emedicine.medscape.com

Bell Palsy
Updated: May 04, 2021
Author: Danette C Taylor, DO, MS, FACN; Chief Editor: Selim R Benbadis, MD 

Overview

Practice Essentials
Bell palsy, also termed idiopathic facial paralysis (IFP), is the most common cause of unilateral facial paralysis. It is one of
the most common neurologic disorders of the cranial nerves (see the image below). In the great majority of cases, Bell palsy
gradually resolves over time, and its cause is unknown.

Signs and symptoms of Bell palsy

Signs and symptoms of Bell palsy include the following:

Acute onset of unilateral upper and lower facial paralysis (over a 48-hr period)

Posterior auricular pain

Decreased tearing

Hyperacusis

Taste disturbances

Otalgia

Weakness of the facial muscles

Poor eyelid closure

Aching of the ear or mastoid

Tingling or numbness of the cheek/mouth

Epiphora

Ocular pain

Blurred vision

Flattening of forehead and nasolabial fold on the side affected by palsy

When patient raises eyebrows, palsy-affected side of forehead remains flat

When patient smiles, face becomes distorted and lateralizes to side opposite the palsy

See Clinical Presentation for more specific information on the signs and symptoms of Bell palsy.

Diagnosis of Bell Palsy

Examination for Bell palsy includes the following:

Otologic examination: Pneumatic otoscopy and tuning fork examination, particularly if evidence of acute or chronic
otitis media

Ocular examination: Patient often unable to completely close eye on affected side

Oral examination: Taste and salivation often affected

 Neurologic examination: All cranial nerves, sensory and motor testing, cerebellar testing

Grading

The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI,[1, 2, 3] as follows:

Grade I: normal facial function

Grade II: mild dysfunction

Grade III: moderate dysfunction

Grade IV: moderately severe dysfunction

Grade V: severe dysfunction

Grade VI: total paralysis

See Clinical Presentation for more specific information on patient history and physical examination for Bell palsy.

Testing

Although there are no specific diagnostic tests for Bell palsy, the following may be useful for identifying or excluding other
disorders:

Rapid plasma reagin and/or venereal disease research laboratory test or fluorescent treponemal antibody absorption
test

HIV screening by enzyme-linked immunosorbent assay and/or Western blot

Complete blood count

Erythrocyte sedimentation rate

Thyroid function

Serum glucose

CSF analysis

Blood glucose

Hemoglobin A1c

Antineutrophil cytoplasmic antibody levels

Salivary flow

Schirmer blotting test

Nerve excitability test

Computed tomography

Magnetic resonance imaging

See Workup for more specific information on testing and imaging modalities for Bell palsy.

Management of Bell Palsy

Goals of treatment: (1) improve facial nerve (seventh cranial nerve) function; (2) reduce neuronal damage; (3) prevent
complications from corneal exposure

Treatment includes the following:

Corticosteroid therapy (prednisone)[4, 5]

Antiviral agents[4, 6]

Eye care: Topical ocular lubrication is usually sufficient to prevent corneal drying, abrasion, and ulcers[7]

Surgical options

Surgical treatment options include the following:

 Facial nerve decompression

Subocularis oculi fat lift

Implantable devices (eg, gold weights) placed into the eyelid

Tarsorrhaphy[2]

Transposition of the temporalis muscle

Facial nerve grafting

Direct brow lift

See Treatment and Medication for more specific information regarding pharmacologic and other therapies for Bell palsy.

Impact of COVID-19 Infection and SARS-CoV-2 Vaccine 

Viruses and vaccinations have been identified as risk factors for development of Bell palsy. Idiopathic facial paralysis (IFP)
has been reported in association with COVID-19 and SARS-CoV-2 as well as the currently available vaccinations. The
specific risk associated with COVID-19, SAR-CoV-2, and the SARS-CoV-2 vaccines has not yet been been determined.[8]

Background
Bell palsy, more appropriately termed idiopathic facial paralysis (IFP), is the most common cause of unilateral facial
paralysis. Bell palsy is an acute, unilateral, peripheral, lower-motor-neuron facial nerve paralysis that gradually resolves over
time in 80–90% of cases.

Controversy surrounds the etiology and treatment of Bell palsy. The cause of Bell palsy remains unknown, though the
disorder appears to be a polyneuritis with possible viral, inflammatory, autoimmune, and ischemic etiologies. Increasing
evidence implicates herpes simplex type I and herpes zoster virus reactivation from cranial-nerve ganglia.[9] (See Etiology.)

Bell palsy is one of the most common neurologic disorders affecting the cranial nerves, and it is the most common cause of
facial paralysis worldwide. It is thought to account for approximately 60–75% of cases of acute unilateral facial paralysis.
Bell palsy is more common in adults, in people with diabetes, and in pregnant women. (See Epidemiology.)

The widespread prevalence of the new coronavirus disease (COVID-19) and associated virus severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2) has led to some reported cases of IFP. In addition, there have been some reports of
IFP associated with the vaccine trials. A study by Ozonoff et al found 7 cases of Bell's palsy among nearly 40,000 vaccine
arm participants. There was only 1 case of Bell's palsy among placebo arm participants. This estimated rate ratio of
approximately 7:0 suggests vaccination might be associated with Bell's palsy (p=0·07). The cases of Bell palsy associated
with COVID-19 and SARS-CoV-2 vaccines, as reported, are not of increased severity and respond to current treatment
protocols.[10, 8]

Anatomy
In 1550, Fallopius noted the narrow foramen in the temporal bone through which a part of the seventh cranial nerve (facial
nerve) passes; this feature is now sometimes called the fallopian canal or the facial canal. In 1828, Charles Bell made the
distinction between the fifth and seventh cranial nerves; he noted that the seventh nerve was involved mainly in the motor
function of the face and that the fifth nerve primarily conducted sensation from the face.

The facial nerve contains parasympathetic fibers to the nose, palate, and lacrimal glands. Its course is tortuous, both
centrally and peripherally. The facial nerve travels a 30-mm intraosseous course through the internal auditory canal (with the
eighth cranial nerve) and through the internal fallopian canal in the petrous temporal bone. This bony confinement limits the
amount that the nerve can swell before it becomes compressed.

The nucleus of the facial nerve lies within the reticular formation of the pons, adjacent to the fourth ventricle. The facial
nerve roots include fibers from the motor, solitary, and salivatory nuclei. The preganglionic parasympathetic fibers that
originate in the salivatory nucleus join the fibers from nucleus solitarius to form the nervus intermedius.

The nervus intermedius is composed of sensory fibers from the tongue, mucosa, and postauricular skin, as well as
parasympathetic fibers to the salivary and lacrimal glands. These fibers then synapse with the submandibular ganglion,
which has fibers that supply the sublingual and submandibular glands. The fibers from the nervus intermedius also supply
the pterygopalatine ganglion, which has parasympathetic fibers that supply the nose, palate, and lacrimal glands.
The fibers of the facial nerve then course around the sixth cranial nerve nucleus and exit the pons at the cerebellopontine
angle. The fibers go through the internal auditory canal along with the vestibular portion of the eighth cranial nerve.

The facial nerve passes through the stylomastoid foramen in the skull and terminates into the zygomatic, buccal,
mandibular, and cervical branches. These nerves serve the muscles of facial expression, which include the frontalis,
orbicularis oculi, orbicularis oris, buccinator, and platysma muscles. Other muscles innervated by the facial nerve include the
stapedius, stylohyoid, posterior belly of the digastric, occipitalis, and anterior and posterior auricular muscles. All muscles
innervated by the facial nerve are derived from the second branchial arch. See the images below.

The facial nerve.

The facial nerve.

Pathophysiology
The precise pathophysiology of Bell palsy remains an area of debate. The facial nerve courses through a portion of the
temporal bone commonly referred to as the facial canal. A popular theory proposes that edema and ischemia result in
compression of the facial nerve within this bony canal. The cause of the edema and ischemia has not yet been established.
This compression has been seen in MRI scans with facial nerve enhancement.[11]

The first portion of the facial canal, the labyrinthine segment, is the narrowest; the meatal foramen in this segment has a
diameter of only about 0.66 mm. This is the location that is thought to be the most common site of compression of the facial
nerve in Bell palsy. Given the tight confines of the facial canal, it seems logical that inflammatory, demyelinating, ischemic,
or compressive processes may impair neural conduction at this site.
Injury to the facial nerve in Bell palsy is peripheral to the nerve’s nucleus. The injury is thought to occur near, or at, the
geniculate ganglion. If the lesion is proximal to the geniculate ganglion, the motor paralysis is accompanied by gustatory and
autonomic abnormalities. Lesions between the geniculate ganglion and the origin of the chorda tympani produce the same
effect, except that they spare lacrimation. If the lesion is at the stylomastoid foramen, it may result in facial paralysis only.

Etiology
Herpes simplex virus

In the past, situations that produced cold exposure (eg, chilly wind, cold air conditioning, or driving with the car window
down) were considered to be the only triggers for Bell palsy. Several authors now believe, however, that the herpes simplex
virus (HSV) is a common cause of Bell palsy, though a definitive causal relationship of HSV to Bell palsy may be difficult to
prove because of the ubiquitous nature of HSV.

The hypothesis that HSV is the etiologic agent in Bell palsy holds that after causing primary infection on the lips (ie, cold
sores), the virus travels up the axons of the sensory nerves and resides in the geniculate ganglion. At times of stress, the
virus reactivates and causes local damage to the myelin.

