meatus via the hiatus of the greater petrosal nerve which is found on the anterior surface of the petrous part of the temporal bone in the middle cranial fossa. The greater petrosal nerve passes forward across the foramen lacerum where it is joined by the deep petrosal nerve (sympathetic from superior cervical ganglion). Together these two nerves enter the pterygoid canal as the nerve of the pterygoid canal. The greater petrosal nerve exits the canal with the deep petrosal nerve and synapses in the pterygopalatine ganglion in the pterygopalatine fossa. The ganglion then gives of nerve branches which supply the lacrimal gland and the mucous secreting glands of the nasal and oral cavities. The other parasympathetic part of the facial nerve travel with the chorda tympani which joins the lingual nerve in the infratemporal fossa. They travel with lingual nerve prior to synapsing in the submandibular ganglion which is located in the lateral floor of the oral cavity. The submandibular ganglion originates nerve fibers that innervate the submandibular and sublingual glands. The visceral motor components of the facial nerve originate in the lacrimal or superior salivatory nucleus. The nerve fibers exit the brainstem via the nervus intermedius. (The nervus intermedius is so called because of its intermediate location between the eighth cranial nerve and the somatomotor part of the facial nerve just prior to entering the brain). There are two sensory (special and general) components of facial nerve both of which originate from cell bodies in the geniculate ganglion. The special sensory component carries information from the taste buds in the tongue and travel in the chorda tympani. The general sensory component conducts sensation from skin in the external auditory meatus, a small area behind the ear, and external surface of the tympanic membrane. These sensory components are connected with cells in the geniculate ganglion. Both the general and visceral sensory components travel into the brain with nervus intermedius part of the facial nerve. The general sensory component enters the brainstem and eventually synapses in the spinal part of trigeminal nucleus. The special sensory or taste fibers enter the brainstem and terminate in the gustatory nucleus which is a rostral part of the nucleus of the solitary tract.
Bell’s Palsy: What Causes It and How Is It Treated?
What is Bell’s palsy?
Bell’s palsy is a condition that causes a temporary weakness or paralysis of the muscles in the face. It can occur when the nerve that controls your facial muscles becomes inflamed, swollen, or compressed.
The condition causes one side of your face to droop or become stiff. You may have difficulty smiling or closing your eye on the affected side. In most cases, Bell’s palsy is temporary and symptoms usually go away after a few weeks.
Although Bell’s palsy can occur at any age, the condition is more common among people between ages 16 and 60. Bell’s palsy is named after the Scottish anatomist Charles Bell, who was the first to describe the condition.
What are the symptoms of Bell’s palsy?
The symptoms of Bell’s palsy can develop one to two weeks after you have a cold, ear infection, or eye infection. They usually appear abruptly, and you may notice them when you wake up in the morning or when you try to eat or drink.
Bell’s palsy is marked by a droopy appearance on one side of the face and the inability to open or close your eye on the affected side. In rare cases, Bell’s palsy may affect both sides of your face.
Other signs and symptoms of Bell’s palsy include:
difficulty eating and drinking
an inability to make facial expressions, such as smiling or frowning
muscle twitches in the face
dry eye and mouth
sensitivity to sound
irritation of the eye on the involved side
Call your doctor immediately if you develop any of these symptoms. You should never self-diagnose Bell’s palsy. The symptoms can be similar to those of other serious conditions, such as a stroke or brain tumor.
What causes Bell’s palsy?
Bell’s palsy occurs when the seventh cranial nerve becomes swollen or compressed, resulting in facial weakness or paralysis. The exact cause of this damage is unknown, but many medical researchers believe it’s most likely triggered by a viral infection.
What are the risk factors for Bell’s palsy?
Your risk of developing Bell’s palsy increases if you:
have a lung infection
have a family history of the condition
How is Bell’s palsy diagnosed?
Your doctor will first perform a physical examination to determine the extent of the weakness in your facial muscles. They’ll also ask you questions about your symptoms, including when they occurred or when you first noticed them.
Your doctor can also use a variety of tests to make a Bell’s palsy diagnosis. These tests may include blood tests to check for the presence of a bacterial or viral infection. Your doctor might also use an MRI or CT scan to check the nerves in your face.
How is Bell’s palsy treated?
In most cases, Bell’s palsy symptoms improve without treatment. However, it can take several weeks or months for the muscles in your face to regain their normal strength.
The following treatments may help in your recovery.
corticosteroid drugs, which reduce inflammation
antiviral or antibacterial medication, which may be prescribed if a virus or bacteria caused your Bell’s palsy
over-the-counter pain medications, such as ibuprofen or acetaminophen, which can help relieve mild pain
an eye patch (for your dry eye)
a warm, moist towel over your face to relieve pain
physical therapy exercises to stimulate your facial muscles
What are the potential complications of Bell’s palsy?
Most people who have an episode of Bell’s palsy will completely recover without complications. However, complications may occur in more severe cases of Bell’s palsy. These include the following:
You may have damage to the seventh cranial nerve. This nerve controls your facial muscles.
