42 Facial Nerve Flashcards
What types of nerve fibers are carried by the facial nerve?
What types of nerve fibers are carried by the facial nerve?
The facial nerve carries both motor and sensory nerve fibers (Figure). These include:
- Special visceral efferent: Motor innervation of the muscles of facial expression, stylohyoid, stapedius, platysma, and posterior belly of the digastric muscle
- General visceral efferent: Parasympathetic innervation of the lacrimal, submandibular, sublingual, minor salivary, mucosal glands of the nose, and palate
- Special sensory afferent: Taste from the anterior two thirds of the tongue, palate, and tonsillar fossa
- Somatic sensory afferent: Sensation from the external ear canal and skin of the concha portion of the auricle
- General visceral afferent sensory: Sensation from the nasal mucosa, palate, and pharynx
What branchial arch is associated with the facial nerve during development?
What branchial arch is associated with the facial nerve during development?
Second branchial arch. All muscles innervated by the facial nerve are second arch derivatives, as well as the stapes suprastructure, styloid process, stylohyoid ligament, and the lesser cornu of the hyoid.
Name the three anatomic segments of the fallopian canal, their course, and their length.
Name the three anatomic segments of the fallopian canal, their course, and their length.
- Labyrinthine segment: From fundus of IAC (meatal foramen) to the geniculate ganglion; 3 to 5 mm. The labyrinthine segment represents the narrowest portion of the fallopian canal at 1 mm.
- Tympanic segment: From geniculate ganglion to pyramidal process; 8 to 11 mm. Begins at the second genu (the first genu is intrapontine). The bony covering of the facial nerve is often dehiscent in this segment. This is the most common site of iatrogenic injury during ear surgery
- Mastoid segment: From pyramidal process to stylomastoid foramen; 10 to 14 mm
What is the nervus intermedius?
What is the nervus intermedius?
The nervus intermedius is a division of the facial nerve that carries its nonbranchial motor components. It is anatomically adjacent to but separate from the main trunk of the facial nerve as it exits the brainstem and then fuses with the facial nerve within the internal auditory canal. The chorda tympani is the terminal extension of the nervus intermedius.
What is the chorda tympani?
What is the chorda tympani?
The chorda tympani carries parasympathetic innervation to both the submandibular and sublingual glands and special sensory afferents from the anterior two thirds of the tongue. It branches off from the mastoid segment of the facial nerve and traverses the middle ear before exiting the tympanic cavity through the petrotympanic fissure to join the lingual branch of the trigeminal nerve. Stretching or cutting of this nerve during middle ear surgery produces transient taste alteration.
What is the pes anserinis?
What is the pes anserinis?
The pes anserinus (“goose’s foot”) is the first major branching of the extratemporal facial nerve after it leaves the stylomastoid foramen. This branching usually splits the nerve into upper and lower divisions. More distally the branching is variable but normally forms five major branches (see Figure):
- Temporal: frontalis, corrugator supercilii, procerus, and upper orbicularis oculi
- Zygomatic: lower orbicularis oculi
- Buccal: zygomaticus major and minor, levator anguli oris, buccinator, and upper orbicularis oris
- Marginal mandibular: lower orbicularis oris, depressor anguli oris, depressor labii inferioris, and mentalis
- Cervical: platysma
During parotid surgery, what are the landmarks for identifying the facial nerve?
During parotid surgery, what are the landmarks for identifying the facial nerve?
There are a number of methods to find the main trunk:
- Identify the tragal pointer, which is a triangular extension of the tragal cartilage. The main trunk of CN VII typically lies 10 mm inferior and 10 mm deep to this landmark.
- Follow the posterior belly of the digastric muscle to the styloid process. The stylomastoid foramen lies deep to this structure and is where the nerve exits the temporal bone. Typically it is 25 mm deep to the skin’s surface. NOTE: In children under the age of 2 the mastoid is not well developed, and the facial nerve lies much closer to the surface of the skin than would otherwise be expected.
- Find the tympanomastoid fissure. The nerve can be found 6 to 8 mm inferior to the end of the fissure.
- Identify a peripheral branch (e.g., marginal mandibular) and follow it proximally.
- Perform a mastoidectomy to find the mastoid portion of the nerve and follow it out of the stylomastoid foramen.
What are the three types of nerve injury?
What are the three types of nerve injury?
- Neuropraxia results when a lesion stops the axoplasm flow within an axon, blocking electrical conduction. Examples would include traumatic swelling or pharmacologic blockade. The nerve is viable and returns to normal function when the blockade is corrected. Electrophysiologic testing reveals normal function, except that the electromyogram fails to show voluntary motor action potentials because they are not conducted across the blockade.
- Axonotmesis is a state of Wallerian degeneration distal to the lesion with preservation of the motor axon endoneural sheaths. Examples would include mild crush or stretch injuries. Electrically, the nerve shows rapid and complete degeneration, with loss of voluntary motor units. Regeneration to the motor end plates will occur, as long as the endoneural tubules are intact.
- Neurotmesis is characterized by both Wallerian degeneration and loss of endoneural tubules. Electrophysiologic studies yield evidence of complete nerve degeneration. Regeneration is dependent on many factors, including the integrity of the endoneurium, perineurium, and epineurium and the extent of ischemia and scarring around the lesion.
What is synkinesis?
What is synkinesis?