This hypothesis was first suggested in 1972 by McCormick.[12] Autopsy studies have since shown HSV in the geniculate
ganglion of patients with Bell palsy. Murakami et al performed polymerase chain reaction (PCR) assay testing on the
endoneural fluid of the facial nerve in patients who underwent surgery for Bell palsy and found HSV in 11 of 14 cases.[13]

Additional support for a viral etiology was seen when intranasal, inactivated influenza vaccine was strongly linked to the
development of Bell palsy.[14, 15] With those cases, however, it is not clear whether another component of the vaccine
caused the paresis, which was then accompanied by a reactivation of HSV infection.

Additional causes of Bell palsy

Besides HSV infection, possible etiologies for Bell palsy include other infections (eg, herpes zoster, Lyme disease, syphilis,
Epstein-Barr viral infection, cytomegalovirus, human immunodeficiency virus [HIV], mycoplasma); inflammation alone; and
microvascular disease (diabetes mellitus and hypertension). Bell palsy has also been known to follow recent upper
respiratory infection (URI).[16, 17, 18, 19, 20, 21]

Bell palsy may be secondary to viral and/or autoimmune reactions that cause the facial nerve to demyelinate, resulting in
unilateral facial paralysis.

A family history of Bell palsy has been reported in approximately 4% of cases. Inheritance in such cases may be autosomal
dominant with low penetration; however, which predisposing factors are inherited is unclear.[22] The family history may also
be positive for other nerve, nerve root, or plexus disorders (eg, trigeminal neuralgia) in siblings.[23] In addition, there are
isolated reports of familial Bell palsy with neurologic deficits, including ophthalmoplegia[24] and essential tremor.[25] A rare
form of familial Bell palsy has a predilection for juvenile females.[26]

Because there is a strong environmental predisposition to Bell palsy, due to the common viral etiology, a positive family
history may or may not indicate a true genetic etiology.

Epidemiology
In the United States, the annual incidence of Bell palsy is approximately 23 cases per 100,000 persons.[5] Very few cases
are observed during the summer months. Internationally, the highest incidence was found in a study in Seckori, Japan, in
1986, and the lowest incidence was found in Sweden in 1971. Most population studies generally show an annual incidence
of 15–30 cases per 100,000 population.

Bell palsy is thought to account for approximately 60–75% of cases of acute unilateral facial paralysis, with the right side
affected 63% of the time. It can also be recurrent, with a reported recurrence range of 4–14%.[17]

Though bilateral simultaneous Bell palsy can develop, it is rare. It accounts for only 23% of bilateral facial paralysis and has
an occurrence rate that is less than 1% of that for unilateral facial nerve palsy.[27, 28] The majority of patients with bilateral
facial palsy have Guillain-Barré syndrome, sarcoidosis, Lyme disease, meningitis (neoplastic or infectious), or bilateral
neurofibromas (in patients with neurofibromatosis type 2).

Persons with diabetes have a 29% higher risk of being affected by Bell palsy than do persons without diabetes. Thus,
measuring blood glucose levels at the time of diagnosis of Bell palsy may detect undiagnosed diabetes. Diabetic patients
are 30% more likely than nondiabetic patients to have only partial recovery; recurrence of Bell palsy is also more common
among diabetic patients.[29]

Bell palsy is also more common in people who are immunocompromised or in women with preeclampsia.[30]
Sex- and age-related demographics

Bell palsy appears to affect the sexes equally. However, young women aged 10–19 years are more likely to be affected than
are men in the same age group. Pregnant women have a 3.3 times higher risk of being affected by Bell palsy than do
nonpregnant women; Bell palsy occurs most frequently in the third trimester.

In general, Bell palsy occurs more commonly in adults. A slightly higher predominance is observed in patients older than 65
years (59 cases per 100,000 people), and a lower incidence rate is observed in children younger than 13 years (13 cases
per 100,000 people). The lowest incidence is found in persons younger than 10 years, and the highest incidence is in
persons aged 60 years or older. Peak ages are between 20 and 40 years. The disease also occurs in elderly persons aged
70–80 years.[31]

Prognosis
The natural course of Bell palsy varies from early complete recovery to substantial nerve injury with permanent sequelae
(eg, persistent paralysis and synkinesis). Prognostically, patients fall into 3 groups:

Group 1 - Complete recovery of facial motor function without sequelae

Group 2 - Incomplete recovery of facial motor function, but with no cosmetic defects that are apparent to the
untrained eye

Group 3 - Permanent neurologic sequelae that are cosmetically and clinically apparent

Approximately 80–90% of patients with Bell palsy recover without noticeable disfigurement within 6 weeks to 3 months. Use
of the Sunnybrook grading scale for facial nerve function at 1 month has been suggested as a means of predicting
probability of recovery.[32]

Most patients who suffer from Bell palsy have neurapraxia or local nerve conduction block. These patients are likely to have
a prompt and complete recovery of the nerve. Patients with axonotmesis, with disruption of the axons, have a fairly good
recovery, but it is usually not complete.

The risk factors thought to be associated with a poor outcome in patients with Bell palsy include (1) age greater than 60
years, (2) complete paralysis, and (3) decreased taste or salivary flow on the side of paralysis (usually 10-25% compared
with the patient’s normal side). Other factors thought to be associated with poor outcome include pain in the posterior
auricular area and decreased lacrimation.

Patients aged 60 years or older have an approximately 40% chance of complete recovery and have a higher rate of
sequelae. Patients younger than 30 years have only a 10–15% chance of less than complete recovery and/or long-term
sequelae.

The sooner the recovery, the less likely are the chances that sequelae will develop, as summarized below:

If some restoration of function is noted within 3 weeks, then the recovery is most likely to be complete

If the recovery begins between 3 weeks and 2 months, then the ultimate outcome is usually satisfactory

If the recovery does not begin until 2–4 months from the onset, likelihood of permanent sequelae, including residual
paresis and synkinesis, is higher

If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the disease, which include
synkinesis, crocodile tears, and (rarely) hemifacial spasm

Bell palsy recurs in 4–14% of patients, with one source suggesting a recurrence rate of 7%. It may recur on the same or
opposite side of the initial palsy. Recurrence usually is associated with a family history of recurrent Bell palsy. Higher
recurrence rates among patients were reported in the past; however, many of these patients were found to have an
underlying etiology for the recurrence, eliminating the diagnosis of Bell palsy, an idiopathic disease.[33]

Patients with recurrent ipsilateral facial palsy should undergo MRI or high-resolution computed tomography (CT) scanning to
rule out a neoplastic or inflammatory (eg, multiple sclerosis, sarcoidosis) cause of recurrence. Recurrent or bilateral disease
should suggest myasthenia gravis.

Sequelae

Most patients with Bell palsy recover without any cosmetically obvious deformities. Approximately 30% of patients, however,
experience long-term symptoms following the paralysis, and approximately 5% are left with an unacceptably high degree of
sequelae. Bell palsy sequelae include incomplete motor regeneration, incomplete sensory regeneration, and aberrant
reinnervation of the facial nerve.
Incomplete motor regeneration

The largest portion of the facial nerve is composed of efferent fibers that stimulate muscles of facial expression. Suboptimal
regeneration of this portion results in paresis of all or some of these facial muscles. This manifests as (1) oral incompetence,
(2) epiphora (excessive tearing), and (3) nasal obstruction.

Incomplete sensory regeneration

Dysgeusia or ageusia (impairment or loss of taste, respectively) may occur with incomplete regeneration of the chorda
tympani. Incomplete regeneration of other afferent branches may result in dysesthesia (impairment of sensation or
disagreeable sensation to normal stimuli).

Aberrant reinnervation of the facial nerve

During regeneration and repair of the facial nerve, some neural fibers may take an unusual course and connect to
neighboring muscle fibers. This aberrant reconnection produces unusual neurologic pathways. When voluntary movements
are initiated, they are accompanied by involuntary movements (eg, eye closure associated with lip pursing or mouth
grimacing that occurs during blinking of the eye). The condition in which involuntary movements accompany voluntary
movements is termed synkinesis.

Patient Education
To prevent corneal abrasions, patients should be instructed about eye care. They also should be encouraged to do facial
muscle exercises using passive range of motion, as well as actively close their eyes and smile. Facial exercises can help
Bell palsy patients increase muscle strength and coordination in the face. Some of these include raising the eyebrows and
holding them in the raised state for 10–15 seconds, curling and snarling the lips, wrinkling the nose, and tilting the head and
stretching the neck, among others.  

For patient education information, see the Brain and Nervous System Center, as well as Bell’s Palsy.

Presentation

History
The diagnosis of Bell palsy must be made on the basis of a thorough history and physical examination, as well as the use of
diagnostic testing when necessary. Bell palsy is a diagnosis of exclusion. Clinical features of the disorder that may help to
distinguish it from other causes of facial paralysis include the sudden onset of unilateral facial paralysis and the absence of
signs and symptoms of CNS, ear, and cerebellopontine angle disease.

Symptoms of Bell palsy include the following:

Acute onset of unilateral upper and lower facial paralysis (over a 48-hr period)

Posterior auricular pain

Decreased tearing

Hyperacusis

Taste disturbances

Otalgia

Early symptoms include the following:

Weakness of the facial muscles

Poor eyelid closure

Aching of the ear or mastoid (60%)

Alteration of taste (57%)

Hyperacusis (30%)

Tingling or numbness of the cheek/mouth

 Epiphora

Ocular pain

Blurred vision

Onset

The onset of Bell palsy is typically sudden, and symptoms tend to peak in less than 48 hours. This sudden onset can be
frightening for patients, who often fear they have had a stroke or have a tumor and that the distortion of their facial
appearance will be permanent.

