Karen Kölln • Jeffrey LaCour • Harold C.

Pillsbury III 131

Bell’s Palsy

Introduction
The muscles of facial expression are intimately involved in our ability to communicate emotions with those
around us. Acute unilateral facial palsy, also known as Bell’s palsy after Sir Charles Bell who described the
disorder in 1821, is the most common cause of facial weakness and the most common cranial neuropathy.
Bell’s palsy has traditionally been a diagnosis of exclusion and attributed to idiopathic origins; however, recent
investigations have implicated herpetic viral infection with associated inflammation as the source of the paresis
or paralysis. Bell’s palsy is the most common cause of unilateral lower motor neuron facial palsy, accounting
for 60% to 75% of all peripheral facial nerve palsies. Bell’s palsy shows no gender or seasonal predilection and
occurs with an incidence of about 20 to 30 per 100,000 population. As many as 71% of untreated patients
recover completely, whereas 84% achieve near-normal facial function. Poor prognostic indicators for return of
function include older age, hypertension, impairment of taste, pain other than in the ear, and complete facial
nerve palsy.

Etiology and Pathogenesis the primary cause of acute unilateral facial palsy. Nucleic
acids from HSV have been found to be present in the
An understanding of the anatomy of the facial nerve is
geniculate ganglion of the facial nerve, and HSV DNA has
critical to the understanding of Bell’s palsy. The facial
been detected in the endoneural fluid of the facial nerve in
nerve primarily carries fibers for motor control to the
patients with acute paralysis undergoing surgical decom-
muscles of facial expression, the stapedius muscle, and the
pression. An animal model of facial paralysis has been
posterior belly of the digastric muscle. In addition to these
developed by inoculating mouse tongues or auricles with
motor fibers, sensory branches and parasympathetic fibers
HSV. It is hypothesized that primary HSV may result in
course within the facial nerve. Taste sensation from the
the entrapment of the virus within the geniculate ganglion,
anterior two thirds of the tongue joins the facial nerve
and its reactivation causes the inflammatory process
through the chorda tympani branch. Parasympathetic
causing the seventh nerve neuropathy. Another herpes
fibers reach the lacrimal and submandibular glands through
virus, varicella-zoster virus, is known to be associated with
the greater superficial petrosal nerve and the chorda
acute facial nerve palsy in the setting of Ramsey Hunt’s
tympani, respectively. Loss of nerve conduction in the
syndrome.
facial nerve can potentially disrupt all these fibers
(Fig. 131-1).
The facial nerve travels through the temporal bone
Clinical Presentation
housed in a bony canal (fallopian canal), entering the tem-
poral bone at the internal auditory canal and exiting from The onset of Bell’s palsy is typically acute, with the pro-
the stylomastoid foramen. The narrowest segment of the gression of weakness in several hours to overnight (Fig.
bony canal is located at the lateral end of the internal audi- 131-2). Bell’s palsy may present as a complete hemifacial
tory canal. Acute unilateral facial palsy has been postulated paralysis or, more commonly, as an incomplete palsy that
to arise from an inflammatory process causing the facial may or may not progress to complete paralysis over several
nerve to swell within the bony canal surrounding it. days. Many patients describe pain behind the affected ear
Although still a controversial topic, a large body of evi- as a prodrome and a sensation of numbness on the affected
dence implicates herpes simplex virus (HSV) infection as side of the face, although this sensation appears to be

923
924 SECTION XIII  Neurologic Disorders

Figure 131-1 Facial (VII) Nerve.

Greater petrosal n.
Motor fibers Deep petrosal n.
Sensory fibers
Lesser petrosal n. Carotid plexus (on internal carotid a.)
Parasympathetic fibers
Geniculate ganglion Motor nucleus of facial n.
Sympathetic fibers Nerve of pterygoid canal
Facial (VII) nerve
Otic ganglion Internal acoustic
Pterygopalatine ganglion
meatus
Facial muscles Nervus intermedius
(of facial n.)
Occipitofrontalis m. (frontal belly) Motor nucleus of
Orbicularis oculi m. facial n.
Corrugator supercilii m. Superior salivatory
Zygomaticus major m. nucleus
Zygomaticus minor m.
Temporal branc
Depressor supercilii m.
Procerus m. Solitary tract
nucleus
Levator labii superioris Occipito-
alaeque nasi m.
h es

frontalis m.
Nasalis m. (occipital belly)

Levator labii superioris m. Occipital branch

of posterior
auricular n.
Levator anguli oris m. Zygomatic branc
hes Branches to
2/3tongue auricular muscles
e ant.
Depressor septi m. Tast Buccal
branches Posterior
auricular n.
h

Orbicularis oris m.
an c
l br
i ca

Depressor anguli oris m.

