Anatomy of the Facial Nerve

The facial nerve is a second pharyngeal (hyoid) arch derivative and therefore supplies structures derived from the same arch. ³ These include the muscles of facial expression, and taste sensation to the anterior two-thirds of the tongue ( ▶ Table 12.1). An understanding of the anatomy of the facial nerve ( ▶ Fig. 12.1) allows prediction of deficits and directs clinical diagnosis. The facial nerve comprises two nerves: the facial motor nerve, which is a purely motor nerve, and the nervus intermedius, which carries afferent taste and parasympathetic secretomotor fibers. These unite at the genu to form the common facial nerve in the temporal bone. To highlight this, the preceding terminology will be used throughout this chapter.

12.3 Central Course

12.3.1 The Facial Motor Nerve

Corticobulbar (upper motor neuron) fibers descend from the precentral motor cortex toward the facial nerve nucleus in the caudal pons. These fibers cross over in the caudal pons, but those innervating the upper facial muscles also synapse in the ipsilateral facial motor nucleus. Sparing of the upper facial muscles in a facial palsy suggests a cortical or corticobulbar lesion. Lower motor neuron nerve fibers wind around the abducens nucleus to emerge from the brainstem at the pontomedullary junction in concert with the nervus intermedius.

The Nervus Intermedius

The nervus intermedius is a smaller mixed nerve carrying afferent taste and parasympathetic secretomotor fibers. It is best considered as comprising two nerves (the greater superficial petrosal nerve and the chorda tympani; ▶ Fig. 12.1) that hitchhike alongside the facial motor nerve in the temporal bone. The nerve fibers arise in the superior salivary nucleus medial to the facial motor nucleus where the cell bodies of the preganglionic parasympathetic fibers lie. Afferent taste fibers run alongside these and synapse in the nucleus tractus solitarius in the medulla.

At their exit from the brainstem, the nerves lack epineurium and bridge an interval to enter the internal auditory meatus. Here they lie at the cerebellopontine angle closely related to the vestibulocochlear nerve. At this point, cranial nerves V to VIII are at risk from space-occupying lesions. Combined palsies strongly suggest this diagnosis and urgent imaging is mandatory.

12.3.2 Intratemporal Course

Upon entering the internal auditory meatus, the facial nerve courses through the petrous temporal bone within the Fallopian canal ( ▶ Fig. 12.2). Here the nerve is readily susceptible to compression from neoplastic, inflammatory, and traumatic events. In children, the nerve occupies proportionally less of the lumen of the canal than in adults; therefore, there is theoretically less likelihood of facial nerve compression. The intratemporal components of the facial nerve can be divided into the following three segments:

• 
  

  Labyrinthine.

  
  
• 
  

  Tympanic.

  
  
• 
  

  Mastoid.

Labyrinthine Segment

The labyrinthine segment courses from the internal acoustic meatus to the geniculate ganglion where the nervus intermedius and facial motor nerve unite. The labyrinthine segment is the shortest and narrowest segment and lies posterior to the cochlea; any compression occurs initially at this point. After traversing the labyrinthine segment, the common facial nerve suddenly changes direction, forming a knee-shaped bend (genu) and thereafter running posteroinferiorly. The main branch of this portion is the greater petrosal nerve.

Tympanic Segment

The tympanic segment extends from geniculate ganglion to the bend at the lateral semicircular canal; here the thin lateral wall of the Fallopian canal separates the nerve from the tympanic cavity.

Mastoid Segment

The mastoid segment is the longest part and runs from the second bend to the stylomastoid foramen; the branches from this portion are the nerve to stapedius and the chorda tympani. The facial nerve runs vertically down the anterior wall of the mastoid process to exit at the stylomastoid foramen.

It is due to the postnatal growth of these structures that the facial nerve eventually has a deeper location in the adult.

12.3.3 Branches of the Nervus Intermedius

Greater Petrosal Nerve

Also known as the greater superficial petrosal nerve, it leaves the common facial nerve and passes through the petrosal bone to enter the middle cranial fossa by running forward in a groove on the petrous temporal bone beneath the dura mater. It exits the cranial cavity through the foramen lacerum until it reaches the opening of the pterygoid canal. Here it is joined by the deep petrosal nerve, which is derived from the sympathetic plexus about the internal carotid artery. They unite to form the nerve of the pterygoid canal (vidian nerve) that will course toward the pterygopalatine fossa where parasympathetic fibers synapse in the pterygopalatine (sphenopalatine) ganglion. Postganglionic fibers join the maxillary nerve and are distributed to the lacrimal gland, nose, and palate through its branches.