Because the condition appears so rapidly, patients with Bell palsy frequently present to the emergency department (ED)
before seeing any other health care professional. More people first notice paresis in the morning. Because the symptoms
require several hours to become evident, most cases of paresis likely begin during sleep.

Facial paralysis

The paralysis must include the forehead and lower aspect of the face. The patient may report the inability to close the eye or
smile on the affected side. He or she also may report increased salivation on the side of the paralysis. If the paralysis
involves only the lower portion of the face, a central cause should be suspected (ie, supranuclear). If the patient complains
of contralateral weakness or diplopia in conjunction with the supranuclear facial palsy, a stroke or intracerebral lesion should
be strongly suspected.

If a patient has gradual onset of facial paralysis, weakness of the contralateral side, or a history of trauma or infection, other
causes of facial paralysis must be strongly considered. Progression of the paresis is possible, but it usually does not
progress beyond 7–10 days. A progression beyond this point suggests a different diagnosis. Patients who have bilateral
facial palsy must be evaluated for Guillain-Barré syndrome, Lyme disease, and meningitis.

Many patients report numbness on the side of the paralysis. Some authors believe that this is secondary to involvement of
the trigeminal nerve, whereas other authors argue that this symptom is probably from lack of mobility of the facial muscles
and not lack of sensation.

Ocular manifestations
Early ocular complications include the following:

Lagophthalmos (inability to close the eye completely)

Paralytic ectropion of the lower lid

Corneal exposure

Brow droop

Upper eyelid retraction

Decreased tear output/poor tear distribution

Loss of the nasolabial fold

Corneal erosion, infection, and ulceration (rare)

Late ocular manifestations include the following:

Mild, generalized mass contracture of the facial muscles, rendering the affected palpebral fissure narrower than the
opposite one (after several months)

Aberrant regeneration of the facial nerve with motor synkinesis

Reversed jaw winking (ie, contracture of the facial muscles with twitching of the corner of the mouth or dimpling of
the chin occurring simultaneously with each blink)

Autonomic synkinesis (ie, crocodile tears—tearing with chewing)

Permanent, disfiguring facial paralysis (rare)

Two thirds of patients complain about tear flow.[9] This results from the reduced function of the orbicularis oculi in
transporting the tears. Fewer tears arrive at the lacrimal sac, and overflow occurs. The production of tears is not
accelerated.

Posterior auricular pain

Half of the patients affected with Bell palsy may complain of posterior auricular pain.[9] The pain frequently occurs
simultaneously with the paresis, but pain precedes the paresis by 2–3 days in about 25% of patients. Ask the patient if he or
she has experienced trauma, which may account for the pain and facial paralysis.

One third of patients may experience hyperacusis in the ear ipsilateral to the paralysis, which is secondary to weakness of
the stapedius muscle.

Taste disorders

While only one third of patients report taste disorders,[9] 80% of patients show a reduced sense of taste. Patients may fail to
note reduced taste, because of normal sensation in the uninvolved side of the tongue. Early recovery of the sense of taste
suggests that the patient will experience a complete recovery.

Facial spasm

Facial spasm, a very rare complication of Bell palsy, occurs as tonic contraction of 1 side of the face. Spasms are more
likely to occur during times of stress or fatigue and may be present during sleep. This condition may occur secondary to
compression of the root of the seventh nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root.

Facial spasm occurs most commonly in patients in the fifth and sixth decades of life. Sometimes the etiology is not found.
The presence of progressive facial hemispasm with other cranial nerve findings indicates the possibility of a brainstem
lesion.

Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It may be mild and result in
slight movement of the mouth or chin when the patient blinks or in eye closure with smiling. Crocodile tears can be
observed; patients shed tears while they eat.

Cranial neuropathies

Some believe that other cranial neuropathies may also be present in Bell palsy; however, this is not uniformly accepted. The
symptoms in question include the following:

Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves

Dysfunction of the vestibular nerve

Hyperesthesia of the cervical sensory nerves

Vagal or trigeminal motor weakness

Physical Examination
Weakness and/or paralysis from involvement of the facial nerve affects the entire face (upper and lower) on the affected
side. A careful examination of the head, ears, eyes, nose, and throat must be carried out in all patients with facial paralysis.
Time must also be taken to examine the patient’s skin for signs of squamous cell carcinoma, which can invade the facial
nerve, and parotid gland disease.

Focus attention on the voluntary movement of the upper part of the face on the affected side; in supranuclear lesions, such
as occur in a cortical stroke (upper motor neuron; above the facial nucleus in the pons), the upper third of the face is spared
in the majority of cases, while the lower two thirds are paralyzed. The orbicularis, frontalis, and corrugator muscles are
innervated bilaterally at the level of the brainstem, which explains the pattern of facial paralysis in these cases.[28]

Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the side affected by the palsy.
When the patient is asked to raise his or her eyebrows, the side of the forehead with the palsy will remain flat. When the
patient is asked to smile, the face will become distorted and lateralize to the side opposite the palsy.

Otologic examination

An otologic examination includes pneumatic otoscopy and tuning fork examination. An otologic cause should be considered
if the history or physical examination demonstrates evidence of acute or chronic otitis media, including a tympanic
membrane perforation, otorrhea, cholesteatoma, or granulation tissue, or if a history of ear surgery is noted. Concurrent
rash or vesicles along the ear canal, pinna, and mouth should raise the suspicion for Ramsay Hunt syndrome (herpes zoster
oticus).

The external auditory canal must be inspected for vesicles, injection or erythema, infection, or trauma. The patient may have
decreased sensation to pinprick in the posterior auricular area. Tympanic membranes should be normal; the presence of
inflammation, vesicles, or other signs of infection raises the possibility of complicated otitis media.
The patient who has paralysis of the stapedius muscle will report hyperacusis. This can be tested clinically using the
stethoscope loudness test. In this, the patient wears a stethoscope, and an activated tuning fork is placed at its bell. The
loud sound will lateralize to the side of the paralyzed stapedius muscle.

Ocular examination

With weakness/paralysis of the orbicularis oculi muscle (facial nerve innervation) and normal function of the levator muscle
(oculomotor nerve innervation) and Mueller muscle (sympathetic innervation), the patient frequently is not able to close the
eye completely on the affected side. On attempted eye closure, the eye rolls upward and outward on the affected side. (This
is known as Bell phenomenon and is considered a normal response to eye closure.) In addition, the tear reflex is absent in
many cases of Bell palsy.

For these reasons, the patient may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye.
The patient may appear to have loss of corneal reflex on the affected side; however, the contralateral eye blinks when
testing the corneal reflex on the affected side.

Oral examination

A careful oral examination must be performed. Taste and salivation are affected in many patients with Bell palsy. Taste may
be assessed by holding the tongue with gauze and testing each side of the tongue independently with salt, sugar, and
vinegar. The mouth must be washed after testing with different substances. The affected side has decreased taste
compared with the normal side.

Neurologic examination

Careful neurologic examination is necessary in patients with facial paralysis. This includes complete examination of all of the
cranial nerves, sensory and motor testing, and cerebellar testing. A neurologic abnormality warrants neurologic referral and
further testing, such as MRI of the brain, lumbar puncture, and EMG where appropriate.

Grading
The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI.[1, 2, 3] Grade I is
normal facial function.

Grade II is mild dysfunction. Characteristics include the following:

Slight weakness is noted on close inspection

Slight synkinesis may be present

Normal symmetry and tone are noted at rest

Forehead motion is moderate to good

Complete eye closure is achieved with minimal effort

Slight mouth asymmetry is noted

Grade III is moderate dysfunction. The following characteristics are found:

An obvious, but not disfiguring, difference is noted between the 2 sides

A noticeable, but not severe, synkinesis, contracture, or hemifacial spasm is present

Normal symmetry and tone are noted at rest

Forehead movement is slight to moderate

Complete eye closure is achieved with effort

A slightly weak mouth movement is noted with maximal effort

Grade IV is moderately severe dysfunction. Signs include the following:

An obvious weakness and/or disfiguring asymmetry is noted

Symmetry and tone are normal at rest

No forehead motion is observed

 Eye closure is incomplete

An asymmetrical mouth is noted with maximal effort

Grade V is severe dysfunction. Characteristics include the following:

Only a barely perceptible motion is noted

Asymmetry is noted at rest

No forehead motion is observed

Eye closure is incomplete

Mouth movement is only slight.

Grade VI is total paralysis. The following are noted:

Gross asymmetry

No movement

In this system, grades I and II are considered good outcomes, grades III and IV represent moderate dysfunction, and grades
V and VI describe poor results. Grade VI is defined as complete facial paralysis; all of the other grades are defined as
incomplete. An incomplete facial paralysis denotes an anatomically and, to some degree, functionally intact nerve. The
degree of facial nerve function should be noted in the chart at the patient’s initial visit.

Complications
Complications of Bell palsy may include the following:

Irreversible damage to the facial nerve

Abnormal regrowth of nerve fibers, resulting in involuntary contraction of certain muscles when trying to move others
(synkinesis) 
Partial or complete blindness of the eye that won't close due to excessive dryness and scratching of the cornea 

DDx

Diagnostic Considerations
In most cases, the diagnosis of Bell palsy is straightforward as long as the patient has undergone a thorough history and
physical examination. Failure to recognize structural, infectious, or vascular lesions leading to seventh cranial (facial) nerve
damage may result in further deterioration of the patient’s condition. For example, if other cranial nerve, motor, or sensory
symptoms are present, then other neurologic diseases should be considered (eg, stroke, Guillain-Barré syndrome, basilar
meningitis, cerebellar pontine angle tumor).

