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 results 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 magnetic
resonance imaging (MRI) scans with facial nerve enhancement. [5]

The first portion of the facial canal, the labyrinthine segment, is 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.

The location of injury of the facial nerve in Bell palsy is peripheral to the nerves 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

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

In 1972, McCormick first suggested that HSV is responsible for idiopathic facial paralysis. [6] This was
based on the analogy that HSV was found in cold sores, and he hypothesized that HSV may remain
latent in the geniculate ganglion. Since then, autopsy studies have shown HSV in the geniculate ganglion
of patients with Bell palsy. Murakami et al, who performed polymerase chain reaction (PCR) testing for
HSV in the endoneural fluid of the facial nerve in 14 patients who underwent surgery for Bell palsy, found
that 11 of the 14 had HSV in the endoneural fluid. [7]

Assuming that HSV is the etiologic agent in Bell palsy is a plausible argument. If this is true, then the virus
is most likely to travel up the axons of the sensory nerves and reside in the ganglion cells. At times of
stress, the virus will reactivate, causing local damage to the myelin.

Additional support for a viral etiology was seen when intranasal inactivated influenza vaccine was strongly
linked to the development of Bell palsy, although whether another component of the vaccine caused the
paresis, which was then accompanied by a reactivation of herpes simplex virus, is not clear. [8, 9]

Besides HSV infection, possible etiologies for Bell palsy include other infections (eg, herpes zoster, Lyme
disease, syphilis, Epstein-Barr viral infection,cytomegalovirus, HIV, and mycoplasma); inflammation
alone; and microvascular disease (diabetes mellitus and hypertension).[10, 11, 12, 13, 14, 15, 16] Bell palsy may be
secondary to viral and/or autoimmune reactions causing 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.
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 (HEENT) must be
carried out in all patients with facial paralysis.

Focus attention on the voluntary movement of the upper part of the face on the affected side: in
supranuclear lesions such as a cortical stroke (upper motor neuron; above the facial nucleus in the pons),
the upper third of the face is spared 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.[19]

Initial inspection
Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the side
affected with the palsy. When the patient is asked to raise the eyebrows, the side of the forehead with the
palsy will remain flat. When the patient is asked to smile, the face becomes distorted and lateralizes 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 previous 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, infection, or trauma. The patient may
have decreased sensation to pinprick in the posterior auricular area. The patient who has paralysis of the
stapedius muscle will report hyperacusis. Tympanic membranes should be normal; the presence of
inflammation, vesicles, or other signs of infection raises the possibility of complicated otitis media.

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 inward on the affected side. This is known as Bell phenomenon and is
considered a normal response to eye closure.

The tear reflex may also be 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 as compared to the normal side.

Neurologic examination
 Careful neurologic examination is necessary in patients with facial paralysis. Neurologic examination
includes complete examination of all 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 electromyography (EMG) where appropriate.

Skin examination
Time must also be taken to examine the patients skin for signs of squamous cell carcinoma, which can
invade the facial nerve, and parotid gland disease.

History
The diagnosis of Bell palsy must be made on the basis of a thorough history and physical examination
and use of diagnostic testing when necessary. Bell palsy is a diagnosis of exclusion. Clinical features of
Bell palsy that may help distinguish it from other causes of facial paralysis include sudden onset of
unilateral facial paralysis, absence of signs and symptoms of central nervous system (CNS) disease, and
absence of signs and symptoms of ear or posterior fossa disease.

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 (see the image below).

Left-sided Bell palsy.

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.

No evidence of CNS disease is noted in patients with Bell palsy. In addition, no evidence of ear or
cerebellopontine angle disease is noted. Bell palsy may follow recent upper respiratory infection (URI).

Symptoms of Bell palsy include the following:

Acute onset of unilateral upper and lower facial paralysis (over a 48-h 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

Facial paralysis

The paralysis must include the forehead and lower aspect of the face. The patient may report inability to
close the eye or to smile on the affected side. He or she also may report increased saliva 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 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-Barr syndrome
(GBS), 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 due to
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 nasolabial fold
Corneal erosion, infection, and ulceration (rare but may occur)

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)
Rare, permanent, disfiguring facial paralysis

Two thirds of patients complain about tear flow.[1] This is due to 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. [1] 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, [1] 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.

