Facial Nerve Embryology 

  • Author: Alexander G Bien, MD; Chief Editor: Arlen D Meyers, MD, MBA   more...
 
Updated: Jun 21, 2011
 

Overview

The anatomy and embryology of the facial nerve are complex. A basic understanding of developmental anatomy is necessary to comprehend and anticipate variations encountered by the surgeon. (See the images below.) Congenital anomalies of the auricle, for example, should raise suspicion for an associated facial nerve anomaly. The objective of this article is to outline the embryology of the facial nerve and its common clinical implications. The reader is referred to Embryology and Anomalies of the Facial Nerve and Their Surgical Implications (Sataloff, 1991) for a comprehensive review of the development of the facial nerve and the associated development of the ear. (See table 1.)[1, 2, 3]

The surgical anatomy and landmarks of the facial nThe surgical anatomy and landmarks of the facial nerve. Schematic illustration shows the facial nerve and Schematic illustration shows the facial nerve and its peripheral connections. Note the interconnections of cranial nerve (CN) VII with CN V, CN IX, and CN X.
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Mature Facial Nerve

While studying the embryology of the facial nerve, keep in mind the mature course and structure that is the end result of developmental events. The motor nucleus of the facial nerve is located in the reticular formation of the caudal pons. Upon leaving the motor nucleus, axons extend dorsally and medially, cranially and superficially, to bend around the abducens (sixth cranial nerve) nucleus. The fibers then exit the central nervous system (CNS) between the olive and the inferior cerebellar peduncle.

The sensory root (nervus intermedius) consists of (1) central projections of neurons located in the geniculate ganglion (general somatic fibers that synapse in the spinal nucleus of the trigeminal nerve and special afferent fibers that synapse in the nucleus solitarius) and (2) axons of parasympathetic neurons from the superior salivatory (lacrimal) nucleus. The nervus intermedius enters the CNS lateral to the motor root at the pontocerebellar groove.

After it exits the internal auditory canal, the facial nerve enters the middle ear, where it bends posteriorly (first, or medial, genu) and courses horizontally through the middle ear. Just anterior to the lateral aspect of the horizontal semicircular canal, the facial nerve curves gently (the second genu) to form the vertical, or mastoid, segment that exits via the stylomastoid foramen.

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Intracranial Embryology of the Facial Nerve

Weeks 0-4 (0-6 mm)

The rhombencephalon (or hindbrain) is divided into the myelencephalon (caudal), which becomes the medulla oblongata, and the metencephalon (cranial), which becomes the pons and cerebellum. The facioacoustic (acousticofacial) primordium appears during the third week of life (4.2 mm crown-rump length [CRL]). It is attached to the metencephalon just cranial to the otic vesicle. The facial part of the acousticofacial primordium migrates cranial and ventral to end adjacent to the epibranchial placode, which is located on the dorsal and caudal aspect of the first branchial cleft.

By the end of the fourth week of gestation (4.8-6.5 mm CRL), the facial nerve splits into 2 parts: the caudal and rostral trunks. The chorda tympani nerve exits rostrally and courses ventrally to the first pharyngeal pouch to enter the mandibular arch. Shortly thereafter, the nerve approaches the epibranchial placode, inducing the appearance of the large, dark nuclei of neuroblasts that represent the future geniculate ganglion.

Weeks 5-6 (7-17mm)

Mesenchymal concentrations that form the cephalic muscles are seen in association with their nerves, while the epibranchial placode disappears and the geniculate ganglion is identifiable. The greater superficial petrosal nerve (GSPN) is present. The chorda tympani nerve enters the mandibular arch and terminates just proximal to the submandibular ganglion, near a branch of the trigeminal nerve that will become the lingual nerve. The posterior auricular nerve appears near the chorda tympani.

