As you go through your day, think about how you interact with other people. You speak to them, yes; but while that is a very direct form of communication, you also use a number of other less obvious–even less conscious–methods to communicate your opinions and emotions on a regular basis.
One of the most important ways we non-verbally communicate with each other is by facial expression. A lift of an eyebrow, the wrinkling of a nose, or the slight twinge of the corner of the mouth can tell us quite a bit: if we are paying attention, we notice these small changes and interpret not only what they indicate about the people we are interacting with, but also what they indicate regarding their demeanor towards us, and the relationships forming between us.
Like Mona Lisa’s mysterious, captivating, and somewhat evasive smile, one small visually-observable change in facial expression can speak volumes without having to say a single word.
Regarding facial expression, there is one vitally important nerve that allows us to partake in this form of communication, and it is aptly named the facial nerve. While it is indeed responsible for innervating the muscles of facial expression, the facial nerve is a complex structure containing many fiber types with a variety of functions, including motor, sensory, and autonomic. The following article will discuss the importance and versatility facial nerve
- The cranial nerves
- The facial nerve
- The muscles of facial expression
- The facial nerve as part of the corticobulbar tract
- Clinical notes
- Related Atlas Images
The cranial nerves
The facial nerve is one of a group of nerves called the cranial nerves (CN), twelve pairs of nerves that, with the exception of the spinal accessory nerve (CN XI), originate in the brain and contribute to the peripheral nervous system (PNS). They are referred to as “cranial” because they arise from the brain and upper spinal cord and supply structures of the head and neck.
The 12 paired cranial nerves include:
- the olfactory nerve (CN I)
- the optic nerve (CN II)
- the oculomotor nerve (CN III)
- the trochlear nerve (CN IV)
- the trigeminal nerve (CN V)
- the abducens nerve (CN VI)
- the facial nerve (CN VII)
- the vestibulocochlear nerve (CN VIII)
- the glossopharyngeal nerve (CN IX)
- the vagus nerve (CN X)
- the accessory nerve (CN XI)
- the hypoglossal nerve (CN XII)
Some of these contain motor fibers, some contain autonomic fibers, some contain somatic sensory fibers, some contain special sensory fibers, and some contain combinations of a number of these aforementioned fiber types. CN I, CN II, CN VII, CN VIII, CN IX and CN X play roles in special sensory functions (i.e. olfaction, vision, gustation, audition, and balance); CN V (all three branches, the ophthalmic, maxillary, and mandibular) and CN IX play roles in somatic sensory functions; CN III, CN IV, CN V (the mandibular branch, V3, only), CN VI, CN VII, CN IX, CN X, CN XI, and CN XII are responsible for motor functions; and CN III, CN VII, CN IX, and CN X have important autonomic functions.
The facial nerve
Components and branches
The facial nerve contains many different types of fibers, including general sensory (afferent) fibers, special sensory fibers, visceral/autonomic motor (efferent) fibers, and somatic motor fibers.
General sensory fibers in the facial nerve are responsible for transmitting signals to the brain from the external acoustic meatus, as well as the skin over the mastoid and lateral pinna. Special sensory fibers in the facial nerve are responsible for receiving and transmitting taste information from the anterior two-thirds of the tongue.
Visceral/autonomic motor fibers in the facial nerve are responsible for innervating the lacrimal gland, submandibular gland, sublingual gland, and the mucous membranes of the nasal cavity and hard and soft palates, allowing for production of tears, saliva, etc., from these locations. Somatic motor fibers in the facial nerve are responsible for innervating the muscles of facial expression and muscles in the scalp (which are derived from the second pharyngeal arch), as well as the stapedius muscle in the ear, the posterior belly of the digastric muscle, and the stylohyoid muscle.
Origin and course
The motor root of the facial nerve originates in the facial (motor) nerve nucleus in the pons of the brainstem, which receives input from a number of other structures and brain regions, including the primary motor cortex and the ophthalmic division of the trigeminal nerve.
The fibers travel towards the floor of IV ventricle and go around the abducens nucleus and descend. The facial nerve emerges from the lateral surface of brainstem at the pontine-medullary junction between the VI and VIII nerves.
The motor root travels with the nervus intermedius (a smaller sensory root containing parasympathetic fibers, general sensory fibers, and special sensory fibers) in the cerebellopontine angle and enters the internal auditory meatus of the temporal bone accompanied by the vestibulocochlear nerve (CN VIII) and the labyrinthine artery and vein.
The facial nerve roots then enter the facial canal in petrous part of temporal bone, where the small sensory and large motor roots fuse, forming the facial nerve. This united nerve enlarges at the geniculate ganglion, which contains cell bodies for sensory neurons.