Facial spasm

Facial spasm is a very rare complication of Bell palsy. It occurs as tonic contraction of one 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. It occurs most commonly in the fifth and sixth decades
of life, and sometimes the etiology is not found. The presence of progressive facial hemispasm with other
cranial nerve findings indicates a 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; 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
 The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI, as
follows[26, 27] :

Grade I - Normal facial function.

Grade II - Mild dysfunction. Slight weakness is noted on close inspection. The patients may have
a slight synkinesis. Normal symmetry and tone is noted at rest. Forehead motion is moderate to good;
complete eye closure is achieved with minimal effort; and slight mouth asymmetry is noted.
Grade III - Moderate dysfunction. 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 is noted at rest. Forehead movement is slight to moderate; complete eye closure is
achieved with effort; and a slightly weak mouth movement is noted with maximum effort.
Grade IV - Moderately severe dysfunction. 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, and an asymmetric mouth is noted with maximal effort.
Grade V - Severe dysfunction. Only a barely perceptible motion is noted. Asymmetry is noted at
rest. No forehead motion is observed. Eye closure is incomplete, and mouth movement is only slight.
Grade VI - Total paralysis. Gross asymmetry is noted. No movement is noted.
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 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 initial visit of the patient

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 nerve (facial nerve) damage may result in further deterioration of the patients
condition. For example, if other cranial nerve, motor, or sensory symptoms were present, then treatable or
preventable nervous system diseases should be sought (eg, stroke, Guillain-Barr syndrome [GBS],
basilar meningitis, or 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, 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 the patient reports sudden onset of hearing loss and severe pain with the onset of facial paralysis,
Ramsay Hunt syndrome must be considered.

Other problems to be considered include the following:

Acoustic neuroma and other cerebellopontine angle lesions

Acute or chronic otitis media
Amyloidosis
 Aneurysm of vertebral, basilar artery, or carotid arteries
Autoimmune syndromes
Botulism
Carcinomatosis
Carotid disease and stroke, including embolic phenomenon
Cholesteatoma of the middle ear
Congenital malformation
Diabetes mellitus
Facial nerve schwannoma
Geniculate ganglion infection
Glomus tumors
Guillain-Barr syndrome
Herpes zoster
HIV
Leukemia/lymphoma
Leukemic meningitis
Lyme disease
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
Pregnancy (especially third trimester)
Ramsay Hunt syndrome
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
Differential Diagnoses
Anterior Circulation Stroke
Benign Skull Tumors
Brainstem Gliomas
Cerebral Aneurysms
Intracranial Hemorrhage
Meningioma
Meningococcal Meningitis
Neurosyphilis
Sarcoidosis
Tick-Borne Diseases, Lyme
Tuberculous Meningitis
In many cases, the history and physical examination lead to the diagnosis of Bell palsy. If the clinical
findings are doubtful or if paralysis lasts longer than 6-8 weeks, further investigations should be
considered.[2]

No specific diagnostic tests are available for Bell palsy, though the following may be useful:

Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or
fluorescent treponemal antibody absorption (FTA-ABS) test
Human immunodeficiency virus (HIV) screening by means of enzyme-linked immunosorbent
assay (ELISA) and/or Western blot
Complete blood cell count
Determination of the erythrocyte sedimentation rate
Thyroid function studies
Serum glucose level
Cerebrospinal fluid analysis
If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging is not
necessary. Imaging is not required 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.

Blood glucose or hemoglobin A1c levels may be obtained to determine if the patient has undiagnosed
diabetes.

Serum titers for herpes simplex virus may be obtained, but this 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 many cases, the history and physical examination lead to the diagnosis of Bell palsy. If the clinical
findings are doubtful or if paralysis lasts longer than 6-8 weeks, further investigations should be
considered.[2]

No specific diagnostic tests are available for Bell palsy, though the following may be useful:

Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or
fluorescent treponemal antibody absorption (FTA-ABS) test
Human immunodeficiency virus (HIV) screening by means of enzyme-linked immunosorbent
assay (ELISA) and/or Western blot
Complete blood cell count
Determination of the erythrocyte sedimentation rate
Thyroid function studies
Serum glucose level
Cerebrospinal fluid analysis
If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging is not
necessary. Imaging is not required 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.