Symptoms associated with seventh nerve neoplasm include slowly progressive paralysis, facial hyperkinesis, severe pain,
recurrent palsy, and other cranial nerve involvement. Cerebellopontine tumors may affect the seventh, eighth, and fifth
cranial nerves simultaneously. Patients with a progressive paralysis of the facial nerve lasting longer than 3 weeks should
be evaluated for neoplasm.

Recurrent ipsilateral facial paralysis must raise the suspicion of a tumor of the facial nerve or parotid gland. Tumors in the
temporal bone, such as facial nerve neuromas, meningiomas, hemangiomas, and malignant primary and metastatic lesions,
should be considered as well.

If a patient is from the Northeast United States, Lyme disease should be considered as a cause of facial paralysis, and
serologic testing should be performed. Approximately 5-10% of untreated Lyme patients may have a peripheral facial nerve
palsy.

If a patient reports the sudden onset of hearing loss and severe pain with the onset of facial paralysis, Ramsay Hunt
syndrome must be considered. Typically, these patients will also have an erythematous vesicular rash involving the ear
canal, auricle, and/or oropharynx.

Other problems to be considered include the following:

Acoustic neuroma and other cerebellopontine angle lesions

 Acute or chronic otitis media

Amyloidosis

Aneurysm of vertebral artery, basilar artery, or carotid arteries

Autoimmune syndromes

Botulism

Carcinomatosis

Carotid disease and stroke - Including embolic phenomenon

Cholesteatoma of the middle ear

Congenital malformation

Facial nerve schwannoma

Geniculate ganglion infection

Glomus tumors

Guillain-Barré syndrome

Herpes zoster

Human immunodeficiency virus (HIV) infection

Leukemia/lymphoma

Leukemic meningitis

Malignant otitis externa

Melkersson-Rosenthal syndrome

Meningitis

Mycoplasma pneumonia

Nasopharyngeal carcinoma

Osteomyelitis of the skull base

Otitis media

Parotid gland disease or tumor

Pontine lesions

Sarcoma

Skull base tumor

Teratoma

Tuberculosis

Viral syndromes

Wegener granulomatosis

Wegener vasculitis

In the setting of an appropriate history, additional considerations include the following:

Alcoholic neuropathy

Anesthesia nerve blocks

Basal skull fractures

Barotrauma
 Benign intracranial hypertension

Birth trauma

Carbon monoxide exposure

Diphtheria

Facial injuries

Facial trauma (blunt, penetrating, iatrogenic)

Forceps delivery

Iatrogenic - As in otologic, neurotologic, skull base, or parotid surgery

Infectious mononucleosis

Kawasaki disease

Leprosy

Metastatic disease

Mumps

Polyneuritis

Temporal bone fracture

Tetanus

Thalidomide exposure

Toxic

Bilateral cases
Bilateral simultaneous Bell palsy is a rare occurrence; the rate of such cases is less than 1% of that of unilateral facial nerve
palsy,[27, 28] and it accounts for only 23% of bilateral facial paralysis cases. The majority of patients with bilateral facial
palsy have Guillain-Barré syndrome, sarcoidosis, Lyme disease, meningitis (neoplastic or infectious), or bilateral
neurofibromas (in patients with neurofibromatosis type 2).

Differential Diagnoses
Acute Complications of Sarcoidosis

Anterior Circulation Stroke

Benign Skull Tumors

Brainstem Gliomas

Cerebral Aneurysms

Intracranial Hemorrhage

Lyme Disease in Emergency Medicine

Meningioma

Neurosyphilis

Tuberculous Meningitis

Workup
 

Workup
Approach Considerations
Determining whether facial nerve paralysis is peripheral or central is a key step in the diagnosis. A lesion involving the
central motor neurons above the level of the facial nucleus in the pons causes weakness of the lower face alone. Thorough
history taking and examination, including the ears, nose, throat, and cranial nerves, must be performed. (See Presentation.)

The minimum diagnostic criteria include paralysis or paresis of all muscle groups on one side of the face, sudden onset, and
absence of central nervous system (CNS) disease. Note that the diagnosis of IFP can be made only after other causes of
acute peripheral palsy have been excluded. (See DDx.)

If the clinical findings are doubtful or if paralysis lasts longer than 6–8 weeks, further investigations, including gadolinium-
enhanced magnetic resonance imaging (MRI) of the temporal bones and pons, should be considered.[34]  Electrodiagnostic
tests (eg, stapedius reflex test, evoked facial nerve electromyography [EMG], audiography) may help to improve the
accuracy of prognosis in difficult cases. (See Workup.)

No specific diagnostic tests are available for Bell palsy, though the following may be useful for identifying or excluding other
disorders:

Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or fluorescent treponemal
antibody absorption (FTA-ABS) test

HIV screening by means of enzyme-linked immunosorbent assay (ELISA) and/or Western blot

Complete blood cell (CBC) count

Erythrocyte sedimentation rate measurement

Thyroid function studies

Serum glucose level

Cerebrospinal fluid analysis

In addition to the above tests, blood glucose or hemoglobin A1c levels may be obtained to determine if the patient has
undiagnosed diabetes. Persons with diabetes have a 29% higher risk of being affected by Bell palsy than do persons
without diabetes.

Serum titers for herpes simplex virus (HSV) may be obtained. However, this test is usually not helpful, owing to the
ubiquitous nature of this virus.

Antineutrophil cytoplasmic antibody (cANCA) levels are indicated, if applicable, to exclude Wegener granulomatosis. In
areas where Lyme disease is endemic, serum titers (immunoglobulin M [IgM] and IgG) for Borrelia burgdorferi should be
obtained.

Serum titers (IgM and IgA) for Mycoplasma pneumoniae may be obtained. A study in Germany measured titers in patients
with Bell palsy and found that several patients had elevated titers for M pneumoniae, though only 2 of those who tested
positive had respiratory symptoms.[35]

Content.

Imaging Studies for Bell Palsy

Imaging considerations

The latest guidelines (2103) from the American Academy of Otolaryngology-Head and Neck Surgery Foundation do not
recommend diagnostic imaging and routine lab testing for patients with new-onset disease.[36]  

If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging is not necessary, because
most patients with Bell palsy improve within 8–10 weeks. If the paralysis does not improve or worsens, imaging may be
useful. If the patient has a palpable parotid mass, imaging may be necessary.

CT scanning and MRI

Imaging with CT scanning or other methods is indicated if there are other associated physical findings or if the paresis is
progressive and unremitting. CT scanning demonstrates the architecture of the temporal bone and may be used if some
other pathology is suspected.
MRI is useful as a means of excluding other pathologies as the cause of paralysis and is preferred for imaging the
cerebellopontine angle.

MRI in patients with Bell palsy may show enhancement of the seventh cranial nerve (facial nerve) at or near the geniculate
ganglion. Alternatively, MRI may demonstrate a neoplasm compressing the facial nerve. Tumors that compress or involve
the facial nerve include schwannoma (most common), hemangioma, meningioma, and sclerosing hemangioma.

Perform gadolinium-enhanced MRI when findings are atypical or when the facial nerve paralysis appears central, to rule out
a tumor or vascular compression.[37] Increased signal intensity of the premeatal or intratemporal segment of the facial
nerve after administration of gadolinium has been noted in patients with Bell palsy.[38, 39] Attempts to correlate outcome
with quantification of signal intensity increases have yielded contradictory results.

Conduction Testing and EMG

Useful tests for evaluation of the function of the facial nerve include nerve conduction testing and EMG. Nerve conduction
velocities and EMG produce a graphic readout of the electrical currents, displayed by stimulating the facial nerve and
recording the excitability of the facial muscles it supplies. These tests may aid in assessing the outcome of a patient who
has persistent and severe Bell palsy.

This testing is not part of the acute workup; the tests are most useful when performed 3–10 days after the onset of paralysis.
Note that most electromyographic/nerve conduction studies do not show an abnormality for 3 weeks following a peripheral
nerve injury.

Comparison to the contralateral side helps to demonstrate the extent of nerve injury and has prognostic implications. Nerve
conduction responses are abnormal if a difference of 50% in amplitude between the paralyzed and normal side is detected;
a difference of 90% between the 2 sides suggests a poorer prognosis.

May et al. demonstrated that prognosis may be favorable if the motor amplitude of the affected side is greater than 25% of
that of the normal side. An incomplete recovery was observed in patients whose results demonstrated less than 25%
amplitude on the paralyzed side.[40] Blink reflexes can be used to measure conduction across the involved segment, but
they are commonly absent in Bell palsy.

Electroneurography
Electroneurography is a physiologic test that uses EMG to objectively measure the difference between potentials generated
by the facial musculature on both sides of the face in response to a supramaximal electrical stimulation of the facial nerve.
Because all electrodiagnostic testing is performed on the nerve distal to the proposed site of injury, sufficient time is needed
for wallerian degeneration to occur, usually 48–72 hours. Testing should begin 3 days from the onset of complete paralysis.