Cerv

Depressor labii inferioris m.

Mentalis m.
Risorius m. Nerve to stapedius m.
Buccinator m. Stylomastoid foramen
Platysma Tympanic plexus
Tympanic n.
Sublingual gland
Submandibular gland Glossopharyngeal (IX) n.
Submandibular ganglion Posterior belly of digastric m.
Lingual n. Stylohyoid m.
Chorda tympani Caroticotympanic n.

secondary to the lack of motion. Dysgeusia (disturbed
taste), hyperacusis (sounds are too loud in the affected ear),
and difficulty drinking are also common complaints.
Physical examination reveals unilateral paresis or paral-
ysis of the muscles of facial expression. An important dis-
tinction is that the unilateral paresis or paralysis involves
both the upper and lower face on the affected side (lower
motor neuron lesion pattern). When severe, the affected
hemiface shows no voluntary movements and obvious
asymmetry at rest. The degree of facial paralysis is often
quantified using the House-Brackmann scale, which incor-
porates gross facial appearance, symmetry at rest, and sym-
metry of the forehead, eye, and mouth in motion (Table
131-1). The skin surrounding the affected side of the
mouth is displaced to the opposite side with smiling, and
often the affected eye cannot be completely closed with
maximal effort. When attempts are made to close the
affected eye, the globe is seen to roll upward into the orbit,
revealing sclera (Bell’s phenomenon).
Thorough history taking and a complete physical exam-
ination with cranial nerve testing is critical to establishing
the diagnosis. The parotid glands must be palpated for
 131  Bell’s Palsy 925

Figure 131-2 Bell’s Palsy.

Course and distribution of facial (VII) nerve

Facial
Occipito-
Orbicularis oculi m. (VII) n.
frontalis m.
Acoustic
Lacrimal gland (VIII) n.
Corrugator Pons
super- Pterygopalatine
Geniculate Sites of lesions and their manifestations
cilii m. ganglion
ganglion
1. Intracranial and/or internal auditory meatus
Greater
All symptoms of 2, 3, and 4, plus deafness
Temporal petrosal n.
2 1 due to involvement of eighth cranial nerve
branch
2. Geniculate ganglion
Stapedius m. All symptoms of 3 and 4, plus pain behind ear.
3 Herpes of tympanum and of external auditory
Tympanum meatus may occur
Stylomas-
Lingual n. toid
3. Facial canal
foramen
All symptoms of 4, plus loss of taste in anterior
tongue and decreased salivation on affected
Posterior
Tongue side due to chorda tympani involvement.
auricu-
Hyperacusis due to effect on nerve branch to
lar n.
4 stapedius muscle
Chorda
tympani 4. Below sytlomastoid foramen (parotid gland
tumor, trauma)
Parotid gland
Facial paralysis (mouth draws to opposite side;
Buccal branch on affected side, patient unable to close eye or
Marginal wrinkle forehead; food collects between teeth
mandibular branch and cheek due to paralysis or buccinator muscle)
Orbicularis Cervical branch
oris m.
Zygomatic branch
Levator Sublingual Platysma m.
anguli oris m. gland
Submandibular ganglion
Depressor Risorius m.
Submandibular gland
anguli oris m.
Buccinator m.

Hyperacusis: patient
holds phone away
In patient's attempts to smile or bare
from ear because
teeth, mouth draws to unaffected side.
of painful sensitivity
Patient cannot wink, close eye,
to sound
or wrinkle forehead on affected side