Blood glucose or hemoglobin A1c levels may be obtained to determine if the patient has undiagnosed
diabetes.

Serum titers for herpes simplex virus may be obtained, but this 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.

Radiological evaluation by computed tomographic (CT) scanning and 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. Magnetic resonance imaging (MRI) of patients with Bell palsy may show enhancement of the
seventh cranial nerve (facial nerve) at, or near, the geniculate ganglion. However, if the paralysis
progresses over weeks, the possibility is high of 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. [29]

Little correlation between the enhancement of the facial nerve and the clinical outcome has been noted.
However, a recent analysis of early MRIs with gadolinium of the intratemporal facial nerve demonstrated
the ability to predict the long-term outcome of the facial paralysis; these findings (increased signal
intensity in the internal auditory canal after administration of gadolinium) correlated favorably with those of
electrodiagnostic testing. Thus, MRI is useful as a means of excluding other pathologies as the cause of
paralysis. MRI is preferred for imaging the cerebellopontine angle.

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.
 Many issues must be addressed in treating patients with Bell palsy. The most important consideration is
the onset of symptoms. Treatment may be considered for patients who have the onset of paralysis within
1-4 days of the initial office visit.

Patients with Bell palsy frequently present to the 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 treatment of Bell palsy. Any
recommendation on facial decompression surgery had insufficient evidence.

A variety of nonpharmacologic measures have been used to treat Bell palsy, including physical therapy
(eg, facial exercises[34] and neuromuscular retraining[35]) and acupuncture.[36] 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.

The most widely accepted treatment for Bell palsy is corticosteroids. 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

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. [37]

This study and other early studies have shown conflicting results using steroids in treating Bell palsy,
[38]
and they have been limited in their size. However, 3 recent randomized, controlled trials showed
significant improvement in outcomes when prednisolone was started within 72 hours of symptom onset. [3, 4,
39]
Based on these 3 studies, steroids should be strongly considered to optimize outcomes. Once the
decision to use steroids is made, the consensus is to start immediately.

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

A larger double-blind, controlled trial showed that prednisolone significantly shortened the time to
complete recovery, whereas valacyclovir did not affect facial recovery compared to placebo. [4]

The recommended dose of prednisone for the treatment of Bell palsy is 1 mg/kg or 60 mg/d for 6 days,
followed by a taper, for a total of 10 days. Caution should be used in patients with tuberculosis,
immunocompromise, pregnancy, an active infection, sarcoidosis, sepsis, peptic ulcer disease, diabetes
mellitus, renal or hepatic dysfunction, or malignant hypertension.
High-dose steroids (>120 mg/d of prednisone) have been safely used to treat Bell palsy in patients with
diabetes[40, 41] ; however, optimal dosing has not been established. Caution should be given in these cases
due to the risk of hyperglycemia.

Antiviral agents

Evidence evaluating the efficacy of antiviral medicines in Bell palsy has shown limited benefit, [42, 29] with 3
recent randomized controlled trials showing no benefit.[3, 4, 39] However, there is evidence to suggest a large
percentage of Bell palsy cases may result from a viral infection. [16, 43] Therefore, antiviral agents may be
reasonable in certain situations.

The AAN guidelines suggest that the use of acyclovir for the treatment of Bell palsy is only possibly
effective and that this agent alone is not effective in facial recovery. The Scottish study cited earlier
suggested that prednisolone, and not acyclovir, is useful for facial recovery in Bell palsy.[3]

A Cochrane review analyzed 7 studies (1987 patients) from 1966-2008 looking at the efficacy of antivirals
in the complete recovery from Bell palsy. In their review, antivirals showed no significant benefit over
placebo in the rate of incomplete recovery (relative risk [RR], 0.88; 95% confidence interval [CI], 0.65-
1.18).[44]

Acyclovir (Zovirax) is administered at a dosage of 400 mg orally 5 times a day for 10 days. Evidence
supports herpes simplex virus (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 a day).

Valacyclovir (Valtrex), 500 mg orally twice a day 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 a day). Because of increased cost and increased risk of
side effects with higher doses, valacyclovir cannot be routinely recommended at this time.