Electrodiagnostic testing measures the facial nerve degeneration indirectly. If a patient does not reach 90% degeneration
within the first 3 weeks of the onset of paralysis, some studies suggest that the prognosis is excellent, with over 80–100% of
the patients recovering with excellent function.

The patients who reach over 90% degeneration within the first 3 weeks of the onset of paralysis have a much more guarded
prognosis, with only 50% having good recovery of facial motion. The rate of degeneration also predicts the prognosis.
Patients who have 90% degeneration by 5 days have a worse prognosis than those with 90% degeneration at 14 days.

Electrodiagnostic testing is not recommended in patients with incomplete facial paralysis; however, it may be offered to
those patients with complete facial paralysis.[36]

Brainstem Auditory Evoked Response and Audiometry

Brainstem auditory evoked response (BAER) may be obtained in patients with peripheral facial nerve lesions and other
neurologic involvement. This test measures the transmission of response through the brainstem and is effective in detecting,
notably, retrocochlear lesions.

Hendrix and Melnick evaluated the BAER of 17 patients with Bell palsy and found no evidence of retrocochlear lesions of
the auditory system in any of the patients.[41] In study by Shannon et al, BAER was recorded in 27 patients with Bell palsy;
only 6 patients had prolonged brainstem transmission but normal auditory function.[42]

These studies were small and do not support routine use of BAER in patients with Bell palsy. However, when a patient
presents with multiple cranial neuropathies (eg, of the seventh and eighth cranial nerves), BAER may be useful.
If hearing loss is suspected, audiography and auditory evoked potentials (AEPs) should be pursued once an underlying
structural lesion has been excluded. Typically, the hearing threshold is not affected by Bell palsy. Impedance testing may
reveal an absent or diminished stapedial reflex because of paresis of the stapedial branch of the facial nerve.

Blepharokymographic Analysis
Blepharokymographic analysis, a high-speed eyelid motion-analysis system, has been used to evaluate movement of the
eyelids. Computer-based analysis may prove helpful in diagnosing Bell palsy, predicting prognosis, and evaluating response
to therapeutic measures such as placement of a gold weight in the affected upper eyelid (used in cases in which
spontaneous recovery has been limited).

Histologic Findings
In a review of 12 autopsy cases of patients with Bell palsy, most cases showed inflammatory changes around the mastoid
cells and walls of the arteries.[43] The most common site of involvement was the geniculate ganglion. Surgical findings
described constriction of the nerve at the stylomastoid foramen, with swelling of the nerve itself. Microscopic findings
showed an inflammatory reaction with infiltration of macrophages on the nerve.

Other Tests
Salivary flow test

Salivary flow also may be tested. The physician places a small catheter into the paralyzed and normal submandibular
glands. The patient is then asked to suck on a lemon, and the salivary flow is compared between the 2 sides. The normal
side is the control.

Schirmer blotting test

The Schirmer blotting test may be used to assess tearing function. The use of benzene will stimulate the nasolacrimal reflex,
and the degree of tearing can be compared between the paralyzed and normal sides.

Nerve excitability test

The nerve excitability test determines the threshold of the electrical stimulus needed to produce visible muscle twitching.
This test is technically challenging and has very limited clinical availability.

Treatment

Approach Considerations
Because persons with true Bell palsy generally have an excellent prognosis, and because spontaneous recovery is fairly
common, treatment of Bell palsy is still controversial. The goals of treatment are to improve facial nerve (seventh cranial
nerve) function and reduce neuronal damage. Treatment of Bell palsy should be conservative and guided by the severity
and probable prognosis in each particular case. Studies have shown the benefit of high-dose corticosteroids for acute
cases.[44, 45]  Although antiviral treatment has also come into use, evidence is now available indicating that it may not be
beneficial.[44]  (See Medication.)

Topical ocular therapy is useful in most cases, with the exception of those in which the condition is severe or prolonged. In
these cases, surgical management is best. Several procedures are aimed at protecting the cornea from exposure and
achieving facial symmetry. These procedures reduce the need for constant use of lubrication drops or ointments, may
improve cosmesis, and may be needed to preserve vision on the affected side.

Many issues must be addressed in treating patients with Bell palsy. The most important is the onset of symptoms. Treatment
may be considered for patients who present within 1–4 days of the onset of paralysis.

Patients with Bell palsy frequently present to the emergency department (ED). The role of the ED clinician consists of the
following:
 Initiate appropriate treatment

Protect the eye

Arrange appropriate medical follow-up care

The American Academy of Neurology (AAN) published a practice parameter in 2001 stating that steroids are probably
effective and acyclovir (with prednisone) is possibly effective for the treatment of Bell palsy. There was insufficient evidence
for recommendations on facial decompression surgery.[46]

In 2012, the AAN released guidelines stating that steroids are highly likely to be effective and increase the likelihood of
recovery of facial nerve function in new-onset Bell palsy[4, 6]  Guidelines from the American Academy of Otolaryngology—
Head and Neck Surgery Foundation also recommend the use of corticosteroids.[36]

A variety of nonpharmacologic measures have been used to treat Bell palsy, including physical therapy (eg, facial exercises,
[47] neuromuscular retraining[48] ) and acupuncture.[49] No adverse effects of these treatments have been reported.
Reviews suggest that physical therapy may result in faster recovery and reduced sequelae, but further randomized,
controlled trials are needed to confirm any benefit.

Many patients with Bell palsy may have problems with eating or drinking, swallowing difficulty (overt or unrecognized), and
speech disturbances caused by muscle weakness and associated facial asymmetry. As such, occupational therapy and
speech therapy assessments are recommended; treatments may contribute to improvement in clarity of speech, reduce
risks associated with dysphagia, and decrease social embarassment or self-consciousness.

Pharmacologic Therapy
The most widely accepted treatment for Bell palsy is corticosteroid therapy. However, the use of steroids is still controversial
because most patients recover without treatment. Antiviral agents have also been studied in this setting, as have
combinations of the 2 types of drugs.

Corticosteroids

As previously mentioned, 2012 guidelines from the AAN state that steroids are highly likely to be effective and increase the
likelihood of recovery of facial nerve function in new-onset Bell palsy[4, 6]

Guidelines from the American Academy of Otolaryngology–Head and Neck Surgery Foundation (AAO-HNSF) were issued in
November 2013 that also support the AAN guidelines. The guidelines recommend use of corticosteroids within 72 hours
from the onset of symptoms. Antiviral agents (eg, acyclovir, valacyclovir) may be considered if a viral etiology is suspected,
but only in combination with corticosteroids.[50]

Many trials have been carried out to study the efficacy of prednisone in Bell palsy. In 1972, for example, Adour et al
conducted a large, controlled clinical trial that found that 89% of patients treated with prednisone had full recovery,
compared with 64% of patients treated with placebo.[51]

This trial and other early studies, however, showed conflicting results for steroid use in treating Bell palsy,[52] and they were
limited in their size.

However, 3 subsequent randomized, controlled trials showed significant improvement in outcomes when prednisolone was
started within 72 hours of symptom onset.[44, 45, 53] Based on these 3 studies, steroids should be strongly considered to
optimize outcomes. Once the decision to use steroids is made, the consensus is that this treatment should be started
immediately.

One of the 3 studies—a double-blind, randomized trial from Scotland involving 551 patients with Bell palsy who were
recruited within 72 hours of symptom onset—demonstrated that early treatment with prednisolone can significantly improve
the chances of complete recovery at 3 and 9 months.[44] In contrast, acyclovir given alone did not show any significant
difference in the rate of facial recovery compared with placebo, and there was no additional benefit from combining acyclovir
and prednisolone compared with prednisolone alone.

A larger double-blind, controlled trial showed that prednisolone significantly shortened the time to complete recovery, while
valacyclovir did not affect facial recovery compared with placebo.[45] Further analysis showed that patients treated with
prednisolone within 48 hours had significantly higher rates of complete recovery than did those who were not treated,
whereas no significant difference in recovery rate was seen between patients treated at 49–72 hours and untreated patients.
[54]

The recommended dose of prednisone for the treatment of Bell palsy is 1 mg/kg or 60 mg/day for 6 days, followed by a
taper, for a total of 10 days. Caution should be used in patients with any of the following:

Tuberculosis
 Immunocompromise

Pregnancy

Active infection

Sarcoidosis

Sepsis

Peptic ulcer disease

Diabetes mellitus

Renal or hepatic dysfunction

Malignant hypertension

High-dose steroids (>120 mg/day of prednisone) have been safely used to treat Bell palsy in patients with diabetes[55, 56] ;
however, optimal dosing has not been established. Caution should be used in these cases because of the risk of
hyperglycemia.

Antiviral agents

Evaluation of the use of antiviral medicines in Bell palsy has shown limited benefit from these drugs,[37, 57] with 3
randomized, controlled trials having demonstrated no benefit from them.[44, 45, 53] However, given the evidence
suggesting that a large percentage of Bell palsy cases may result from a viral infection,[21, 58] the use of antiviral agents
may be reasonable in certain situations.

The 2001 AAN practice perameter suggested that the use of acyclovir for the treatment of Bell palsy is only possibly
effective and that therapy with this agent alone is not effective in facial recovery.[46] According to the academy's 2012
guidelines, benefit from antivirals has not been established and, at best, is likely to be modest.[4, 6]

The Scottish study cited earlier suggested that prednisolone, and not acyclovir, is useful for facial recovery in Bell palsy.[44]

A Cochrane review found no significant benefit to the use of antivirals over placebo in reducing the rate of incomplete
recovery from Bell palsy.[59] This meta-analysis looked at 7 studies involving a total of 1987 patients treated between 1966
and 2008.