Complete separation of the facial and acoustic nerves is apparent, and a discrete nervus intermedius develops, making this an important temporal reference point for gestational disorders that affect both systems. The GSPN courses to the lateral aspect of the developing internal carotid artery (ICA), where it joins the deep petrosal nerve and continues as the nerve of the pterygoid canal. It terminates in a group of cells that will become the pterygopalatine ganglion. At this point, the most distal branches of the facial nerve are a loose network or interconnecting twigs.

Week 7 (18-31 mm)

The nervus intermedius is now smaller than the motor root and enters the brainstem between the vestibulocochlear nerve and the motor root of the facial nerve. The chorda tympani and lingual nerve unite proximal to the submandibular gland. The posterior auricular nerve now divides into cranial and caudal branches.

Several branches are visible in the peripheral portion of the seventh nerve. All of the peripheral branches lie deep to the myoblastic laminae that will form the facial muscles. At the end of the seventh week, the separations between the terminal branches continue to increase to the extent that all peripheral divisions can be identified.

The parotid gland is beginning to develop from the parotid bud at this stage. The temporal, zygomatic, and upper buccal branches are superficial to the parotid primordium, while the lower buccal, mandibular, and cervical branches are deeper. Multiple facial muscles appear at this time as well, including the zygomaticus major and minor, depressor anguli oris, buccinators, and frontalis.

Week 8 (32-49 mm)

A sulcus develops around the facial nerve that is the beginning of the fallopian canal. The orbicularis oris, levator anguli oris, and orbicularis oculi muscles appear.

Week 9 (50-60 mm)

Auricularis anterior, corrugator supercilii, occipital and mandibular platysma, and levator labii superioris alaeque nasi muscles appear. All the cranial nerves more closely resemble their adult relationships.

Weeks 10-15 (61-80 mm)

Extensive branching of the peripheral portions of the facial nerve occurs at this stage. Communication with the trigeminal nerve (via infraorbital, buccal, auriculotemporal, and mental branches) occurs in the perioral and infraorbital regions. The vertical portion of the facial nerve begins in the middle ear, and its overall relationship to external and middle ear structures is far more anterior than in the adult. Branches that will supply sensation to the external auditory canal arise between the stapedius and chorda tympani nerves.

Intricate connections between the superficial and deep lobes of the parotid and their relation to the facial nerve develop. By the fifteenth week, the geniculate ganglion is fully developed, and the facial nerve's relationship to middle ear structures is more fully developed.

Week 16 to birth (146 mm)

All definitive communications of the facial nerve are established by the 16th week. At 26 weeks, ossification has progressed to partial closure of the previously formed sulcus into the fallopian canal.

In late fetal life, the fallopian canal is closed by bone in most areas, except in the anterior cranial portion, where it remains open to form the facial hiatus along the floor of the middle cranial fossa. At least 25%, and as many as 55%, of fallopian canals are dehiscent, with the most common location adjacent to the oval window.[4]

At birth, the anatomy of the facial nerve approximates that of the adult, except for its exit through the more superficially located stylomastoid foramen. Adult anatomy will form in this region as the mastoid tip develops after birth. (See Table 1, below.)

Table 1. Summary of the Derivatives of the Second Branchial Arch (Open Table in a new window)

Pharyngeal ArchNerveArteryMusclesSkeleton
II = Hyoid (Reichert cartilage)Cranial nerve VII (Facial nerve)Stapedial
  • Muscles of facial expression
  • Buccinator
  • Posterior belly of digastric
  • Stylohyoid muscle
  • Stapedius muscle
  • Manubrium of malleus
  • Long process incus
  • Stapes (except for footplate)
  • Facial canal
  • Styloid process
  • Stylohyoid ligament
  • Lesser cornu of hyoid
  • Upper body of hyoid
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Congenital Facial Paralysis

Abnormalities of the facial nerve may occur in conjunction with malformations of the ear, in isolation without associated anomalies, or in conjunction with a variety of syndromes that include abnormalities elsewhere in the body.

