All 12 Cranial Nerves | Anatomy & Physiology

The olfactory nerve is a sensory nerve responsible for transmitting information about olfaction, or smell, to the brain. The nerve begins in the olfactory epithelium, a specialized collection of cells that lines the nasal cavity in humans. The olfactory epithelium contains millions of olfactory receptor cells. The axons of the olfactory receptor cells form bundles called

fila that travel up through a structure called the cribriform plate, which is part of the bone called the ethmoid bone that separates the nasal cavity from the brain. The cribriform plate has holes that allow the fila to pass through it. The fila make up the olfactory nerve.

The olfactory nerve travels to an adjacent structure called the olfactory bulb, where it forms synaptic connections with several types of olfactory bulb neurons, like cells called mitral cells. These olfactory bulb neurons carry information about smell to the olfactory cortex as part of the olfactory tract.

Damage to the olfactory nerve can happen in a number of ways, such as head trauma or tumors.

When the olfactory nerve is damaged, the sense of smell is affected. The deficits can include anosmia, which is a complete loss of the sense of smell, or varying levels of impaired or distorted olfaction. Olfactory nerve damage is also linked to abnormalities in flavor perception due to

olfaction. Olfactory nerve damage is also linked to abnormalities in flavor perception due to the role of the olfactory system in flavor. The ability to smell can be assessed through tests where patients are exposed to a variety of odorants and asked to identify them. An impaired

sense of smell alone, however, can be due to a number of causes and doesn’t necessarily indicate olfactory nerve damage, so more testing must be done to verify the cause of the deficit.

The optic nerve is a sensory nerve responsible for transmitting information about vision to the brain. The nerve begins in the retina as the axons of cells called retinal ganglion cells. These

brain. The nerve begins in the retina as the axons of cells called retinal ganglion cells. These

axons come together to leave the eye at a region called the optic disc and form the optic nerve.

The optic nerve leaves the eye and extends to a structure called the optic chiasm where it meets the optic nerve from the other eye. At the optic chiasm, the optic nerve fibers carrying information from the sides of the retina closest to the nose cross over to the other side of the brain, while those carrying information from the sides of the retina closest to the temples

remain on the side of the brain where they are. After leaving the optic chiasm, the nerve fibers are referred to as the optic tract. Most of the nerve fibers in the optic tract end in the lateral geniculate nucleus of the thalamus, and from there the information will be passed on to the visual cortex.

Damage to the optic nerve can occur due to a variety of causes like trauma, tumors, stroke, or glaucoma. The deficit that occurs after damage depends on where the nerve is damaged,

or glaucoma. The deficit that occurs after damage depends on where the nerve is damaged, and involves some degree of visual defect or anopsia. If the damage occurs before the optic chiasm, then the patient will experience blindness in the eye supplied by that optic nerve. Damage

to the middle of the optic chiasm will cause loss of the lateral visual field of both eyes, due to the way fibers from the nasal side of the retina cross over at this point. If the

optic tract is damaged, one half of the visual field will be lost in both eyes.

The oculomotor nerve is responsible for supplying 4 of the 6 extraocular muscles: the medial rectus, which moves the eye towards the nose; the superior rectus, which moves the eye upwards; the inferior rectus, which moves the eye downwards; and the inferior oblique, which moves the eye up and out. Additionally, the nerve supplies the levator palpebrae superioris,

which is the muscle that elevates the eyelid. It also forms connections with neurons in the ciliary ganglion, which innervate the pupillary sphincter to control the constriction of the pupil and the ciliary muscle, which adjusts the shape of the lens to see clearly at close distances.

Oculomotor nerve fibers originate in the oculomotor nucleus in the midbrain. From here,

they travel to the orbit of the eye, along the way separating into branches that control the different extraocular muscles. The fibers that control the pupillary sphincter and ciliary muscle originate in the Edinger-Westphal nucleus and travel with the oculomotor nerve.

Damage to the oculomotor nerve causes deficits in the ipsilateral eye. A common symptom is a deviation of the affected eye to the side and downwards due to the paralysis of the medial rectus and inferior oblique, and the unopposed action of the unaffected extraocular muscles.

Medial eye movements may also be impaired due to paralysis of the medial rectus, and vertical eye movements may be impaired due to the paralysis of the superior and inferior recti and inferior oblique. Diplopia, or double-vision, is common.

Ptosis, or drooping of the eyelid may occur due to the paralysis of the levator palpebrae superioris. Because the pupillary constriction muscle is impaired, the pupil on the side of

superioris. Because the pupillary constriction muscle is impaired, the pupil on the side of the damage may remain dilated, a condition known as mydriasis. And the patient may have a difficult time focusing the lens for close-up vision due to effects on the ciliary muscle.