Chorda Tympani

The chorda tympani traverses the middle ear along the superior inner surface adjacent to the tympanum. At the anterior border of the tympanum, it enters the petrotympanic fissure and turns downward and forward to reach the infratemporal fossa to join the lingual nerve, which distributes taste fibers to the anterior two-thirds of the tongue, and the parasympathetic secretomotor fibers, which synapse in the submandibular ganglion, to the submandibular and sublingual glands. It is these branches that are responsible for the intraoral eruption of herpes zoster in Ramsay Hunt syndrome. The chorda tympani is at risk in the middle ear and mastoid surgery. Trauma to the nerve, which can be caused by transection or by excessive manipulation and stretching, leads to alteration in taste sensation (dysgeusia) typically manifest as a metallic taste; this is much more severe when bilateral and is a significant but underreported cause of morbidity following tympanomastoid surgery.

12.3.4 The Facial Motor Nerve in the Face

Upon exiting the stylomastoid foramen, the facial nerve gives a posterior auricular branch and lies between the posterior belly of digastric and the stylohyoid muscles giving a branch to each before entering the substance of the parotid gland. In infants and young children, the intraparotid portion lies very superficial, where it can easily be damaged (see ▶ Fig. 26.4).

All the facial muscles are supplied from their deep surface with the exception of buccinator, mentalis, and depressor anguli oris. ⁴ There are several common branching patterns, but each patient has a unique arrangement of branches, making knowledge of such patterns of limited value. There are surface anatomy landmarks that are helpful in identifying specific divisions. ⁵ A caveat is that such landmarks are determined in adults and the relative proportions in children are different, nonetheless they are a useful guide. The temporal branch that innervates the frontalis and orbicularis oculi muscles can be located using a line drawn from 1 cm below the inferior border of the tragus to a finger’s breadth behind the eyebrow. This is termed Pitanguy’s line and represents the vector along which the temporal division runs immediately under the temporoparietal fascia. In reality, it comprises numerous smaller branches over a defined area ⁶ and clinically its function is manifest by raising the eyebrows and by eyelid closure.

The midpoint of a line that runs from the root of the helix to the oral commissure is termed Zuker’s point, which is the point at which a buccal or zygomatic branch innervates the oral (smile) musculature. The buccal and zygomatic divisions have overlapping innervation of the midfacial musculature. Evaluation of the zygomatic division is by assessing lower eyelid tone, eye closure, and the smile. The buccal division is examined by puckering the lips and blowing out the cheeks to establish lip seal.

The mandibular division (marginal mandibular nerve) may be at risk during surgery in the submandibular region, for example, in removal of lymph nodes, excision of the submandibular gland, or drainage of septic neck swellings. The nerve runs in the superficial tissues and is best avoided by ensuring that incisions are kept at least 2 cm below the inferior mandibular border. ⁵ In this way, the nerve is kept out of harm’s way as it is lifted upward in the superior flap as dissection progresses in the subplatysmal plane. This nerve innervates the depressor anguli oris and damage is manifest as an asymmetric smile, where the lower lip rides higher than the contralateral normal side. The cervical branch can be located 1 cm below the angle of the mandible on a line perpendicular to that drawn from the mentum to the mastoid process. Dysfunction of the cervical branch is of far less clinical or aesthetic importance.

12.4 Classification of Facial Palsy

Facial palsy is a sign with many causes, and comprehensive classification systems have been proposed. ⁷ The most efficient method to classify causes for diagnostic purposes is to consider the anatomical location of the nerve (central, temporal, and facial) and then apply the “surgical sieve” ( ▶ Table 12.2). Rare systemic causes, such as fetal acetylcholine receptor inactivation syndrome, ⁸ may be considered further down the diagnostic pathway.

Facial palsy at birth occurs in approximately 0.2 to 2% of live births, 80 to 90% of which are due to birth trauma. Overall, a cause for pediatric facial palsy is determined in 70% of cases. ⁹ Acquired idiopathic facial palsy is a diagnosis of exclusion and termed Bell’s palsy. In children, additional weight should be given to considering a congenital cause, but the commonest etiology overall is obstetric birth injury and most recover within a month. ^{10,​ 11} Congenital idiopathic isolated palsy of the mandibular division is a typical presentation, but the true incidence is hard to define. Syndromic facial palsy is infrequent but is most commonly part of hemifacial microsomia where there is hypoplasia affecting one side of the face, often in association with other congenital anomalies of the head and neck. The most common causes of facial palsy in children are outlined as follows.

