SVE: Fibers originate from nucleus of facial nerve, and supply facial muscles
GVE: Fibers derived from superior salivatory nucleus and relayed in pterygopalatine and submandibular ganglia. The postganglionic fibers supply lacrimal, submandibular and sublingual glands.
SVA: Fibers from taste buds of anterior two thirds of tongue with cell bodies in the geniculate ganglion of the facial nerve end by synapsing with cells of nucleus of solitary tract
Figure 2: Facial Nerve in the Petrous Part of Temporal Bone
GSA: Fibers from skin of external ear.
The facial nerve arises by two roots from the brainstem (Pons) in the posterior cranial fossa.
Figure 1: Nuclei of the Facial Nerve in Pons
Like the trigeminal nerve, one root is special visceral motor. But unlike the trigeminal nerve, the other contains preganglionic parasympathetic axons as well as sensory axons. The other name of this root is the “nervus intermedius”. It gives no information about fiber type. Rather, it refers to its position between the motor root and cranial nerve VIII.
The special visceral motor root and nervus intermedius enter the internal acoustic meatus in the petrous temporal bone along with the VIII cranial nerve.
All three are enveloped by an arachnoid / dural sheath that extends the length of the meatus.
The nervus intermedius and motor root of the facial join to form the complete facial nerve just before the end of the meatus, and this complete nerve pierces the arachnoid and dura to enter the facial canal.
The facial canal runs anterolaterally in the petrous bone for one or two millimeters and then comes upon the labyrinthine wall of the tympanic cavity.
Here the facial nerve bifurcates in two forks that move off in opposite directions perpendicular to the path of their parent nerve.
The larger fork passes posterolaterally and the smaller passes anteromedially.
Both forks run parallel to the long axis of petrous temporal bone.
At the site of the bifurcation there is a collection of cells that form the sensory ganglion of the facial nerve.
The larger fork retains the name “facial nerve” and the channel within the petrous bone through which it travels retains the name “facial canal”.
Figure 2: Intracranial Course of the Facial Nerve
When the facial nerve encounters the labyrinthine wall of the tympanic cavity it undergoes a 90o bend in its course that takes it posterolaterally.
This bend is called the genu of the facial nerve (Lt: knee).
That is why the sensory ganglion located at the facial bifurcation is most often called the “geniculate ganglion”.
Beyond the geniculate ganglion the facial nerve runs posterolaterally in the bone that forms the labyrinthine wall of the tympanic cavity.
Figure 3: Intracranial branches of the Facial Nerve
This course takes it above the oval window but inferior to the lateral semicircular canal to the mastoid wall of the tympanic cavity.
Upon reaching the bony mastoid wall of the tympanic cavity, the facial nerve passes below the aditus ad antrum into this wall.
The nerve then continues downward in the mastoid wall of the tympanic cavity to emerge from the stylomastoid foramen.
Near the vicinity of the geniculate ganglion, the facial nerve gives off a tiny twig that participates in a nerve plexus that lies beneath the mucous membrane that covers the promontory of the tympanic cavity.
The plexus is called the tympanic plexus, and it receives its main input from the tympanic branch of the glossopharyngeal nerve. The internal carotid plexus also sends a caroticotympanic nerve backwards to join in the tympanic plexus.
While it descends in the mastoid wall of the middle ear cavity, the facial nerve gives off two branches.
The first one is the minute nerve to the stapedius muscle.
The second one “the chorda tympani” is given off a little further along its descent.
This nerve passes forward out of the bony mastoid wall into the tympanic cavity (but remains outside its mucous membrane).
Figure 4: The Chorda Tympani
Here it continues anteriorly, crossing lateral to the long process of the incus and then medial to the neck of the malleus.
The chorda tympani then passes out of the carotid wall of the tympanic cavity through a slit (petrotympanic fissure) that leads to the infratemporal fossa just behind the medial end of the jaw joint.
Its course beyond this point is linked to the lingual branch of VIII.
The chorda tympani carries:
Preganglionic parasympathetic axons for the submandibular and sublingual salivary glands, and
Taste fibers from the anterior two thirds of the tongue.
Figure 5: Extracranial Course & Branches of the Facial Nerve
While traveling in the mastoid wall of the tympanic cavity, the facial nerve also sends a small twig to communicate with the auricular branch of the vagus.
This twig carries somatic sensory axons from the external auditory meatus.
Upon exiting the skull through the stylomastoid foramen, the facial nerve enters the retromandibular region of the neck.
Here it gives branches to the auricularis posterior, stylohyoid, and the posterior belly of digastric muscles.
After these are given off, the nerve enters the parotid gland and divides into upper and lower divisions, which turn forward, pass lateral to the retromandibular vein, and thereby reach the part of the parotid lying in the face.
Here, within the gland, the two divisions join again to form the “ansa facialis.”
From this loop spray out the branches of the facial nerve to the remaining facial muscles.
These branches are given names according to the general area of the face to which they run (temporal, zygomatic, buccal, mandibular, cervical).
The smaller, anteromedially coursing fork of the facial nerve is called the greater superficial petrosal nerve.
Figure 7: Course & Distribution of the Facial Nerve
It emerges into the middle cranial fossa on the anterior surface of the petrous temporal (between bone and endocranium) through a hole called the hiatus of the facial canal.
From here, its course continues across the depth of the trigeminal ganglion and onto the cartilage that fills the foramen lacerum, where the nerve is located just lateral to the internal carotid artery.
Here, postganglionic sympathetic fibers from the internal carotid plexus join the greater superficial petrosal nerve. These sympathetic axons are said to form the deep petrosal nerve.
The product of this joining will leave the cranial cavity by passing obliquely through the cartilage of the foramen lacerum to enter a canal in the sphenoid bone at the root of the medial pterygoid plate.