Acyclovir (Zovirax) is administered at a dosage of 400 mg orally 5 times daily for 10 days. Evidence supports HSV as a
major cause of Bell palsy; if varicella zoster virus (VZV) is suspected, higher doses may be needed (800 mg orally 5 times
daily).

Valacyclovir (Valtrex), taken orally in doses of 500 mg twice daily for 5 days, may be used instead of acyclovir. Although it is
more expensive, it may be associated with better compliance. If VZV is the cause of Bell palsy, higher doses may be
needed (1000 mg orally 3 times daily). Because of the increased cost and greater risk of side effects with higher doses,
however, valacyclovir cannot be routinely recommended for the treatment of Bell palsy at this time.

Corticosteroid-antiviral combinations
A prospective randomized trial with 101 patients comparing prednisone with acyclovir demonstrated that the prednisone
group had better clinical recovery.[60] In another prospective, randomized trial, with 99 patients, the combination of
prednisone and acyclovir was more effective than prednisone monotherapy in preventing nerve degeneration, as measured
by electrodiagnostic tests.[61]

A Japanese randomized, prospective study of 221 patients with Bell palsy showed significant improvement in facial function
using a combination of prednisone and valacyclovir therapy versus using prednisone alone. This improvement was noted in
patients who had severe to complete facial palsy.[58]

Quant et al conducted a meta-analysis of published studies from 1984 to January 2009 that showed no improved benefit
(with respect to degree of facial muscle recovery in patients with Bell palsy) from the use of corticosteroids plus antiviral
agents as compared with corticosteroid therapy alone.[62] Six trials (representing pooled data from 1145 patients) were
examined and included 574 patients who received corticosteroids alone and 571 patients who received corticosteroids and
antiviral agents.

Quant et al suggest that the routine use of antiviral agents is not warranted; however, future studies should improve
diagnostic efforts to identify herpes virus as a potential etiology. Additionally, newer antiviral agents may prove more
beneficial than older antiviral agents used in the studies analyzed to date.[62]

Contrary to the meta-analyses by Quant et al and Cochrane, de Almeida and colleagues found that antiviral agents, when
combined with corticosteroids, were associated with greater risk reduction of borderline significance than were
corticosteroids alone.[63] Their meta-analysis examined 18 trials involving a total of 2786 patients.
If antiviral agents are used, they should be initiated in conjunction with corticosteroids. Future studies will be needed to
determine which population will most benefit from antiviral therapy.

Local Treatment
It is universally accepted that eye care is imperative in Bell palsy. The patient’s eye is at risk for drying, corneal abrasion,
and corneal ulcers.

In most cases, topical ocular lubrication (with artificial tears during the day and lubricating ophthalmic ointment at night, or
occasionally ointment day and night) is sufficient to prevent the complications of corneal exposure.[7] Punctal plugs may be
helpful if dryness of the cornea is a persistent problem.

Occluding the eyelids by using tape or by applying a patch for 1 or 2 days may help to heal corneal erosions. Care must be
taken to prevent worsening the abrasion with the tape or patch by ensuring that the eyelid is securely closed. Clear plastic
wrap, cut to 8x10 cm and applied with generous amounts of ointment as a nighttime occlusive bandage, may be required.

External eyelid weights are available to improve mechanical blink. The weights are attached to the upper lid with an
adhesive and are available in different skin tones.

Lower-lid ectropion or droop can temporarily be helped by applying tape below the lid margin in the center of the lower lid;
the lid is pulled laterally and upward to anchor on the orbital rim.

Botulinum toxin can be injected transcutaneously or subconjunctivally at the upper border of the tarsus and aimed at the
levator muscle to produce complete ptosis and to protect the cornea.[2] Botulinum toxin may help in relaxing the facial
muscles after they have developed mass contraction, though the results are not as satisfying in patients with Bell palsy as in
patients with idiopathic hemifacial spasm.

Facial Nerve Decompression

Surgery to decompress the facial nerve is controversial. Patients with a poor prognosis, identified by facial nerve testing or
persistent paralysis, appear to benefit the most from surgical intervention. However, studies have been mixed as far as
benefit from surgery.[46]

Surgery may be considered in patients with complete Bell palsy that has not responded to medical therapy and with greater
than 90% axonal degeneration, as shown on facial nerve EMG within 3 weeks of the onset of paralysis.[64, 28] The problem
must be localized with MRI. The surgeon can then decide if the maxillary segment should be decompressed externally or if
the labyrinthine segment and geniculate ganglion should be decompressed with a middle fossa craniotomy.

A study in patients with greater than 90% degeneration demonstrated superior results in the cohort that underwent middle
fossa decompression, compared with the cohort that chose not to pursue surgical decompression. In the surgical group,
91% of cases exhibited a postoperative House-Brackmann grade of I or II. In the nonsurgical group, 58% of the patients had
a poor result, with a House-Brackmann grade of III or IV at 7 months. The best surgical results were obtained when the
procedure was done within 14 days after the onset of paralysis.[65]

Subocularis Oculi Fat Lift

The SOOF is deep to the orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim. An SOOF
lift is designed to lift and suspend the midfacial musculature. The procedure may also elevate the upper lip and the angle of
the mouth to improve facial symmetry.

Lateral tarsal strip procedure

An SOOF lift is commonly performed in conjunction with a lateral tarsal strip procedure to correct horizontal lower-lid laxity
and to improve apposition of the lid to the globe.[66] First, lateral canthotomy and cantholysis is performed. Then, the
anterior lamella is removed, and the lateral tarsal strip is shortened and attached to the periosteum at the lateral orbital rim.

Implants in Eyelid
Implantable devices have been used to restore dynamic lid closure in cases of severe, symptomatic lagophthalmos. These
procedures are best for patients with poor Bell phenomenon and decreased corneal sensation. Gold or platinum weights, a
weight-adjustable magnet, or palpebral springs can be inserted into the eyelids. Pretarsal gold-weight implantation is most
commonly performed.

The implants are inert and composed of 99.99% pure gold or platinum. Sizes range from 0.6–1.8 g. The weight allows the
upper eyelid to close with gravity when the levator palpebrae are relaxed. Therefore, patients must sleep with their head
slightly elevated.

The implants are easily removed if nerve function returns. Complications include migration of the implant, inflammation,
allergic reaction, and extrusion.

Tarsorrhaphy
Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together, increasing support of the precorneal
lake of tears and improving coverage of the eye during sleep. The procedure can be done in the office and is particularly
suitable for patients who are unable or unwilling to undergo other surgery. It can be completed as either a temporary or a
permanent measure. Permanent tarsorrhaphy is performed if nerve recovery is not expected.

Tarsorrhaphy can be performed laterally, centrally, or medially. The lateral procedure is the most common; however, it can
restrict the monocular temporal visual field. Central tarsorrhaphy offers good corneal protection, but it occludes vision and
can be cosmetically unacceptable. Medial or paracentral tarsorrhaphy is performed lateral to the lacrimal puncta and can
offer good lid closure without substantially affecting the visual field.

Muscle Transposition, Nerve Grafting, and Brow Lift

Transposition of temporalis

Transposition of the temporalis muscle can be used to reanimate the face and to provide lid closure by using the fifth cranial
nerve. Strips from the muscle and fascia are placed in the upper and lower lids as an encircling sling. Patients initiate
movement by chewing or clenching their teeth.

Facial nerve grafting or hypoglossal-facial nerve anastomosis

Reinnervation of the facial nerve by means of facial nerve grafting or hypoglossal-facial nerve anastomosis can be used in
cases of clinically significant permanent paralysis to help restore relatively normal function to the orbicularis oculi muscle or
eyelids.

Direct brow lift

Brow ptosis is repaired with a direct brow lift. Care should be taken in the presence of corneal decompensation because
lifting the brow can cause worsening of lagophthalmos, especially if lid closure is poor. A gold-weight implant can be placed
or lower-lid resuspension can be performed simultaneously to prevent this complication.

Consultations and Monitoring

Consultations

If the patient’s paralysis is not resolving or is progressing to complete paralysis, a thorough neurologic assessment and an
examination of the head, eyes, ears, nose, and throat should be performed to rule out neoplastic causes of facial nerve
palsy.

If the initial diagnostic impression based on the history and physical examination of the patient is not Bell palsy, then
consultation with a neurologist or otolaryngologist is needed. For example, consultation with an otolaryngologist should be
made for the patient who has facial palsy and pain and in whom the ear, nose, and throat examination does not show
auricular vesicles (as in Ramsay Hunt syndrome). These patients should be evaluated for malignancy or other structural
lesions of the facial nerve.

Consultation with a neurologist or otolaryngologist should also be sought if the paralysis persists for several months.

An evaluation by an otolaryngologist may be indicated for patients with a prolonged course, for the consideration of surgical
decompression of the facial nerve. Patients who report persistent dry eye or painful eye should be referred to an
ophthalmologist. An evaluation by a specialist in infectious disease may be indicated if results of laboratory studies are
positive for Lyme disease, syphilis, or HIV infection.
Monitoring
The patient should be monitored if the initial EMG shows that the function of the involved facial muscles is less than 25% of
the normal side’s facial muscle function. If the residual paralysis is severe, the patient should be referred for counseling.