12.4.1 Congenital

This term refers to facial palsy present at birth that does not rapidly improve; supportive management is indicated with consideration of reconstruction when the child is older.

Idiopathic Facial Palsy

In children, the most common congenital cause is idiopathic facial nerve palsy. There are a number of presentations typically affecting the mandibular division (discussed next) or multiple divisions; the lower face is most obviously affected during animation.

Neonatal Asymmetric Crying Facies

The term neonatal indicates that the condition is present at birth rather than acquired. It classically presents as normal appearance at rest but an asymmetric lower lip position with crying or smiling.

It affects 0.6% live births, and in approximately 10% of cases, there are significant associated malformations. Whether the defect is due to muscle hypoplasia or nerve dysfunction is the subject of debate; electrodiagnostic studies have suggested muscle hypoplasia, whereas an ultrasonographic study (USS) found that six of seven patients had normal muscles. ¹² Cayler’s (cardiofacial) syndrome is asymmetric crying facies in association with cardiac malformations; fluorescence in situ hybridization (FISH) analysis has demonstrated the 22q.11 microdeletion in these instances. Positive FISH testing is an indication for echocardiogram and referral to pediatric cardiologist. Electrodiagnostic testing and USS of muscle is of little practical value and difficult to perform in infants.

Hemifacial Microsomia

This is a spectrum of morphogenetic anomalies of the tissues derived from the first and second pharyngeal arches. Facial palsy has been reported to be present in 22 to 45% of patients ¹³ and forms part of the OMENS (orbit, mandible, ear, nerve, soft tissue) classification, ¹⁴ whereby the palsy is classified as upper face, lower face, or complete involvement. It is managed in the same way as other cases of established facial palsy. One consideration is that these patients typically require orthognathic surgery at skeletal maturity, and planning of a cross-facial nerve graft should be undertaken with care.

Möbius’ Syndrome

Möbius’ syndrome is a rare sporadic congenital form of cranial nerve palsy that affects the abducens and facial nerves bilaterally, together with numerous other cranial and extracranial anomalies in a variable fashion ( ▶ Fig. 12.4). It is estimated that it affects 1 per 300,000 live births and approximately 200 cases of all ages are present in the United Kingdom. At birth, severe strabismus is noted together with a “masklike” facies; ophthalmology is often the first surgical specialty to have contact with these babies either due to the strabismus or lagophthalmos necessitating corneal protection. Other cranial nerve palsies lead to swallowing and feeding difficulties necessitating nasogastric feeding, percutaneous gastroenterostomy, or even tracheostomy for airway protection in severe cases. Other signs include the Poland’s syndrome of chest and hand malformations and lower limb malformations such as talipes.

In addition to the lack of facial expression, a delay in speech development and hearing loss can add to the impression of learning disabilities, which is present in 10 to 75%, ¹⁵ the wide range in percentage indicating that the very low numbers in the study groups make it difficult to ascertain a true incidence.

The facial palsy in these patients is bilateral but typically has a mixed picture with partial activity in some divisions of the facial nerve in an asymmetric pattern. Like most cases of congenital pediatric facial palsy, the lower face has a greater impact to the overall appearance upon animation. Therapy may be of some benefit in these patients, but if the child desires a smile, surgical reconstruction can be considered around the age of 7 years or above.

CHARGE Syndrome

CHARGE syndrome (coloboma, heart defects, atresia of the choanae, retardation of growth/development, genitourinary, and ear malformations) is a rare genetic syndrome affecting 1 to 3 per 10,000 live births and the acronym refers to the clinical features. There are specific clinical criteria for diagnosis, and a mutation in the CHD7 gene occurs in approximately two-thirds of patients. Facial palsy occurs in some cases, typically as part of multiple cranial nerve anomalies with consequent hearing loss and swallowing problems. As a consequence of the choanal atresia, the otolaryngologist will often be the first surgical specialty to assess these children; airway and feeding considerations take precedence (see ▶ 16).

12.4.2 Acquired

An acquired facial palsy may present at birth after traumatic delivery and rapidly improves, or presents later following a period of normal function.

Obstetric Facial Palsy (Trauma/Facial)

The most common form of facial palsy in children is obstetric facial palsy. ^{10,​ 11}

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