You may have excessive dryness in the eye, which can lead to eye infections, ulcers, or even blindness.
You may have synkinesis, which is a condition in which moving one body part causes another to move involuntarily. For example, your eye may close when you smile.
What is the long-term outlook for people with Bell’s palsy?
The outlook for people with Bell’s palsy is usually good. Recovery time may vary depending on the severity of nerve damage. In general, however, people can see an improvement within two weeks after the initial onset of symptoms. Most will completely recover within three to six months, but it may be longer for people with more severe cases of Bell’s palsy. In rare cases, symptoms may continue to return or may be permanent.
Call your doctor immediately if you’re showing any signs of Bell’s palsy. Prompt treatment can help speed up your recovery time and prevent any complications.
CN VIII. Vestibulocochlear Nerve
The vestibulocochlear nerve is a sensory nerve that conducts two special senses: hearing (audition) and balance (vestibular). The receptor cells for these special senses are located in the membranous labyrinth which is embedded in the petrous part of the temporal bone. There are two specialized organs in the bony labyrinth, the cochlea and the vestibular apparatus. The cochlear duct is the organ that is connected to the three bony ossicles which transduce sound waves into fluid movement in the cochlea. This ultimately causes movement of hair cells which activate the auditory part of the vestibulocochlear nerve. The vestibular apparatus is the organ that senses head position changes relative to gravity. Movement causes fluid vibration resulting in hair cell displacement that activates the vestibular part of the eighth nerve. The peripheral parts of the eighth nerve travel a short distance to nerve cell bodies at the base of the corresponding sense organs. From these peripheral sensory nerve cells the central part of the nerve then travels through the internal auditory meatus with the facial nerve. The eighth nerve enters the brain stem at the junction of the pons and medulla lateral to the facial nerve. The auditory component of the eighth nerve terminates in a sensory nucleus called the cochlear nucleus which is located at the junction of the pons and medulla. The vestibular part of the eight nerve ends in the vestibular nuclear complex located in the floor of the fourth ventricle.
CN IX. Glossopharyngeal Nerve
The glossopharyngeal nerve as its name suggests is related to the tongue and the pharynx. The ninth cranial nerve exits the brain stem as a the most rostral of a series of nerve rootlets that protrude between the olive and inferior cerebellar peduncle. These nerve rootlets come together to form the ninth cranial nerve and leave the skull through the jugular foramen. The tympanic nerve is a branch that is occurs prior to exit the skull. The visceromotor or parasympathetic part of the ninth nerve originate in the inferior salivatory nucleus. Nerve fibers from this nucleus join the other components of the ninth nerve during their exit from the brain stem. They branch in the cranium as the tympanic nerve. The tympanic nerve exits the jugular foramen and passes by the inferior glossopharyngeal ganglion. It re-enters the skull through the inferior tympanic canaliculus and reaches the tympanic cavity where it forms a plexus in the middle ear cavity. The nerve travels from this plexus through a canal and out into the middle cranial fossa adjacent to the exit of the greater petrosal nerve. It is here the nerve becomes the lesser petrosal nerve. The lesser petrosal nerve exits the cranium via the foramen ovali and synapses in the otic ganglion. The otic ganglion provides nerve fibers that innervate and control the parotid gland, an important salivary gland. The branchial motor component supplies the stylopharyngeas muscle which elevates the pharynx during swallowing and talking. In the jugular foramen are two sensory ganglion connected to the ninth cranial nerve: the superior and inferior glossopharyngeal ganglia. General sensory components from the skin of the external ear, inner surface of the tympanic membrane, posterior one-third of the tongue and the upper pharynx join either the superior or inferior glossopharyngeal ganglia. The ganglia send central processes into the brain stem which terminate in the caudal part of the spinal trigeminal nucleus. Visceral sensory nerve fibers originate from the carotid body (oxygen tension measurement) and carotid sinus (blood pressure changes). The visceral sensory nerve components connect to the inferior glossopharngeal ganglion. The central process extend from the ganglion and enter the brain stem to terminate in the nucleus solitarius. Taste from the posterior one-third of the tongue travels via nerve fibers that enter the inferior glossopharnygeal ganglion. The central process that carry this special sense travel through the jugular foramen and enter the brain stem. They terminate in the rostral part of the nucleus solitarius (gustatory nucleus).
CN X. Vagus Nerve.
