Facial nerve (7th cranial nerve) palsy is often idiopathic (formerly called Bell palsy). Idiopathic facial nerve palsy is sudden, unilateral peripheral facial nerve palsy. Symptoms of facial nerve palsy are hemifacial paresis of the upper and lower face. Tests (eg, chest x-ray, serum ACE level) are done to diagnose treatable causes. Treatment may include lubrication of the eye, intermittent use of an eye patch, and, for idiopathic facial nerve palsy, corticosteroids.
Historically, Bell palsy was thought to be idiopathic facial nerve (peripheral 7th cranial nerve) palsy. However, facial nerve palsy is now considered a clinical syndrome with its own differential diagnosis, and the term "Bell palsy" is not always considered synonymous with idiopathic facial nerve palsy. About half the cases of facial nerve palsy are idiopathic. The mechanism for idiopathic facial nerve palsy is presumably swelling of the facial nerve due to an immune or viral disorder. Recent evidence suggests that herpes simplex virus infection is the most common cause and that herpes zoster may be the second most common viral cause. Other viral causes include coxsackievirus, cytomegalovirus, adenovirus, and the Epstein-Barr, mumps, rubella, and influenza B viruses. The swollen nerve is maximally compressed as it passes through the labyrinthine portion of the facial canal, resulting in ischemia and paresis.
Various other disorders (eg, Lyme disease, sarcoidosis) can cause facial nerve palsy.
The upper facial muscles are innervated primarily by the peripheral nervous system via the facial nerve; however, the lower facial muscles are innervated by both the facial nerve (peripheral nervous system) and the ipsilateral cerebral hemisphere (CNS). Thus, when the lesion is central or supranuclear (eg, in stroke), the lower face is typically affected more than the upper face. In contrast, when the lesion is peripheral (involving the facial nerve nucleus and/or the facial nerve), the upper and lower face are affected equally.
Symptoms and Signs
Pain behind the ear often precedes facial paresis in idiopathic facial nerve palsy. Paresis, often with complete paralysis, develops within hours and is usually maximal within 48 to 72 h. Patients may report a numb or heavy feeling in the face. The affected side becomes flat and expressionless; the ability to wrinkle the forehead, blink, and grimace is limited or absent. In severe cases, the palpebral fissure widens and the eye does not close, often irritating the conjunctiva and drying the cornea.
Sensory examination is normal, but the external auditory canal and a small patch behind the ear (over the mastoid) may be painful to the touch. If the nerve lesion is proximal to the geniculate ganglion, salivation, taste, and lacrimation may be impaired, and hyperacusis may be present.
Facial nerve palsy is diagnosed based on clinical evaluation. There are no specific diagnostic tests. Facial nerve palsy can be distinguished from a central facial nerve lesion (eg, due to hemispheric stroke or tumor), which causes weakness primarily of the lower face, sparing the forehead muscle and allowing patients to wrinkle their forehead; also, patients with central lesions can usually furrow their brow and close their eyes tightly.
Other disorders that cause peripheral facial nerve palsies include the following:
The other disorders that cause peripheral facial nerve palsy typically develop more slowly than idiopathic facial nerve palsy and may have other distinguishing symptoms or signs. Thus, if patients have any other neurologic symptoms or signs or if symptoms developed gradually, MRI should be done.
In idiopathic facial nerve palsy, MRI may show contrast enhancement of the facial nerve at or near the geniculate ganglion or along the entire course of the nerve. However, its enhancement may reflect other causes, such as meningeal tumor. If the paralysis progresses over weeks to months, the likelihood of a tumor (eg, most commonly schwannoma) compressing the facial nerve increases. MRI can also help exclude other structural disorders causing facial nerve palsy. CT, usually negative in Bell palsy, is done if a fracture is suspected or if MRI is not immediately available and stroke is possible.
In addition, acute and convalescent serologic tests for Lyme disease are done if patients have been in a geographic area where ticks are endemic. For all patients, a chest x-ray is taken and serum ACE is measured to check for sarcoidosis. Serum glucose is measured. Viral titers are not helpful.
in idiopathic facial nerve palsy, the extent of nerve damage determines outcome. If some function remains, full recovery typically occurs within several months. Nerve conduction studies and electromyography are done to help predict outcome. The likelihood of complete recovery after total paralysis is 90% if nerve branches in the face retain normal excitability to supramaximal electrical stimulation and is only about 20% if electrical excitability is absent.
Regrowth of nerve fibers may be misdirected, innervating lower facial muscles with periocular fibers and vice versa. The result is contraction of unexpected muscles during voluntary facial movements (synkinesia) or crocodile tears during salivation. Chronic disuse of the facial muscles may lead to contractures.
Corneal drying must be prevented by frequent use of natural tears, isotonic saline, or methylcellulose drops and by intermittent use of tape or a patch to help close the eye, particularly during sleep. Tarsorrhaphy is occasionally required.
In idiopathic facial nerve palsy, corticosteroids, if begun within 48 h after onset, result in faster and more complete recovery. Prednisone 60 to 80 mg po once/day is given for 1 wk, then decreased gradually over the 2nd wk. Antiviral drugs effective against herpes simplex virus (eg, valacyclovir 1 g po tid for 7 to 10 days, famciclovir 500 mg po tid for 5 to 10 days, acyclovir 400 mg po 5 times/day for 10 days) have been prescribed, but recent data suggest that antiviral drugs provide no benefit.
Last full review/revision July 2012 by Michael Rubin, MDCM