Surgical Care
Surgical options for Bell Palsy

Surgical options for Bell palsy include the following:

Facial nerve decompression

Subocularis oculi fat (SOOF) lift

Implantable devices (eg, gold weights) placed into the eyelid

Tarsorrhaphy

Transposition of the temporalis muscle

Facial nerve grafting

Direct brow lift

Anecdotal evidence suggests that surgical repair by using a combination of procedures tailored to the patients’ clinical
findings works well for improving symptoms and exposure. Most patients who have had severe corneal exposure from
lagophthalmos with or without paralytic ectropion have received a combination of lateral tarsal strip placement, SOOF lift,
and gold-weight implantation. Patients without severe exposure have received a single procedure or combinations of
procedures.

Medication

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Agents used in cases of Bell palsy
include corticosteroids and antiviral agents. Early treatment with corticosteroids is the most widely accepted treatment, but it
remains controversial because most patients recover without treatment. The literature offers less support for the use of
antiviral agents in either monotherapy or combination therapy, although treatment with combinations of corticosteroids and
antiviral agents is somewhat better supported.

Corticosteroids

Class Summary
Prednisone can be used in the treatment of Bell palsy but has many adverse effects, including the following:

- Fluid retention

- Hypokalemia

- Myopathy

- Peptic ulcer

- Headache (pseudotumor)
- Menstrual irregularities

- Cataracts

- Glaucoma

- Manifestation of latent diabetes mellitus

In addition, signs of infection may be masked in patients taking prednisone. Physicians should use caution when using
prednisone in patients with the aforementioned conditions.

Prednisone (Deltasone, Orasone, Sterapred)

Prednisone, the standard drug used in Bell palsy, is a glucocorticoid that is absorbed readily from the gastrointestinal tract. It
has anti-inflammatory and immune-modulating effects, as well as profound and varied metabolic effects. For best outcome,
prednisone treatment should be initiated within 72 hours of symptom onset.

Antivirals

Class Summary
Acyclovir and valacyclovir have been administered in the treatment of Bell palsy in combination with prednisone or have
been used alone in patients who cannot take prednisone. The use of antivirals has proved most beneficial in patients with
severe to complete facial palsy.[58]

Acyclovir (Zovirax)
Acyclovir is a prodrug activated by phosphorylation, by way of virus-specific thymidine kinase (TK), that inhibits viral
replication. Herpes virus TK, but not host cell TK, uses acyclovir as a purine nucleoside, converting it into acyclovir
monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate form into diphosphate and
triphosphate analogues that inhibit viral DNA replication.

Acyclovir has an affinity for viral TK and, once phosphorylated, causes DNA chain termination when acted on by DNA
polymerase.

The drug inhibits the activity of HSV-1 and HSV-2. Patients experience less pain and faster resolution of cutaneous lesions
when acyclovir is used within 48 hours after rash onset. Acyclovir may also prevent recurrent outbreaks. Early initiation of
therapy is imperative.

Valacyclovir (Valtrex)
Valacyclovir is a prodrug that is rapidly converted to acyclovir. It is more expensive than acyclovir, but it has a more
convenient dosing regimen.

Questions & Answers

Overview

What is Bell palsy (idiopathic facial paralysis) (IFP)?

What are the signs and symptoms of Bell palsy (idiopathic facial paralysis) (IFP)?

Which exams are performed in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the House-Brackmann grading system for Bell palsy (idiopathic facial paralysis) (IFP)?

Which lab tests may be used in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the goals of treatment for Bell palsy (idiopathic facial paralysis) (IFP)?

What is included in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?
What are the surgical treatment options for Bell palsy (idiopathic facial paralysis) (IFP)?

What is Bell palsy (idiopathic facial paralysis) (IFP)?

What causes Bell palsy (idiopathic facial paralysis) (IFP)?

What is the prevalence of Bell palsy (idiopathic facial paralysis) (IFP)?

What is a key step in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the minimum diagnostic criteria for Bell palsy (idiopathic facial paralysis) (IFP)?

When is gadolinium-enhanced MRI indicated in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What should be the basis for treatment selection in Bell palsy (idiopathic facial paralysis) (IFP)?

Which treatment is indicated in most cases of Bell palsy (idiopathic facial paralysis) (IFP)?

What information should patients be given for prevention of corneal abrasions in Bell palsy (idiopathic facial paralysis)
(IFP)?

What are the roles of the fifth and seventh cranial nerves?

What is the anatomy of the facial nerve?

What is the role of the nervus intermedius in Bell palsy (idiopathic facial paralysis) (IFP)?

Which muscles are innervated by the facial nerve in Bell palsy (idiopathic facial paralysis) (IFP)?

What is the pathophysiology of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the pathophysiology of injury to the facial nerve in Bell palsy (idiopathic facial paralysis) (IFP)?

Is herpes simplex virus (HSV) an etiological factor in Bell palsy (idiopathic facial paralysis) (IFP)?

Can inactivated influenza vaccines cause Bell palsy (idiopathic facial paralysis) (IFP)?

What are possible infectious etiologies for Bell palsy (idiopathic facial paralysis) (IFP)?

Is there a genetic etiology of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the incidence of Bell palsy (idiopathic facial paralysis) (IFP) in the US?

What is the prevalence of bilateral simultaneous Bell palsy (idiopathic facial paralysis) (IFP)?

Which groups are at higher risk for Bell palsy (idiopathic facial paralysis) (IFP)?

Is there a gender predilection for Bell palsy (idiopathic facial paralysis) (IFP)?

Doe the incidence of Bell palsy (idiopathic facial paralysis) (IFP) vary among age groups?

What is the prognosis of Bell palsy (idiopathic facial paralysis) (IFP)?

How likely is complete recovery from Bell palsy (idiopathic facial paralysis) (IFP)?

Which factors increase the likelihood of a full recovery from Bell palsy (idiopathic facial paralysis) (IFP)?

Which factors are associated with a poor outcome in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Does the prognosis for complete recovery from Bell palsy (idiopathic facial paralysis) (IFP) vary among age groups?

How does the risk sequelae will develop in patients with Bell palsy (idiopathic facial paralysis) (IFP) increase over time?

How likely is recurrence of Bell palsy (idiopathic facial paralysis) (IFP)?

Which imaging studies are performed in patients with recurrent Bell palsy (idiopathic facial paralysis) (IFP)?

What is the long-term sequelae of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the manifestation of incomplete motor regeneration in Bell palsy (idiopathic facial paralysis) (IFP)?

What is the pathophysiology of incomplete sensory regeneration in Bell palsy (idiopathic facial paralysis) (IFP)?

What is synkinesis in Bell palsy (idiopathic facial paralysis) (IFP)?

Presentation

How is the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP) made?

What are the signs and symptoms of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the early signs and symptoms of Bell palsy (idiopathic facial paralysis) (IFP)?

Is the onset of Bell palsy (idiopathic facial paralysis) (IFP) sudden or gradual?

How is the facial paralysis of Bell palsy (idiopathic facial paralysis) (IFP) characterized?

How is the facial paralysis in Bell palsy (idiopathic facial paralysis) (IFP) differentiated from other disorders?

What does numbness on the side of the paralysis indicate in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What are the early ocular complications of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the late ocular complications of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the cause of tear flow in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Is posterior auricular pain a symptom of Bell palsy (idiopathic facial paralysis) (IFP)?

How common is hyperacusis in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Is early recovery of taste a positive prognostic factor in Bell palsy (idiopathic facial paralysis) (IFP)?

What are the possible causes of facial spasm in Bell palsy (idiopathic facial paralysis) (IFP)?

Which patients are at increased risk for facial spasms with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the presentation of synkinesis in Bell palsy (idiopathic facial paralysis) (IFP)?

Which symptoms of cranial neuropathy may occur in Bell palsy (idiopathic facial paralysis) (IFP)?

Which exams are performed when Bell palsy (idiopathic facial paralysis) (IFP) is suspected?

Which physical findings are consistent with a diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

When should an otologic cause be considered for Bell palsy (idiopathic facial paralysis) (IFP)?

How should the external auditory canal be examined for Bell palsy (idiopathic facial paralysis) (IFP)?

How is hyperacusis tested in Bell palsy (idiopathic facial paralysis) (IFP)?

Which ocular exam findings are consistent with a diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

Which oral exam findings are consistent with a diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of a neurologic exam in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the House-Brackmann grading system for Bell palsy (idiopathic facial paralysis) (IFP)

What are the characteristics of grade II Bell palsy (idiopathic facial paralysis) (IFP)?

What are the characteristics of grade III Bell palsy (idiopathic facial paralysis) (IFP)?

What are the characteristics of grade IV Bell palsy (idiopathic facial paralysis) (IFP)?

What are the characteristics of grade V Bell palsy (idiopathic facial paralysis) (IFP)?

What are the characteristics of grade VI Bell palsy (idiopathic facial paralysis) (IFP)?

What prognosis is given to each grade of Bell palsy (idiopathic facial paralysis) (IFP)?

DDX

What should be considered in the differential diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

How is seventh nerve neoplasm differentiated from Bell palsy (idiopathic facial paralysis) (IFP)?

How are tumors of the facial nerve or parotid gland differentiated from Bell palsy (idiopathic facial paralysis) (IFP)?

When should Lyme disease be considered in the differential diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?
When should Ramsay Hunt syndrome be considered in the differential diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

Which disorders should be considered in the differential diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

Which disorders should be considered in differential diagnosis of Bell palsy (idiopathic facial paralysis) (IFP) based on
history?

Which disorders should be considered in the differential diagnosis of bilateral simultaneous Bell palsy (idiopathic facial
paralysis) (IFP)?