Corticosteroid-antiviral combinations

A prospective randomized trial with 101 patients comparing prednisone and acyclovir demonstrated that
the prednisone group had a better clinical recovery.[45]In another prospective, randomized trial with 99
patients, prednisone monotherapy was compared with the combination of prednisone and acyclovir. This
study demonstrated that combination therapy was more effective in preventing nerve degeneration as
measured by electrodiagnostic tests.[46]

A Japanese randomized, prospective study of 221 patients with Bell palsy showed significant
improvement in facial function using both prednisone and valacyclovir therapy as compared with those
who used prednisone alone. This improvement was noted in those who had severe to complete facial
palsy.[12]

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) with
corticosteroids plus antivirals as compared to corticosteroids alone (odds ratio 1.50; 95% confidence
interval, 0.83-2.69).[47] Six trials (representing pooled data of 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 antivirals 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. [47]

Contrary to the Quant et al and Cochrane meta-analyses, de Almeida et al found that antiviral agents,
when combined with corticosteroids, were associated with greater risk reduction of borderline significance
than were corticosteroids alone (relative risk, 0.75; 95% CI, 0.56-1.00). [48] Their meta-analysis examined
18 trials including 2786 patients. If antivirals are to be initiated, they should be done so in conjunction with
corticosteroids. Future studies will be needed to determine which population will most benefit from
antiviral therapy.

Whether to use prednisone alone or combination therapy is left to the discretion of the treating physician

It is universally accepted that eye care is imperative in Bell palsy. The patients 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.[49] 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 a patch by ensuring that
the eyelid is securely closed. Clear plastic wrap, cut to 8 X 10 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; pull the lid 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. [26] 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.

Surgical options include facial nerve decompression, subocularis oculi fat (SOOF) lift, implantable devices
placed into the eyelid, tarsorrhaphy, transposition of the temporalis muscle, facial nerve grafting, and
direct brow lift.

In the authors experience, 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 due to lagophthalmos with or without paralytic ectropion 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.
Decompression of facial nerve

Surgery to decompress the facial nerve is controversial when performed 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 electromyography (EMG) within 3 weeks of the onset of paralysis. [50, 19] The problem
must be localized with magnetic resonance imaging (MRI); then, the surgeon can 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.

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.[51]

A study compared a cohort of patients with degeneration greater than 90% who underwent middle-fossa
decompression with a cohort of similar patients who chose not to pursue surgical decompression. The
surgical group exhibited a House-Brackmann grade I or II in 91% of the cases. The nonsurgical group had
a poor result in 58% of the patients, with a House-Brackmann grade III or IV at 7 months. This study also
demonstrated that best results were obtained if the decompression was attempted within 14 days after
the onset of paralysis.[52]

Subocularis oculi fat lift with lateral tarsal strip procedure

The SOOF lift is designed to lift and suspend the midfacial musculature. The SOOF is deep to the
orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim. Lifting the SOOF
may also elevate the upper lip and the angle of the mouth to improve facial symmetry. A SOOF lift is
commonly done in conjunction with a lateral tarsal strip procedure to tighten the eyelid. [53]

A lateral tarsal strip procedure is performed to correct horizontal lower-lid laxity and to improve apposition
of the lid to the globe. 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 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 inert and composed of 99.99% pure gold or platinum. Sizes range from 0.6-1.8 g. They
are easily removed if nerve function returns. Complications include migration of the implant, inflammation,
allergic reaction, or extrusion.

Tarsorrhaphy
Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together to improve support of
the precorneal lake of tears and to improve 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 done if
nerve recovery is not expected.

Tarsorrhaphy can be performed laterally, centrally, or medially. The lateral procedure is 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.

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.

Prednisone can be used but has many adverse effects, including fluid retention, hypokalemia, myopathy,
peptic ulcer, headache (pseudotumor), menstrual irregularities, cataracts, glaucoma, and manifestation of
latent diabetes mellitus. Signs of infection may also be masked in patients taking prednisone. Physicians
should use caution when using prednisone in patients with the aforementioned conditions.
View full drug information
Prednisone (Deltasone, Orasone, Sterapred)
Prednisone 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