The vagus nerve is the longest of the cranial nerve. Its name is derived from Latin meaning "wandering". True to its name the vagus nerve wanders from the brain stem through organs in the neck, thorax and abdomen. The nerve exits the brain stem through rootlets in the medulla that are caudal to the rootlets for the ninth cranial nerve. The rootlets form the tenth cranial nerve and exit the cranium via the jugular foramen. Similar to the ninth cranial nerve there are two sensory ganglia associated with the vagus nerve. They are the superior and inferior vagal ganglia. The branchial motor component of the vagus nerve originates in the medulla in the nucleus ambiguus. The nucleus ambiguus contributes to the vagus nerve as three major branches which leave the nerve distal to the jugular foramen. The pharyngeal branch travels between the internal and external carotid arteries and enters the pharynx at the upper border of the middle constrictor muscle. It supplies the all the muscles of the pharynx and soft palate except the stylopharyngeas and tensor palati. These include the three constrictor muscles, levator veli palatini, salpingopharyngeus, palatopharyngeus and palatoglossal muscles. The superior laryngeal nerve branches distal to the pharyngeal branch and descends lateral to the pharynx. It divides into an internal and external branch. The internal branch is purely sensory and will be discussed later. The external branch travel to the cricothyroid muscle which it supplies. The third branch is the recurrent branch of the vagus nerve and it travels a different path on the left and right sides of the body. On the right side the recurrent branch leave the vagus anterior to the subclavian artery and wraps back around the artery to ascend posterior to it. The right recurrent branch ascends to a groove between the trachea and esophagus. The left recurrent branch leaves the vagus nerve on the aortic arch and loops posterior to the arch to ascend through the superior mediastinum. The left recurrent branch ascends along a groove between the esophagus and trachea. Both recurrent branches enter the larynx below the inferior constrictor and supply intrinsic muscles of larynx excluding the cricothyroid. The visceromotor or parasympathetic component of the vagus nerve originates from the dorsal motor nucleus of the vagus in the dorsal medulla.
These cells give rise to axons that travel in the vagus nerve. The visceromotor part of the vagus innervates ganglionic neurons which are located in or adjacent to each target organ. The target organs in the head-neck include glands of the pharynx and larynx (via the pharyngeal and internal branches). In the thorax branches go to the lungs for bronchoconstriction, the esophagus for peristalsis and the heart for slowing of heart rate. In the abdomen branches enter the stomach, pancreas, small intestine, large intestine and colon for secretion and constriction of smooth muscle. The viscerosensory component of the vagus are derived from nerves that have receptors in the abdominal viscera, esophagus, heart and aortic arch, lungs, bronchia and trachea. Nerves in the abdomen and thorax join the left and right vagus nerves to ascend beside the left and right common carotid arteries. Sensation from the mucous membranes of the epiglottis, base of the tongue, aryepiglottic folds and the upper larynx travel via the internal laryngeal nerve. Sensation below the vocal folds of the larynx is carried by the recurrent laryngeal nerves. The cell bodies that give rise to the peripheral processes of the visceral sensory nerves of the vagus are located in the inferior vagal ganglion. The central process exits the ganglion and enters the brain stem to terminate in the nucleus solitarius. The general sensory components of the tenth cranial nerve conduct sensation from the larynx, pharynx, skin the external ear and external auditory canal, external surface of the tympanic membrane, and the meninges of the posterior cranial fossa. Sensation from the larynx travels via the recurrent laryngeal and internal branches of the vagus to reach the inferior vagal ganglion. Sensory nerve fibers from the skin and tympanic membrane travel with auricular branch of the vagus to reach the superior vagal ganglion. The central processes from both ganglia enter the medulla and terminate in the nucleus of the spinal trigeminal tract.
CN XI. Spinal Accessory Nerve
The spinal accessory nerve originates from neuronal cell bodies located in the cervical spinal cord and caudal medulla. Most are located in the spinal cord and ascend through the foramen magnum and exit the cranium through the jugular foramen. They are branchiomotor in function and innervate the sternocleidomastoid and trapezius muscles in the neck and back. The cranial root of the accessory nerve originates from cells located in the caudal medulla. They are found in the nucleus ambiguus and leave the brainstem with the fibers of the vagus nerve. They join the spinal root to exit the jugular foramen. They rejoin the vagus nerve and distribute to the same targets as the vagus. Most consider the cranial part of the eleventh cranial nerve to be functionally part of the vagus nerve.
CN XII. Hypoglossal Nerve
The hypoglossal nerve as the name indicates can be found below the tongue. It is a somatomotor nerve that innervates all the intrinsic and all but one of the extrinsic muscles of the tongue. The neuronal cell bodies that originate the hypoglossal nerve are found in the dorsal medulla of the brain stem in the hypoglossal nucleus. This nucleus gives rise to axons that exit as rootlets that emerge in the ventrolateral sulcus of the medulla between the olive and pyramid. The rootlets come together to form the hypoglossal nerve and exit the cranium via the hypoglossal canal. The nerve passes laterally and inferiorly between the internal carotid artery and internal jugular vein. The twelfth cranial nerve travels lateral to the bifurcation of the common carotid and loops anteriorly above the greater horn of the hyoid bone to run on the lateral surface of the hyoglossus muscle. It then travels above the edge of the mylohyoid muscle. The hypoglossal nerve then separates into branches that supply the intrinsic muscles and three of the four extrinsic muscles of the tongue.