If a facial nerve lesion results in Wallerian degeneration, subsequent axon regeneration may result in “cross-wiring” in which voluntary movement of one facial muscle group induces involuntary movement of another. For example, after recovering from a facial palsy a patient may have squinting whenever he or she smiles. Although this is usually thought to occur from aberrant routing of regenerating axons, it is also proposed to be the result of ephaptic transmission (abnormal connections between axons) and postsynaptic hyperexcitability.
What is the House-Brackmann Facial Nerve Grading System?
What is the House-Brackmann Facial Nerve Grading System?
This grading system is used to classify the degree of function of the facial nerve following its recovery after injury (Table 42-1).
What is Bell’s palsy?
What is Bell’s palsy?
Bell’s palsy is the most commonly diagnosed cause of facial paralysis. The etiology is thought to be a viral neuropathy caused by the herpes simplex virus. Most importantly, it is a diagnosis of exclusion with the following minimum diagnostic criteria:
- Paralysis or paresis of all facial muscle groups on one side of the face
- Sudden onset
- Absence of signs of central nervous system (CNS) disease, ear disease, or a parotid mass
It often follows a viral prodrome with a typical 3- to 5-day duration and a peak in symptoms at 48 hours. The patient may have a widened palpebral fissure, diminished taste, difficulty chewing, hyperesthesia in one or more branches of the fifth cranial nerve, facial pain, and hyperacusis. In 14% of patients with Bell’s palsy, family history will be positive. Some 12% of patients may have recurrent facial paralysis, either ipsilateral or contralateral.
HSV has been shown to be present within the geniculate ganglion of affected individuals, in contrast to the normal population in which this is rare. It has been proposed that reactivation of this virus in the geniculate ganglion causes swelling and subsequent paralysis. Bell’s palsy accounts for roughly 70% of acute facial palsies. However, it is important to remember that this is a diagnosis of exclusion.
List the common etiology categories of facial paralysis.
List the common etiology categories of facial paralysis.
- Congenital: Möbius syndrome, congenital unilateral lower lip paralysis, Melkersson-Rosenthal syndrome, dystrophic myotonia
- Traumatic: Temporal bone fractures, intrauterine compression, birth trauma/forceps delivery, facial contusions or lacerations, penetrating wounds to face or ear, iatrogenic injury (parotid/ear/cranial surgery, embolization for epistaxis, mandibular block anesthesia)
- Infection: Bell’s palsy, herpes zoster oticus, otitis media with effusion, acute mastoiditis, malignant otitis externa, tuberculosis, Lyme disease, acquired immunodeficiency syndrome, mononucleosis, influenza, encephalitis, malaria, syphilis, botulism
- Idiopathic: Recurrent facial palsy
- Neoplasia: Cholesteatoma, carcinoma, acoustic neuroma, meningioma, facial neuroma, glomus jugulare or tympanicum, leukemia, hemangioblastoma, osteopetrosis, histiocytosis, rhabdomyosarcoma
- Metabolic/systemic: Diabetes, hyperthyroidism, pregnancy, autoimmune disorders, sarcoidosis, hypertension
- Neurologic: Guillain-Barré syndrome, multiple sclerosis, Millard-Gubler syndrome
What elements of the history and physical examination are important in evaluating a facial paralysis?
What elements of the history and physical examination are important in evaluating a facial paralysis?
With a good history, the wide differential diagnosis listed above can be narrowed significantly. Identifying factors for systemic and/or infectious causes is mandatory. Any palsy with slow progression or without improvement after 3 months should be considered a neoplasm until proven otherwise. Additional signs of possible tumor involvement include facial twitching, other cranial nerve involvement, hearing loss, recurrent episodes of facial paralysis, a mass behind the tympanic membrane or in the parotid gland, unilateral eustachian tube dysfunction, skin lesions suggesting skin cancer, and/or prolonged ear pain.
Bell’s palsy and herpes zoster oticus may also have associated numbness in the middle and lower face, otalgia, hyperacusis, decreased tearing, or altered taste sensation.
How can you distinguish whether the lesion causing facial paralysis is peripheral or central?
How can you distinguish whether the lesion causing facial paralysis is peripheral or central?
A unilateral central lesion (supranuclear) will spare the upper face, since these muscles receive both crossed and uncrossed fibers. Lesions of the peripheral system involve both the upper and the lower face. A central lesion is also suggested by the lack of emotional facial movement as well as decreased lacrimation, taste, and salivation on the ipsilateral side. Cortical lesions are also frequently associated with tongue or hand dysfunction.
Which radiologic studies should be part of the diagnostic workup for a patient with a facial paralysis?
Which radiologic studies should be part of the diagnostic workup for a patient with a facial paralysis?
Routine radiologic tests are not indicated for the assessment of every patient presenting with a facial nerve paralysis. The need for such studies is based on both the clinical history and the course of the paralysis (i.e., if a neoplasm is suspected). If radiologic imaging is deemed necessary, high-resolution computed tomography (CT) or magnetic resonance imaging (MRI) are the studies of choice. MRI scans are superior to CT in imaging the nerve at the cerebellopontine angle and internal auditory canal. Gadolinium-enhanced MRI is the test of choice for facial nerve paralysis secondary to inflammatory, neoplastic, and other nontraumatic etiologies. CT, on the other hand, is preferred for the evaluation of traumatic seventh nerve paralysis and other etiologies involving the temporal bone such as cholesteatoma.