In the newborn, the otolaryngologist evaluating a facial paresis or facial palsy must decide whether it is congenital or acquired. One in 2000 live births has a unilateral facial palsy, with a 90% spontaneous recovery rate. Approximately 75-80% of palsies in newborns are related to birth trauma. A history of forceps delivery, prolonged labor, ecchymosis over the mastoid, or hemotympanum raises suspicion for birth trauma.

The presence of bilateral facial paralysis, other cranial nerve deficits, or other anomalies suggests a developmental etiology. Early, accurate diagnosis is important if the etiology is traumatic. In rare cases, surgery and facial nerve repair may be required in the newborn if the etiology is determined to be traumatic.

The evaluation of facial nerve paralysis includes the use of electromyograms (EMGs), evoked electromyograms (EEMGs), and computed tomography (CT) scans. If the etiology is traumatic, the nerve can be stimulated for 3-5 days postnatal; fibrillation potentials on EMG develop 14-21 days after birth. If the cause is not traumatic, treatment generally is delayed. Eye protection is rarely required in congenital facial paralysis.

In patients with congenital malformations, eliciting the fetal age at which development was arrested is usually possible. This allows for elucidation of the anatomy of the malformed structure based on its normal course of embryologic development. Furthermore, if anomalies are present in other organ systems (in particular, the kidney), they often reflect arrested development at the same time during development. In this way, the surgeon should be able to predict the location of the facial nerve, particularly in the case of middle ear malformation.

Most hereditary conditions that include facial paralysis are manifest at the time of birth. However, a few hereditary syndromes are associated with the development of facial paralysis later in life. (See Table 2, below.)

In addition, many hereditary and congenital malformations are associated with abnormal facial nerve anatomy in the presence of normal nerve function. The otolaryngologist must be familiar with these conditions, because abnormal development may place the nerve at increased risk of injury during otologic surgery.[2]

Table 2. Developmental Syndromes Associated With Facial Nerve Abnormalities* (Open Table in a new window)

SyndromeFacial Nerve AbnormalityDescription
Bulbopontine paralysis with progressive sensorineural hearing loss
  • Facial paresis common
  • Complete facial paralysis uncommon
  • Autosomal recessive inheritance
  • More females affected than males
  • Involvement of bulbar musculature
  • Slowly progressive, bilateral sensorineural hearing loss
DiGeorge syndromeFacial paralysis reported
  • Multiple anomalies of craniofacial, cardiovascular, and visceral structures
  • Absent and/or hypoplastic thymus and parathyroid glands
  • Abnormal aural development
Dominant craniometaphyseal dysplasiaUnilateral and bilateral facial paralysis reported
  • Autosomal dominant
  • Metaphyseal widening of limbs and bony overgrowth of facial bones and skull
  • Obliteration of mastoid air cells
  • Conductive and sensorineural hearing loss
  • Manifest in early infancy or childhood
Hemifacial microsomiaFacial paralysisFacial asymmetry, including unilateral microtia, macrostomia, and failure of mandibular ramus and condyle to form
Hereditary acoustic neuromasFacial paresis and/or palsy
  • Autosomal dominant
  • Manifests in third decade
  • Symptoms secondary to tumor encroachment on nerves
Melkersson-Rosenthal syndromeRecurrent alternating facial paralysis
  • Recurrent alternating facial paralysis
  • Edema of lips, face, and eyelids
  • Cheilitis and fissured tongue
  • Positive family history
Möbius syndrome
  • Bilateral facial paralysis
  • Masklike facies
  • Unilateral or bilateral abducens paralysis
  • Deformities of extremities
  • Aplasia of brachial and thoracic muscles
OsteopetrosisFacial paralysis, which may be acute and recurring
  • "Marble bone disease"
  • Uncommon genetic disorder characterized by increasing skeletal density
  • Two forms, benign and malignant
  • Benign form is autosomal dominant and not commonly associated with facial paralysis
  • Malignant form is autosomal recessive (known as Albers-Schönberg disease) and is associated with facial paralysis, deafness, blindness, and abnormal ear and mastoid; death often results at a young age due to infection
Recessive craniometaphyseal dysplasiaUnilateral facial paralysis
  • Autosomal recessive bone disease
  • Major features - Glabella and paranasal prominence with severe mandibular prognathism
  • Nasal obstruction (complete)
  • Ocular hypertelorism
  • Progressive visual disturbance and blindness
  • Severe hearing loss
Sclerostenosis
  • Facial paralysis possibly apparent at birth
  • Often appears early in childhood
  • Generally unilateral, eventually becoming bilateral
  • Autosomal recessive
  • Generalized osteosclerosis, hyperostosis of mandible, calvaria, pelvis, and clavicles
  • Hearing loss usually bilateral, may be conductive, sensorineural, or mixed
Sickle cell diseaseFacial paralysis observed to occur during a crisis
  • Hemoglobinopathy observed primarily in African Americans
  • Recurrent attacks of fatigue, weakness, abdominal pain, anorexia, and jaundice
  • May have sensorineural hearing loss during a crisis
von Recklinghausen neurofibromatosisFacial paralysis possible from a neurofibroma of the facial nerve or secondary to encroachment by an acoustic schwannoma
  • Autosomal dominant
  • Multiple skin tumors, cutaneous pigmentation (cafe-au-lait spots)
  • Incidence of 1 in 2000
  • Malignant degeneration in 3-12%
*Modified from Sataloff, 1991
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Contributor Information and Disclosures
Author