The trochlear nerve, also known as cranial nerve IV, is responsible for supplying one of the extraocular muscles of the eye: the superior oblique muscle. The superior oblique helps the eye to move down and out. To create this type of movement, the muscle passes through a pulley-like structure called the trochlea of the superior oblique, which is where the nerve gets its name.

The trochlear nerve originates in a small nucleus in the midbrain. The nerve fibers decussate, or cross over to the other side, of the brainstem before leaving the brainstem near the junction of the midbrain and pons. The trochlear nerve is the only cranial nerve that leaves the brainstem from the back, or posterior surface, of the brainstem. It’s also the only cranial

nerve to completely originate from a nucleus contralateral to the structure it supplies.

The trochlear nerve is a very delicate nerve that is relatively easily damaged. Damage can

be congenital or occur due to other causes like trauma. The symptoms of trochlear nerve palsy, however, are typically not as noticeable as those that result from damage to the oculomotor or abducens nerve. Because the superior oblique helps to move the eye downwards, when the nerve is damaged the eye tends to deviate upwards since there is no opposing force coming

from the superior oblique. This can result in diplopia, or double-vision. Some patients will adopt a head tilt as a compensatory mechanism to better align the eyes and reduce the diplopia. If

the palsy does not resolve on its own or through less invasive treatments, patients may undergo surgery to weaken an opposing muscle (usually the inferior oblique) to minimize the deviation.

The trigeminal nerve is the main sensory nerve of the head. It carries information about touch, pain, temperature, and proprioception, or the awareness of the position of muscles and joints. It also controls the muscles involved with chewing, as well as the tensor tympani,

joints. It also controls the muscles involved with chewing, as well as the tensor tympani, a small muscle in the middle ear that helps to dampen the sound of loud noises, and the tensor veli palatini, a muscle that both helps prevent food from entering the nasopharynx during swallowing and opens a small tube called the eustachian tube, which connects the upper

throat with the middle ear. This helps to equalize pressure between the middle ear and outside air.

The trigeminal nerve has three divisions, the ophthalmic, maxillary, and mandibular divisions, which supply three different regions of the head and face as seen in the image. The ophthalmic and maxillary divisions carry sensory information,

image. The ophthalmic and maxillary divisions carry sensory information, while the mandibular division has sensory and motor components.

There are three sensory nuclei and a motor nucleus associated with the trigeminal nerve. They form a column of cells that reaches from the midbrain of the brainstem

trigeminal nerve. They form a column of cells that reaches from the midbrain of the brainstem to the upper spinal cord. The main sensory nucleus receives information from the head about touch and proprioception. The spinal trigeminal nucleus receives information about pain and temperature sensations. The mesencephalic nucleus receives proprioceptive information from the jaw and teeth to prevent damage while biting and

chewing. The motor nucleus controls the muscles of chewing and other muscles mentioned earlier.

chewing. The motor nucleus controls the muscles of chewing and other muscles mentioned earlier.

Damage to the trigeminal nerve or its associated nuclei can cause varying levels of abnormal sensation. The patient may experience decreased sensation, increased pain, and/or weakening of

sensation. The patient may experience decreased sensation, increased pain, and/or weakening of the muscles of chewing. Trigeminal nerve damage can also lead to a condition called trigeminal neuralgia, in which patients experience short but intense bouts of facial pain.

The abducens nerve, also known as cranial nerve VI, is a motor nerve responsible for supplying one of the extraocular muscles of the eye: the lateral rectus muscle.

The lateral rectus muscle abducts the eye, or moves it laterally toward the side of the head.

The abducens nerve originates in the abducens nucleus, which is located in the pons. Fibers

from the facial nerve wrap around the abducens nucleus, and the combination of the nucleus and facial nerve fibers creates a bulge in the floor of the fourth ventricle known as the facial colliculus. The abducens nerve fibers exit the brainstem at the junction between the pons and medulla and supply the lateral rectus muscle on the same side of the head.

Neurons from the abducens nucleus also travel through a pathway called the medial longitudinal fasciculus to the oculomotor nucleus, where they synapse on neurons that control the medial rectus muscle of the other eye. The medial rectus moves the eye inward.

This pathway allows for coordination of eye movement, as when your abducens nerve allows you to look laterally with your left eye, the fibers that travel in the medial longitudinal fasciculus cause your right eye to look medially.

Damage to the abducens nerve causes impairment in the ability of the eye the nerve supplies to to move laterally, and a condition called esotropia in which the eye that’s affected deviates medially. In this case, the medial deviation is due to the loss of abducens function and the

medially. In this case, the medial deviation is due to the loss of abducens function and the unopposed action of the medial rectus muscle. This also leads to diplopia, or double vision.