What are the differential diagnoses for Bell Palsy?

Workup

When is testing indicated in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

Which tests are performed to identify or exclude other disorders in the diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

What is the role of serum titers for herpes simplex virus (HSV) in the diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

Which test is performed to exclude Wegener granulomatosis in Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of serum titers (IgM and IgA) for M pneumoniae in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of salivary flow testing in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

How is the Schirmer blotting test used in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of a nerve excitability test in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the AAO-HNSF recommendations for diagnostic imaging and routine lab testing for Bell palsy (idiopathic facial
paralysis) (IFP)?

What is the role of conduction testing and electromyography (EMG) in the diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

Which nerve conductions findings have prognostic significance in Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of electroneurography in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of electrodiagnostic testing in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

When is electrodiagnostic testing not recommended in Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of brainstem auditory evoked response (BAER) in the diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

When is brainstem auditory evoked response (BAER) indicated in the diagnosis of Bell palsy (idiopathic facial paralysis)
(IFP)?

When are audiography and auditory evoked potentials (AEPs) indicated in the diagnosis of Bell palsy (idiopathic facial
paralysis) (IFP)?

What is the role of blepharokymographic analysis in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the histologic findings of Bell palsy (idiopathic facial paralysis) (IFP)?

When are imaging studies indicated in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of MRI in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

When is gadolinium-enhanced MRI indicated in the diagnosis of Bell palsy (idiopathic facial paralysis) (IFP)?

Treatment

What are the goals of treatment for Bell palsy (idiopathic facial paralysis) (IFP)?

When is treatment considered for patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of the emergency department (ED) in treating patients with Bell palsy (idiopathic facial paralysis) (IFP)?
What are the AAN recommendations for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Which nonpharmacologic therapies may be beneficial in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the surgical options for treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the efficacy of surgical treatments for Bell palsy (idiopathic facial paralysis) (IFP)?

What is the most widely accepted treatment for Bell palsy (idiopathic facial paralysis) (IFP)?

Do the AAN and the AAO-HNSF both recommend corticosteroids for the treatment of Bell palsy (idiopathic facial paralysis)
(IFP)?

What is the efficacy of prednisone and prednisolone for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Is acyclovir (Zovirax) effective in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Is valacyclovir (Valtrex) effective for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the recommended dose of prednisone for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Are high-dose steroids safe for the treatment of Bell palsy (idiopathic facial paralysis) (IFP) in patients with diabetes?

What is the role of antiviral agents in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the AAN recommendation for the use of acyclovir (Zovirax) in the treatment of Bell palsy (idiopathic facial paralysis)
(IFP)?

Does acyclovir (Zovirax) reduce the rate of incomplete recovery from Bell palsy (idiopathic facial paralysis) (IFP)?

What is the dosage of acyclovir (Zovirax) for treating Bell palsy (idiopathic facial paralysis) (IFP)?

What is the dosage of valacyclovir (Valtrex) for treating Bell palsy (idiopathic facial paralysis) (IFP)?

What is the efficacy of combination therapy with prednisone and an antiviral agent for the treatment of Bell palsy (idiopathic
facial paralysis) (IFP)?

Are corticosteroids plus antiviral agents more effective than corticosteroid therapy alone for the treatment of Bell palsy
(idiopathic facial paralysis) (IFP)?

Should antiviral agents be used as monotherapy for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the options for eye care for patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Which treatment is required for corneal erosions in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of external eyelid weights in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Which measures help lower-lid ectropion or droop in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of botulinum toxin (BTX) in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

Which patients with Bell palsy (idiopathic facial paralysis) (IFP) may receive the most benefit from surgical intervention?

When is surgery indicated in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of middle fossa decompression in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What is a suborbicularis oculi fat (SOOF) lift for the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

How is a suborbicularis oculi fat lift (SOOF) performed in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

When are eyelid implants indicated in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What are the possible complications of eyelid implants in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of tarsorrhaphy in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

What is the role of transposition of the temporalis in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?

When is facial nerve grafting or hypoglossal-facial nerve anastomosis indicated in the treatment of Bell palsy (idiopathic
facial paralysis) (IFP)?

When is direct brow lift indicated in the treatment of Bell palsy (idiopathic facial paralysis) (IFP)?
Which tests should be performed if paralysis is not resolving or is progressing to complete paralysis in Bell palsy (idiopathic
facial paralysis) (IFP)?

When is a consultation with a neurologist or otolaryngologist indicated in patients with suspected Bell palsy (idiopathic facial
paralysis) (IFP)?

When is an evaluation by an otolaryngologist or an ophthalmologist indicated for patients with Bell palsy (idiopathic facial
paralysis) (IFP)?

When is monitoring indicated for patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Medications

What are the goals of pharmacotherapy in patients with Bell palsy (idiopathic facial paralysis) (IFP)?

Which medications in the drug class Corticosteroids are used in the treatment of Bell Palsy?

Which medications in the drug class Antivirals are used in the treatment of Bell Palsy?

Contributor Information and Disclosures

Author

Danette C Taylor, DO, MS, FACN Medical Director, Movement Disorders, Mercy Health St Mary's; Clinical Assistant
Professor, Department of Neurology and Ophthalmology, Michigan State University College of Osteopathic Medicine

Danette C Taylor, DO, MS, FACN is a member of the following medical societies: American Academy of Neurology,
American College of Osteopathic Neurologists and Psychiatrists, American Medical Association, American Osteopathic
Association, International Parkinson and Movement Disorder Society

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Acorda<br/>Received research grant from:
Neurocrine.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and
Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy
of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Bioserenity, Ceribell, Eisai,
Jazz, LivaNova, Neurelis, Neuropace, SK life science, Sunovion, Takeda, UCB<br/>Serve(d) as a speaker or a member of a
speakers bureau for: Aquestive, Bioserenity, Eisai, Jazz, LivaNova, Neurelis, SK life science, Stratus, Sunovion,
UCB<br/>Received research grant from: Cerevel Therapeutics, Ovid Therapeutics, Neuropace, Greenwich Jazz, SK Life
Science, Xenon Pharmaceuticals, UCB, Marinus, Neuroelectrics Corporation, Longboard, Janssen, Equilibre
Biopharmaceuticals.

Additional Contributors

Sally B Zachariah, MD Associate Professor, Department of Neurology, University of South Florida College of Medicine;
Director, Department of Neurology, Division of Strokes, Veteran Affairs Medical Center of Bay Pines

Sally B Zachariah, MD is a member of the following medical societies: American Academy of Neurology, American Heart
Association, American Society of Neuroimaging

Disclosure: Partner received none from none for none.

Acknowledgements

Edward Bessman, MD Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant
Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine,
American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Dominique Dorion, MD, MSc, FRCSC, FACS Vice Dean and Associate Dean of Resources, Professor of Surgery, Division of
Otolaryngology-Head and Neck Surgery, University of Sherbrooke Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Thomas R Hedges III, MD Director of Neuro-Ophthalmology, New England Eye Center; Professor, Departments of
Neurology and Ophthalmology, Tufts University School of Medicine

Thomas R Hedges III, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Ophthalmology, American Medical Association, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine,
University of Virginia Health Sciences Center

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American
Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Suzan Khoromi, MD Fellow, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Cranial Research,
National Institutes of Health

Suzan Khoromi, MD is a member of the following medical societies: American Academy of Neurology, American Pain
Society, and International Association for the Study of Pain

Disclosure: Nothing to disclose.

Milind J Kothari, DO Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of
Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association
of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association

Disclosure: Nothing to disclose.

Andrew W Lawton, MD Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center,
Baptist Health Medical Center

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas
Medical Society, and Southern Medical Association

Disclosure: Nothing to disclose.

Bruce Lo, MD Medical Director, Sentara Norfolk General Hospital; Assistant Professor, Assistant Program Director, Core
Academic Faculty, Department of Emergency Medicine, Eastern Virginia Medical School

Bruce Lo, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency
Medicine Residents Association, Medical Society of Virginia, Norfolk Academy of Medicine, and Society for Academic
Emergency Medicine

Disclosure: Nothing to disclose.

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

Kim Monnell, DO Neurology Consulting Staff, Department of Medicine, Bay Pines VA Medical Center

Kim Monnell, DO, is a member of the following medical societies: American Academy of Neurology and American
Osteopathic Association

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical
Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American
College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Reference Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center;
Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor,
Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular
Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology,
American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National
Multiple Sclerosis Society

Disclosure: Nothing to disclose.

B Viswanatha, MBBS, MS, DLO Professor of Otolaryngology (ENT), Chief of ENT III Unit, Sri Venkateshwara ENT Institute,
Victoria Hospital, Bangalore Medical College and Research Institute; PG and UG Examiner, Manipal University, India and
Annamalai University, India

B Viswanatha, MBBS, MS, DLO is a member of the following medical societies: Association of Otolaryngologists of India,
Indian Medical Association, and Indian Society of Otology

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American
Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Craig H Zalvan, MD Director of Laryngology, Assistant Professor of Otolaryngology, Head and Neck Surgery, Department of
Otorhinolaryngology-Head and Neck Surgery, ENT Faculty Practice

Craig H Zalvan, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck
Surgery, American Bronchoesophagological Association, American College of Surgeons, American Laryngological
Association, American Laryngological Rhinological and Otological Society, American Medical Association, Medical Society of
the State of New York, New York County Medical Society, Triological Society, and Voice Foundation

Disclosure: Nothing to disclose.

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