Alexander G Bien, MD  Staff Physician, Department of Otolaryngology-Head and Neck Surgery, University of Nebraska Medical Center

Alexander G Bien, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery and American Rhinologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Daniel D Lydiatt, DDS, MD  Professor, Department of Otolaryngology-Head and Neck Surgery, University of Nebraska Medical Center

Disclosure: Nothing to disclose.

Daphne A Bascom, MD, PhD  Fellow, Department of Otolaryngology-Head and Neck Surgery, University of Oregon Health Sciences University

Daphne A Bascom, MD, PhD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association

Disclosure: Nothing to disclose.

Barry M Schaitkin, MD  Chief, Department of Surgery, Division of Otolaryngology, Shadyside Hospital; Professor, Department of Otolaryngology-Head and Neck Surgery, University of Pittsburgh School of Medicine

Barry M Schaitkin, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, and American College of Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael E Hoffer, MD  Director, Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center of San Diego

Michael E Hoffer, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: American biloogical group Royalty Other

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christopher L Slack, MD  Private Practice in Otolaryngology and Facial Plastic Surgery, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders

Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA  Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting; GYRUS ACMI Honoraria Consulting

References
  1. Sataloff RT. Embryology and Anomalies of the Facial Nerve and Their Surgical Implications. New York, NY: Raven Press; 1991.

  2. Rasweiler CL. Surgical causes of facial paresis. In: Rubin RL, ed. The Paralyzed Face. St. Louis, Mo: Mosby-Year Book; 1991:101-3.

  3. Schaitkin BM, Eisenman DJ. Anatomy of the facial muscles. In: The Facial Nerve. New York, NY: Thieme Medical Pubs; 2000:95-105.

  4. Cisneros A, Orozco JR, Nogues JA, et al. Development of the stapedius muscle canal and its possible clinical consequences. Int J Pediatr Otorhinolaryngol. Feb 2011;75(2):277-81. [Medline].