The facial nerve, also known as cranial nerve VII, is best known for its role in controlling the muscles of facial expression, as well as a number of other muscles of the face and head such as certain muscles involved with swallowing and jaw movement, muscles of the external ear, and the stapedius muscle, which is found in the middle ear and is involved with dampening

loud noises. The facial nerve also receives sensory information from the outer ear and from

loud noises. The facial nerve also receives sensory information from the outer ear and from the taste buds on the anterior two-thirds of the tongue, and it supplies most major glands in the head, including the lacrimal glands for tear production, the submandibular and sublingual

salivary glands, and the mucous glands of the nose, paranasal sinuses, and palate.

The facial nerve is associated with several nuclei in the brainstem. The motor portion of the facial nerve originates in the facial motor nucleus in the pons. The portion of the nerve that supplies the glands mentioned previously originates from the superior salivatory nucleus in the pons. Taste information travels to the nucleus of the solitary tract in the medulla. And the

pons. Taste information travels to the nucleus of the solitary tract in the medulla. And the

sensory information from the outer ear travels to the spinal trigeminal nucleus in the medulla.

Facial nerve damage can cause a variety of symptoms, but the most recognizable of them is weakness and/or paralysis of the muscles of facial expression on the same side of the head that the damaged nerve supplies. The patient’s mouth on the affected side may droop, and he may be unable to close the eye on the affected side. In most cases of facial nerve palsy, the

cause of the dysfunction is not known; when this is the case it is referred to as Bell’s palsy.

The vestibulocochlear nerve consists of a vestibular and cochlear component, which have the functions of carrying information to the brain from the vestibular system and the cochlea, respectively. The information from the cochlea deals with hearing,

cochlea, respectively. The information from the cochlea deals with hearing, while the information from the vestibular system deals with vestibular sensations, which include information about head position and movement. This vestibular information enables us to keep our balance, stabilize our head and body during movement, and maintain posture.

The cochlear component of cranial nerve eight begins with neurons that make connections with hair cells, the sensory receptor cells of the auditory system. When hair cells are activated, they relay auditory signals to the the cochlear portion of the nerve through changes in levels of neurotransmitter release.

The cochlear nerve travels from the cochlea to the dorsal and ventral cochlear nuclei, which are found at the junction between the pons and medulla. From there, the auditory information is sent to areas in the brainstem and cortex that are involved with auditory processing.

The vestibular component of the nerve also receives stimulation from hair cells, but these cells are found in the vestibular apparatus. From there, the nerve travels to the vestibular nuclei in the pons and medulla. The vestibular nuclei consist of four subnuclei: the inferior, medial, lateral, and superior vestibular nuclei. Neurons leave each of these

nuclei to project to various areas in the brain, brainstem, and spinal cord to coordinate head, eye, and body movements to maintain balance and equilibrium, along with other related functions.

Damage to the vestibulocochlear nerve can cause disruption of hearing and/or vestibular functions, generating symptoms like hearing loss, tinnitus, dizziness, loss of balance, and nausea.

The glossopharyngeal nerve is associated with the tongue and the pharynx, or throat, and has both sensory and motor functions. It carries sensory information about touch, pain, and temperature from the posterior third of the tongue, the upper part of the throat, the tonsils, part of the outer ear, the inner surface of the eardrum, and the eustachian tube. It also conveys

sensory information from the carotid body and carotid sinus, structures that detect oxygen, carbon dioxide, and ph levels in the blood along with changes in blood pressure. The

nerve also conveys taste information from the posterior ⅓ of the tongue and carries motor signals to the stylopharyngeus muscle, which plays a role in swallowing and speech.

And it innervates the parotid gland, the largest of our salivary glands.

The glossopharyngeal nerve is associated with a number of nuclei in the medulla. The fibers

that supply the stylopharyngeus muscle originate in the nucleus ambiguus. The

sensory fibers that carry taste information, and those that carry sensory information from the carotid body and carotid sinus, synapse in the nucleus solitarius, and the fibers that convey touch and pain synapse in the spinal trigeminal nucleus.

The fibers that innervate the parotid gland arise from the inferior salivatory nucleus.

Damage to the glossopharyngeal nerve can cause a variety of symptoms, including a loss of taste on the posterior ⅓ of the tongue, trouble swallowing, and generally decreased sensation on the back of the tongue, the soft palate, and pharynx. Patients may also have a diminished gag reflex, and the uvula will often deviate

and pharynx. Patients may also have a diminished gag reflex, and the uvula will often deviate to the side opposite from where the damage has occurred. In rare cases, patients may experience glossopharyngeal neuralgia, which involves brief but intense pain in the tongue and throat.

