Anatomy and Physiology
The facial nerve is a mixed nerve containing:
Motor fibers from the motor nucleus within the pons to the posterior belly of the digastric muscle, stylohyoid muscle, stapedius muscle, and muscles of facial expression. Of note, the upper face receives bilateral central innervation; therefore, an upper motor neuron lesion will spare the upper face. A lower motor neuron lesion will involve the entire hemiface.
Parasympathetic fibers arising from the superior salivary nucleus within the pons. Preganglionic, parasympathetic afferent fibers form following two nerves:
Greater superficial petrosal nerve. Branches off the main trunk at the geniculate ganglion, synapses at the pterygopalatine ganglion, and provides input to lacrimal, nasal, and palatine glands.
Chorda tympani nerve. Branches off the main trunk along the mastoid/vertical segment, joins the lingual nerve, synapses at the submandibular ganglion, and provides input to sublingual and submandibular glands.
Special sensory afferent fibers travel in the lingual nerve to the chorda tympani nerve and provide taste to the anterior two-thirds of the tongue, and travel to the nucleus solitarius.
Afferent fibers also provide sensation from the concha, external auditory canal, and earlobe.
The facial nerve is divided into following six segments:
Intracranial segment (17-24 mm) from brain stem to internal auditory canal (IAC).
Meatal segment (8-10 mm) from the fundus of the IAC, running in the anteriosuperior quadrant, to the meatal foramen.
Labyrinthine segment (4 mm) from the meatal foramen to the geniculate ganglion. The meatal foramen is the narrowest segment of the intratemporal bony channel, and the nerve is most susceptible to inflammation at this point.
Tympanic segment (11 mm) from the geniculate ganglion to the second genu.
Mastoid/vertical segment (13 mm) from the second genu to the stylomastoid foramen.
Extratemporal segment from the stylomastoid foramen, divides into the temporal, zygomatic, buccal, marginal mandibular, and cervical branches to innervate the muscles of facial expression.
Etiology of Facial Paralysis
There are hundreds of etiologies of facial paralysis with the most common causes being:
Benign or malignant tumors
The most common causes of synchronous, bilateral facial paralysis are
Neurofibromatosis type 2
Cavernous brain stem hemangioma and other brain stem pathologies
Bilateral temporal bone fractures
Assessment of Facial Paralysis
Assessment of facial paralysis begins with a detailed history and physical examination. The physical examination includes thorough head and neck examination with attention to otologic findings, cranial nerves, and palpation of the parotid gland and neck. In some cases, additional workup is required and may include laboratory testing, imaging, audiogram, and electrophysiologic testing.
Facial paralysis may be classified into flaccid facial paralysis (FFP), post-paralysis facial palsy (PPFP) characterized by hypertonicity and synkinesis, and mixed facial paralysis (MFP) with elements of flaccidity and hypertonicity. Facial function is documented with the following:
Complete set of photographs, with eight standard expressions including patient at rest, brows elevated, gentle eye closure, tight eye closure, small smile, large smile, pucker, and saying “eeee” along with the basal view of nose.
Video clip of eight standard expressions and articulation of plosives.
Facial nerve examination of patient at rest and during movement with documentation of:
Static parameters. Brow height, palpebral fissure width, oral commissure position, nasolabial fold depth.
Dynamic parameters. Brow elevation, gentle and full eye closure, oral commissure excursion, nasolabial fold depth and orientation with smile, lower lip movement.
Synkinesis parameters. Evaluate for ocular, midfacial, mentalis, and platysmal synkinesis.
Comprehensive intake and analysis of facial nerve patients may include the following:
Clinician-graded scales of facial function. There are numerous instruments available.
House-Brackmann and Sunnybrook are most frequently employed.
Automated assessments of facial function are emerging in the literature (eg, electronic facial paralysis assessment [eFACE]).
Patient-reported outcome measures.
Quality of life assessment (eg, facial clinimetric evaluation (FaCE) instrument).
Synkinesis assessment questionnaire (SAQ).
Nasal obstruction and septoplasty effectiveness (NOSE) scale.
Quantitative facial measurements.
Facial assessment by computer evaluation (FACE-gram).
Treatment of Acute Facial Paralysis
Viral-associated facial paralysis is the most common cause of facial paralysis. Facial paralysis involves all zones of the face (upper, middle, and lower), may be complete or incomplete, and should be fully evolved within 72 hours of onset. Bell palsy is thought to be caused by herpes simplex virus reactivation within the geniculate ganglion. The incidence of Bell palsy is 15 to 30 per 100,000 people. Ramsay Hunt syndrome or herpes zoster oticus is caused by varicella-zoster virus reactivation and is characterized by auricular vesicles, sensorineural hearing loss, and vestibular symptoms, in addition to facial paralysis. Workup for viral-associated facial paralysis is minimal. Routine imaging and laboratories are not indicated, aside from Lyme titer in Lyme-endemic areas. Treatment includes the following:
Oral steroids within 48 to 72 hours.
10-day course with at least 5 days at high dose (eg, prednisone 60 mg for 5 days followed by a 5-day taper).
Antivirals may provide a benefit when combined with oral steroids.
Meticulous eye care with drops, ointment, and nightly eye taping.
Consider electrodiagnostic testing in patients with acute facial paralysis within 12 days of onset.
If electroneuronography (ENoG) is less than 10% compound action potentials and needle electromyography (EMG) demonstrates no voluntary motor units, patient may be a candidate for surgical facial nerve decompression, though this remains controversial.
May offer facial nerve physical therapy to patients at risk for prolonged recovery.