It is here, at the geniculate ganglion in the facial canal of the temporal bone, that the facial nerve gives off the greater petrosal nerve, the first in a series of nerves which eventually carry preganglionic parasympathetic fibers to the lacrimal gland, stimulating lacrimation (tearing). It passes beneath the trigeminal ganglion and reach the foramen lacerum where it is joined by deep petrosal nerve to become the nerve of the pterygoid canal (Vidian nerve). The greater petrosal nerves contain parasympathetic fibers for the pterygopalatine ganglion and taste fibers. As the facial nerve continues to travel along bony canal, two more branches emerge: the nerve to stapedius, the chorda tympani, and preganglionic parasympathetic fibers.The nerve to stapedius innervates the stapedius muscle, as its name suggests. The stapedius muscle attaches to the posterior surface of the stapes, one of the three ossicles of the middle ear. The stapedius muscle contracts in response to loud noises, preventing excessive oscillation of the stapes, thereby dampening its vibrations and controlling the amplitude of sound waves.
The chorda tympani leaves the facial nerve above the stylomastoid foramen and is responsible for transmitting taste sensation, via the aforementioned special sensory fibers, from the anterior two-thirds of the tongue. It passes through the posterior wall of the middle ear, crosses the neck of the malleus and emerges at the medial end of petrotympanic fissure. It joins the posterior aspect of lingual nerve at an acute angle and carries taste fibers for the anterior two-third of tongue and efferent preganglionic parasympathetic fibers to the submandibular ganglion which are responsible for innervating the submandibular gland, stimulating salivary secretions.
The facial nerve exits skull via stylomastoid foramen; nearby, it gives off the posterior auricular nerve which is meant to supply the occipital belly of the occipitofrontalis muscle and some of the auricular muscles, and nerves to the posterior belly of the digastric and the stylohyoid. The nerve then enters the parotid gland, from whence it gives off five terminal branches–the temporal, zygomatic, buccal, marginal mandibular, and cervical branches–which emerge from around the parotid gland and innervate structures across the entire face.
The muscles of facial expression
Now we will return to the topic of conversation first introduced in our discussion of the facial nerve: the facial muscles that it innervates, which allow for us to nonverbally communicate with others via our facial expressions.
The muscles of facial expression, innervated by the branches of the facial nerve, are divided into groups by their locations: these include the orbital group, the nasal group, and the oral group, as well as a group of auricular muscles and the occipitofrontalis.
The orbital group of facial muscles consists of the corrugator supercilii muscle and the orbicularis oculi muscle. The corrugator supercilii muscle pulls the eyebrows medially and downward. The orbicularis oculi muscle has two parts: a palpebral part and an orbital part. The palpebral part is responsible for gently closing the eyelids, while the orbital part is responsible for forcefully closing the eyelids.
The orbicularis oculii are the effector muscles of the efferent limb of the corneal reflex, or blink reflex: when sensory nerve endings of the ophthalmic branch of the trigeminal nerve in the cornea are stimulated, these nerve endings transmit a signal to the trigeminal sensory nucleus, which communicates this signal to both facial motor nuclei. The facial motor nuclei then send signals to the orbicularis oculi muscles of both eyes to contract via the temporal and zygomatic branches of the facial nerve. This causes the eyelids to close, effectively protecting the eyes from foreign bodies.
The nasal group of facial muscles consists of the nasalis muscle, the procerus muscle, and the depressor septi muscle. The nasalis muscle has two parts: the transverse part, which compresses the nasal aperture, and the the alar part, which pulls the alar cartilage laterally and downward, allowing the nostrils to open. The procerus muscle pulls the medial angle of the eyebrows downward, producing wrinkling across the bridge of the nose. As it suggests, in the region of the nasal septum, the depressor septi pulls the tip of the nose downward.
The oral group of facial muscles consists of:
- the depressor anguli oris muscle
- the depressor labii inferioris muscle
- the mentalis muscle
- the risorius muscle
- the zygomaticus major and minor muscles
- the levator labii superioris muscle
- the levator labii superioris alaeque nasi muscle
- the orbicularis oris muscle
- the buccinator muscle
The depressor anguli oris muscle pulls the corners of the mouth downward and laterally into a frown. The depressor labii inferioris muscle, as its name suggests, pulls the lower lip downward and laterally. The mentalis muscle wrinkles the skin on the chin, and raises and protrudes the lower lip. The risorius muscle and zygomaticus major and minor muscles work together to facilitate smiling: the risorius retracts the corners of the mouth upward, the zygomaticus major pulls the corners of the mouth upward and laterally, and the zygomaticus minor raises the upper lip.
The levator labii superioris, as suggested by its name, raises the upper lip; and, along with the levator anguli oris which raises the corners of the mouth, forms the nasolabial furrow. The levator labii superioris alaeque nasi acts to raise the upper lip and open the nostril. The orbicularis oris acts to close and protrude the lips; and, finally, the buccinator compresses the cheeks against the teeth.