The vagus nerve is an extremely long nerve that travels from the brainstem to the colon and has a long list of functions. It carries sensory information about pain, touch, and temperature from the throat, parts of the inner and outer ear, and the meninges near the back of the head. It plays a very minor role in taste. It also

receives sensory information from internal organs in the neck, chest and abdomen like the esophagus, heart, and digestive tract. And it carries sensory information from both baroreceptors in the aorta that detect changes in blood pressure, and chemoreceptors in the aorta that sense oxygen levels in the blood. The vagus nerve controls the movement of a number of muscles in the pharynx,

soft palate, and larynx (as well as one muscle in the tongue) to play a critical role in the control of speaking and swallowing. It is also the main parasympathetic nerve of the body, providing parasympathetic innervation to organs throughout the neck, thorax, and abdomen, contributing to a variety of functions such as slowing of the heart rate.

There are several nuclei in the medulla associated with the vagus nerve and the different types of information it carries. Information about touch, pain, and temperature travels to the spinal trigeminal nucleus. Sensory information from internal organs, or visceral sensory information, travels to the solitary nucleus. Motor signals originate in the

nucleus ambiguus. Parasympathetic fibers originate primarily in the dorsal vagal motor nucleus,

nucleus ambiguus. Parasympathetic fibers originate primarily in the dorsal vagal motor nucleus, while some parasympathetic fibers that travel to the heart begin in the nucleus ambiguus.

Symptoms of vagus nerve damage may include hoarseness of the voice, difficulty swallowing, and a deficient gag reflex. The uvula may deviate away from the side where the damage has occurred. Because the nerve supplies a number of organs, however, damage can result in many

has occurred. Because the nerve supplies a number of organs, however, damage can result in many other symptoms as well, like abnormalities in heart rate or gastrointestinal problems. The accessory nerve is primarily considered a motor nerve that supplies two muscles: the

sternomastoid muscle and the trapezius muscle. The sternomastoid helps to turn your head to the side, as well as bend your neck down or to the side. The trapezius is involved with the movement of the neck and scapula, or shoulder blade. The trapezius is important to a variety of shoulder and arm movements, such as shrugging your shoulders or raising your arms above your head.

Traditionally, the accessory nerve has been divided into a spinal component, which originates in the accessory nucleus in the spinal cord, and a cranial component, which originates in the nucleus ambiguus in the medulla. The fibers that make up the spinal portion of the nerve leave the spinal cord as a series of rootlets, which then come together to form what is known as the spinal root. The spinal root ascends to join the cranial root that extends

from the medulla. The cranial and spinal roots travel together briefly as they exit the skull, but then the cranial portion travels with the vagus nerve while the spinal portion extends to the sternomastoid and trapezius muscles. Because the cranial portion can be functionally considered part of the vagus nerve, often the spinal portion is considered the true accessory nerve.

Damage to the accessory nerve can cause weakness or paralysis of the sternomastoid and/or trapezius muscles, but trapezius dysfunction is typically the more incapacitating problem. Trapezius

dysfunction may impair arm and shoulder movement, cause the shoulder to droop, and cause the shoulder blade to abnormally protrude from the back--a condition known as a “winged scapula.” The patient may also experience shoulder and neck pain, along with muscle fatigue because other muscles in the shoulder and arm that are unaccustomed to supporting the shoulder must be utilized.

The hypoglossal nerve is a motor nerve that controls all of the muscles of the tongue (except for one, the palatoglossus, which is controlled by the vagus nerve). The tongue muscles consist of what are known as intrinsic muscles, which control the shape of the tongue, and extrinsic muscles, which act to protrude, retract, elevate, and move the tongue side to side. Healthy function

of the hypoglossal nerve is thus critical for things like eating, swallowing, and speaking.

The hypoglossal nuclei are found in the medulla. Hypoglossal nerve fibers leave the hypoglossal nuclei on each side of the brainstem and descend to travel to the same side of the tongue to stimulate the muscles of the tongue from below, hence the term hypoglossal, which comes from the Greek for under the tongue. There are three other branches that extend from the hypoglossal nerve to supply various other muscles in the neck as well as the dura mater

at the back of the head. Only the fibers that supply the tongue originate in the hypoglossal nucleus, however, and thus they are often considered the true hypoglossal nerve.

Damage to the hypoglossal nerve can cause tongue weakness and impair tongue dexterity.

It may also lead to small muscle twitches, or fasciculations, in the tongue as well as atrophy of the tongue--especially at the tip or borders of the organ.

If the hypoglossal nerve on only one side is damaged, then atrophy will typically be seen in the tongue muscles on that same side. If the patient is asked to protrude his or her tongue, the tongue will often deviate toward the side of the damaged nerve. Patients with

damage to only one hypoglossal nerve, however, are often able to compensate for the deficiency of the tongue muscles on one side. But if both nerves are damaged, the patient may be unable to

protrude the tongue at all and may experience severe problems with speech and swallowing.