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The surgical anatomy and landmarks of the facial nerve.
Schematic illustration shows the facial nerve and its peripheral connections. Note the interconnections of cranial nerve (CN) VII with CN V, CN IX, and CN X.
Table 1. Summary of the Derivatives of the Second Branchial Arch
Pharyngeal ArchNerveArteryMusclesSkeleton
II = Hyoid (Reichert cartilage)Cranial nerve VII (Facial nerve)Stapedial
  • Muscles of facial expression
  • Buccinator
  • Posterior belly of digastric
  • Stylohyoid muscle
  • Stapedius muscle
  • Manubrium of malleus
  • Long process incus
  • Stapes (except for footplate)
  • Facial canal
  • Styloid process
  • Stylohyoid ligament
  • Lesser cornu of hyoid
  • Upper body of hyoid
Table 2. Developmental Syndromes Associated With Facial Nerve Abnormalities*
SyndromeFacial Nerve AbnormalityDescription
Bulbopontine paralysis with progressive sensorineural hearing loss
  • Facial paresis common
  • Complete facial paralysis uncommon
  • Autosomal recessive inheritance
  • More females affected than males
  • Involvement of bulbar musculature
  • Slowly progressive, bilateral sensorineural hearing loss
DiGeorge syndromeFacial paralysis reported
  • Multiple anomalies of craniofacial, cardiovascular, and visceral structures
  • Absent and/or hypoplastic thymus and parathyroid glands
  • Abnormal aural development
Dominant craniometaphyseal dysplasiaUnilateral and bilateral facial paralysis reported
  • Autosomal dominant
  • Metaphyseal widening of limbs and bony overgrowth of facial bones and skull
  • Obliteration of mastoid air cells
  • Conductive and sensorineural hearing loss
  • Manifest in early infancy or childhood
Hemifacial microsomiaFacial paralysisFacial asymmetry, including unilateral microtia, macrostomia, and failure of mandibular ramus and condyle to form
Hereditary acoustic neuromasFacial paresis and/or palsy
  • Autosomal dominant
  • Manifests in third decade
  • Symptoms secondary to tumor encroachment on nerves
Melkersson-Rosenthal syndromeRecurrent alternating facial paralysis
  • Recurrent alternating facial paralysis
  • Edema of lips, face, and eyelids
  • Cheilitis and fissured tongue
  • Positive family history
Möbius syndrome
  • Bilateral facial paralysis
  • Masklike facies
  • Unilateral or bilateral abducens paralysis
  • Deformities of extremities
  • Aplasia of brachial and thoracic muscles
OsteopetrosisFacial paralysis, which may be acute and recurring
  • "Marble bone disease"
  • Uncommon genetic disorder characterized by increasing skeletal density
  • Two forms, benign and malignant
  • Benign form is autosomal dominant and not commonly associated with facial paralysis
  • Malignant form is autosomal recessive (known as Albers-Schönberg disease) and is associated with facial paralysis, deafness, blindness, and abnormal ear and mastoid; death often results at a young age due to infection
Recessive craniometaphyseal dysplasiaUnilateral facial paralysis
  • Autosomal recessive bone disease
  • Major features - Glabella and paranasal prominence with severe mandibular prognathism
  • Nasal obstruction (complete)
  • Ocular hypertelorism
  • Progressive visual disturbance and blindness
  • Severe hearing loss
Sclerostenosis
  • Facial paralysis possibly apparent at birth
  • Often appears early in childhood
  • Generally unilateral, eventually becoming bilateral
  • Autosomal recessive
  • Generalized osteosclerosis, hyperostosis of mandible, calvaria, pelvis, and clavicles
  • Hearing loss usually bilateral, may be conductive, sensorineural, or mixed
Sickle cell diseaseFacial paralysis observed to occur during a crisis
  • Hemoglobinopathy observed primarily in African Americans
  • Recurrent attacks of fatigue, weakness, abdominal pain, anorexia, and jaundice
  • May have sensorineural hearing loss during a crisis
von Recklinghausen neurofibromatosisFacial paralysis possible from a neurofibroma of the facial nerve or secondary to encroachment by an acoustic schwannoma
  • Autosomal dominant
  • Multiple skin tumors, cutaneous pigmentation (cafe-au-lait spots)
  • Incidence of 1 in 2000
  • Malignant degeneration in 3-12%
*Modified from Sataloff, 1991
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