Other muscles innervated by branches of the facial nerve are the anterior, superior, and posterior auricular muscles; and the occipitofrontalis muscle. The anterior, superior, and posterior auricular muscles all elevate the ear by pulling it upward. As their names suggest, the anterior auricular muscle pulls the ear anteriorly in addition to superiorly, and the posterior auricular muscle pulls the ear posteriorly in addition to superiorly. The occipitofrontalis muscle has two parts: the frontal belly, which raises the eyebrows resulting in wrinkling of the forehead, and the occipital belly, which pulls the scalp backward.
The facial nerve as part of the corticobulbar tract
The corticobulbar tract, or corticonuclear tract, influences the motor nuclei of many of the cranial nerves with motor components. In addition to the facial nerve, these include:
- the oculomotor (III)
- trochlear (IV)
- mandibular component of the trigeminal (V3)
- abducens (VI)
- glossopharyngeal (IX)
- vagus (X)
- spinal accessory (XI)
- hypoglossal (XII) nerves
For the innervation of facial muscles, the corticobulbar tract sends motor signals via a sequence of two motor neurons: signals originating in the cell bodies of the upper motor neurons (UMNs) of the lateral cerebral cortex corresponding to the different parts of the face descend from the cortex, through the internal capsule, and synapse on the cell bodies of lower motor neurons (LMNs) which are located in the facial nerve nuclei of the pons in the upper brainstem. These signals are then transmitted from LMN cell bodies into their axons, which project via the facial nerve motor root to the muscles of facial expression. Axons originating from UMNs are considered part of the corticobulbar tract, whereas axons originating from LMNs are considered part of the cranial nerves themselves.
Surgical removal of the parotid gland
The five terminal branches of the facial nerve–the temporal, zygomatic, buccal, marginal mandibular, and cervical branches–are closely anatomically related to the parotid gland: they emerge from the parotid gland’s upper, anterior, and lower borders. Because of this close association, removal of the parotid gland (i.e. in the removal of an adenoma or neoplasm) without damaging these branches is a particularly delicate procedure. Damage to any of these five branches would result in weakness or paralysis of the muscles supplied.
Facial nerve palsy
Facial nerve palsy can be associated with a variety of etiologies and syndromes. Additional symptoms depend on the level at which the lesion occurs. Although most facial nerve palsies are considered idiopathic, common causes include infection, trauma, iatrogenic injury, and neoplasia. The incidence of facial palsy in neonates is reported to be 0.6–1.8 per 1000 live births, but is primarily associated with forceps delivery. The incidence in adults ranges between 17-35 per 100000.
Vascular damage to the facial nerve usually occurs at the supranuclear, pontine, and (rarely) cerebellopontine angle. Upper motor neuron (UMN) lesions occur in strokes and can easily be differentiated with lower motor neuron (LMN) lesions by their presentation. A LMN lesion causes paralysis of the whole side of face, while an UMN lesion results in sparing of the forehead. The muscles in the forehead remain unaffected because they receive input from both the left and right cerebral hemispheres: input from the ipsilateral hemisphere maintains the function of the muscles in the upper face even when input from the contralateral hemisphere is lost. This is unlike the muscles in the lower part of the face, which receive input from the contralateral hemisphere only.
Lesions at the level of the geniculate ganglion typically result in weakness or paralysis of the muscles on the entire ipsilateral side of the face. Because the greater petrosal nerve and chorda tympani have not yet branched off of the facial nerve at that level, lacrimation, salivation, and taste sensation in the anterior two-thirds of the tongue are also likely to be affected.
If the facial nerve itself is damaged prior to dividing into the temporal, zygomatic, buccal, marginal mandibular, and cervical branches, the muscles of facial expression in the entire side of the face supplied by the damaged nerve may be weakened or paralyzed. This is most commonly associated with viral inflammation of the facial nerve before it exits the stylomastoid foramen. If the lesion occurs distally to the branching of the greater petrosal nerve and chorda tympani, lacrimation, salivation, and taste sensation in the anterior two-thirds of the tongue may be unaffected.
When the stapedius muscle, the nerve to stapedius, or the facial nerve is damaged, paralysis of the stapedius muscle may lead to hyperacusis. In this condition, loss of inhibition of oscillation of the stapes results in its excessive vibration: as a result, sounds that would otherwise be considered of normal volume are perceived as being uncomfortably loud.
Bell’s palsy is most common form of peripheral facial nerve palsy. Although there is usually no detectable cause (i.e. idiopathic), some evidence suggest that latent infection with herpes simplex virus type 1 (HSV-1) plays a role, causing inflammation of the nerve and subsequent symptoms. It presents with sudden onset of impairment of facial expression, typically on one side. It is frequently preceded by periauricular paraesthesia or otalgia and may be associated with dry eyes, xerostomia, tinnitus, and hyperacusis.