This is the pterygoid canal, and the bundle formed by the conjoined deep petrosal and greater superficial petrosal nerves is called the nerve of the pterygoid canal.
The pterygoid canal ends by opening into the pterygopalatine fossa located inferomedial to the foramen rotundum.
As soon as the nerve of the pterygoid canal enters this fossa, it encounters the pterygopalatine ganglion, on whose cells the preganglionic parasympathetic axons synapse.
The postganglionic parasympathetic axons from the ganglion are distributed with branches of the maxillary nerve.
Some of these enter the zygomatic nerve and are carried into the orbit, where they cross to the lacrimal branch of VI for supply of the lacrimal gland.
The postganglionic sympathetic axons within the nerve of the pterygoid canal pass right through the pterygopalatine ganglion, without synapse, to distribute with branches of the maxillary nerve.
The taste fibers from the palate travel through palatine nerves up to the ganglion, and then pass through it into the nerve of pterygoid canal and greater superficial petrosal nerve, which carries them to their cells of origin in the geniculate ganglion.
The symptoms of damage to the facial nerve depend on where along its course the damage has occurred.
One of the most common sites is the region of the facial canal just above the stylomastoid foramen.
Here, an inflammatory disease of unknown etiology causes a condition known as Bell's palsy.
All the facial muscles on one side are paralyzed, but the glandular and taste functions of the facial nerve remain intact.
Bell’s palsy is characterized by a multitude of symptoms that can be predicted from paralysis of facial muscles:
In older persons, in whom elasticity of skin is diminished, paralysis of facial muscles causes the normal creases in facial skin to be diminished or absent on the affected side.
In all persons, both young and old, the eye of the affected side cannot be completely closed.
Because blinking is impossible, the normal cleansing of the surface of the eye is impossible.
The lacrimal gland increases its secretion in an attempt to compensate.
However, without blinking, the tears are not distributed toward the lacrimal puncta.
Furthermore, paralysis of the lacrimal portion of orbicularis oculi causes the lacrimal puncta to lift off the surface of the eyeball, and paralysis (or loss of passive elasticity) of the palpebral orbicularis oculi of the lower lid causes it to fall forward away from the eye.
Figure 8: Facial Nerve Palsy (Bell’s Palsy)
The effect of all these changes is for the excess tears to pool beneath the lower lid and then spillover onto the cheek.
The potential for irritation to the cornea is great, and persons with a Bell's palsy must wear an eye patch to keep the lids closed.
The corner of the mouth and the lower lip droop on the side of the paralysis, allowing saliva to run out of the mouth.
Paralysis of the buccinator allows food to accumulate between the cheek and lower gum.
The patient prefers to chew on the un paralyzed side, but often must manually push on the lower cheek of the affected side in order to express food out of the oral vestibule.
Occasionally, a facial paralysis may be psychosomatic in nature. It can be diagnosed by availing oneself of the oculoauricular reflex. Normally, when a person looks very strongly to one side, the opposite ear is pulled back by the auricularis posterior muscle. This reflex is absent in Bell's palsy, but it is intact if the facial paralysis is psychosomatic.
Pathology of the facial nerve within the facial canal may extend upward to involve the communicating twig to the vagus and the origin of the chorda tympani.
Since so many other nerves provide sensation to the external auditory meatus, loss of function in the “facial axons” that do so is undetectable.
However, irritative lesions of, the facial nerve may lead to pain in the external auditory meatus. If the chorda tympani is damaged, taste from the anterior two thirds of the tongue will be lost (or greatly diminished).
Some patients with damage to the chorda tympani also complain of partial numbness of the tongue on the ipsilateral side. Progress of the disease even more superiorly in the facial canal leads to paralysis of the stapedius and a resultant increased sensitivity to loud sounds, known as hyperacusis.
Tumors within the petrous temporal may affect the facial nerve at the site of the geniculate ganglion.
This leads to all the symptoms just described, plus loss of tearing on the affected side.
Lesions of the facial nerve between the brain and the facial canal may affect one root and not the other because the two roots are actually separate during this part of their courses.
There is a peculiarity about the cortical input to the facial nuclei of the brainstem that is useful in diagnostics.
The facial motor neurons projecting to the upper third of the face receive cortical control from both the right and left cerebral hemispheres, whereas the facial motor neurons to the lower two thirds of the face receive cortical control only from the opposite cerebral hemisphere.
Thus, if a facial paralysis is due to interruption in the corticobulbar pathway on one side, the symptoms due to paralysis of the mouth and cheek on the opposite side are full-blown, but the orbicularis oculi and frontalis of this same side are not nearly as weakened as in Bell’s palsy.
Testing of the facial nerve during a routine physical examination is confined to assessing the major facial muscles.
The patient is asked to raise the eyebrows or wrinkle the forehead (occipitofrontalis) and the examiner looks to see if this is done symmetrically.
The patient is asked to close the eyes very tightly (orbicularis oculi --- orbital and palpebral portions) and the examiner tries to force them open by pushing up on the eyebrows.
A broad smile is requested (mainly zygomaticus major) and assessed for symmetry.
The, patient is asked to puff out the cheeks.
Puffing out one's cheeks is made possible by the action of orbicularis auris in preventing escape of air between the lips. If one side is very weak, air escapes on that side.
If air does not escape, the examiner applies a test of strength by pushing in on both cheeks to see if the orbicularis auris on one side can be overwhelmed.
Only if these tests of facial muscles reveal deficit does the examination progress to a test of taste or lacrimation.
Taste on the anterior two thirds of the tongue can be evaluated by applying a strong tasting solution (e.g., salt, sugar, citric acid, quinine) to its right and left edges, where most of the taste buds are concentrated.
There exist special absorbent paper strips that can be applied to the surface of the eye for assessing tear production.