Ramsay Hunt Syndrome results from reactivation of the varicella zoster virus in the geniculate ganglion. It presents as a triad of facial nerve palsy, vertigo, and vesicles in the ipsilateral external ear, palate or anterior tongue. Treatment typically consists of steroids and antivirals.
Facial nerve paralysis secondary to acute otitis media is more common in young children. The most common cause of otitis media is the gram-positive bacteria Streptococcus pneumoniae, and the majority of cases resolve with antibiotics.
Facial nerve paralysis is also a feature of skull-base osteomyelitis, a condition which occurs primarily in elderly / immunocompromised patients. The characteristic features are severe pain, aural discharge, and progressive cranial neuropathies.
As in an infant injured during a forceps delivery, facial nerve palsy in an adult can also be due to any trauma affecting temporal bone.
Inferior medial pontine syndrome
Inferior medial pontine syndrome, also called Foville syndrome, typically occurs when there is occlusion of the paramedian branches of the basilar artery and subsequent ischemia of the medial aspect of the pons. This can result in damage to a number of structures, including: the corticospinal fibers, resulting in contralateral hemiplegia; the medial lemniscus, resulting in contralateral diminution or potential loss of vibration, proprioception, and fine touch sensation; and the PPRF, abducens nucleus, or abducens nerve, resulting in ipsilateral paralysis of the lateral rectus muscle and subsequently diplopia, or a potential loss of conjugate gaze toward the side of the lesion via interruption of communication between the abducens nucleus of one side of the brain with the oculomotor nucleus on the opposite side.
If the lesion is in the caudal pons and extends laterally, in may involve: the lateral lemniscus, resulting in hyperacusis; the middle cerebellar peduncle, resulting in ataxia; the motor nucleus of the facial cranial nerve, resulting in ipsilateral facial paralysis; the spinal trigeminal nucleus and tract, resulting in ipsilateral loss of pain and temperature sensation in the face; and the anterolateral system resulting in contralateral loss of pain and temperature sensation in the body.
A lesion at this level resulting in corticospinal deficits on one side of the body with motor cranial nerve deficits on the opposite side of the face is referred to as a middle alternating hemiplegia.
If the lesion is in the rostral pons and extends medially, it may involve: the part of the medial lemniscus that contains fibers carrying sensory information from the upper extremity, leading to contralateral loss of vibration, proprioception, and fine touch sensation in the upper extremity; the trigeminal motor nucleus, resulting in ipsilateral paralysis of the muscles of mastication; the anterolateral system and parts of the spinal trigeminal tract and nucleus, resulting in contralateral loss of pain and temperature sensation in the body and ipsilateral loss of pain and temperature sensation in the face, respectively.
It’s a warm day in late June, and a 23 year-old man presents to the emergency department with the complaint that he is unable to move the right side of his face. Observation of the patient reveals that he is speaking mostly out of the left side of his mouth, while the right side of his mouth droops downward. You notice that his right eyelid droops slightly, and when you ask him to close his right eye, he is unable to do so completely. You ask him to raise his eyebrows and wrinkle his forehead, and while he is able to do this on the left side, the right eyebrow and forehead remain unchanged. You take a history, during which the young man tells you his family has no significant history of atherosclerosis, heart disease, or strokes. When you start asking about his travel history, he tells you he has never left the United States, but he did go camping with friends last month on the Appalachian Trail. You ask the patient if he has experienced any rashes or skin symptoms since that trip, and he tells you that he recalls a round, reddish pink spot with central clearing forming on his arm, but says he did not think anything of it as it went away on its own after a couple of days. You continue with a physical examination, and cardiac auscultation alarmingly reveals that his heart is skipping beats.
This patient is suffering from Bell’s palsy and other cardiac symptoms associated with stage two Lyme disease. Lyme disease is contracted when someone is bitten by an Ixodes tick and infected with the bacteria Borrelia burgdorferi, a Gram-positive spirochete. In stage one of Lyme disease, the bacteria enter the human body through the tick bite, forming a red, bulls-eye rash around the bite. As the bacteria disseminate outward from the bite into the body, the bulls-eye rash spreads outward as well, and for this reason is called erythema migrans. A few weeks to months after the initial infection occurs, and the bacteria have disseminated throughout the body, patients may develop stage two Lyme disease, common features of which include facial muscle weakness or paralysis and various cardiac symptoms, including palpitations, skipped heartbeats, or even heart block (a block in the propagation of electrical signaling from the atria to the ventricles, across the atrioventricular node in the heart). Later on, stage three Lyme disease may develop, with symptoms of severe joint swelling and arthritis, muscle weakness, paresthesia (a tingling sensation or numbness), and even neurological symptoms from bacterial invasion of the central nervous system.
Once diagnosed, Lyme disease may be treated with antibiotics, including doxycycline, ceftriaxone, and the aminopenicillins.