masses, and the otoscopic examination must establish clear
tympanic membranes with no evidence of infection or
lesions. Examination of the tongue will often reveal inflam-
mation of the fungiform papillae on the affected side. Lac-
rimation may be decreased in the affected eye. Audiometric
assessment will often reveal stapedial muscle dysfunction
and hyperacusis on the affected side.
Other etiologies of facial nerve palsy should be explored
in the following scenarios: a history of recurrent facial
palsy, other cranial nerve involvement, facial twitching, no
recovery after 3 to 6 weeks or only partial recovery after 3
to 6 months, and a slowly progressive palsy lasting longer
than 3 weeks.
Differential Diagnosis
Bell’s palsy is a diagnosis of exclusion. The reported inci-
dence of misdiagnosing facial palsy as Bell’s palsy is between
13% and 20%. The differential diagnosis for unilateral
facial palsy must include infectious causes, neoplasms,
trauma, inflammatory processes, and metabolic dis-
orders; symptoms also may result from a central insult,
such as cerebrovascular accident or multiple sclerosis
(Table 131-2).
Infectious etiologies include Lyme disease, Ramsey
Hunt’s syndrome (varicella-zoster), HIV, and otitis media
or mastoiditis. Varicella-zoster virus facial paralysis
926 SECTION XIII  Neurologic Disorders

Table 131-1 House-Brackmann Facial Nerve Grading System

Grade Description Findings

I Normal Normal facial function in all areas

II Mild dysfunction Gross: slight weakness on close inspection, very slight synkinesis
At rest: normal symmetry and tone
In motion: forehead—moderate to good function; eye—complete closure with
minimal effort; mouth—slight asymmetry
III Moderate dysfunction Gross: obvious but not disfiguring difference between sides, noticeable but
not severe synkinesis
At rest: normal symmetry and tone
In motion: forehead—slight to moderate movement; eye—complete closure
with effort; mouth—slightly weak with maximal effort
IV Moderately severe dysfunction Gross: obvious weakness or disfiguring asymmetry
At rest: normal symmetry and tone
In motion: forehead—no movement; eye—incomplete closure; mouth—
asymmetrical with maximal effort
V Severe dysfunction Gross: barely perceptible motion
At rest: asymmetry
In motion: forehead—no movement; eye—incomplete closure; mouth—slight
movement
VI Total paralysis No movement

Table 131-2 Differential Diagnosis of Peripheral Facial Palsy

Category Signs and Symptoms

Infectious
Lyme disease History of tick bite, other neurologic symptoms, and constitutional
symptoms (asthenia, anorexia, headache)
Ramsey Hunt’s syndrome (varicella zoster) Painful vesicular lesions on external ear or within ear canal; occasional
lesions on soft palate
Human immunodeficiency virus (HIV) History of HIV
Otitis media, mastoiditis Evidence of middle ear purulence on otoscopy; postauricular erythema,
edema
Neoplastic
Middle ear tumor Lesion seen on otoscopy
Parotid tumor Mass palpated on physical examination
Cerebellopontine angle tumor (acoustic neuroma) Sensorineural hearing loss, vertigo, facial hypesthesia (impingement of
cranial nerve V)
Cholesteatoma History of chronic draining ear, otoscopic examination with squamous
debris
Traumatic
Temporal bone fracture History of trauma, possible sensorineural hearing loss, computed
tomography scan demonstrating fracture along course of facial nerve
Middle ear trauma History of penetrating trauma to middle ear, tympanic membrane
perforation
Inflammatory
Sjögren’s syndrome Sicca complex—dryness of mucous membranes of eyes and mouth
Amyloidosis Possible proteinuria, hepatomegaly, heart failure, arrhythmia
Sarcoidosis History with pulmonary symptoms
Guillain-Barré syndrome Caudal to cranial progression of weakness, tingling starting in lower
extremities
Metabolic
Diabetes mellitus History of diabetes; visual or renal problems
Preeclampsia Pregnant patient with hypertension and proteinuria
Central Insult
Multiple sclerosis Visual changes, vertigo, weakness or numbness
Cerebral vascular accident Hemiparesis, hemisensory loss, hemineglect with sparing of the
forehead on the affected side

(Ramsey Hunt’s syndrome) is the second most common
cause of hemifacial palsy. Typical varicella-zoster infection
is associated with skin blistering or blebs involving the
tympanic membrane, external auditory canal, or post-
auricular skin. Often these patients complain of severe pain
around the affected auricle and may experience sensori-
neural hearing loss. The severity and prognosis for recov-
ery of facial function is much graver in varicella-zoster
infection.
Other infectious sources of unilateral facial palsy merit
consideration. Acute otitis media may present as unilateral
facial palsy. This is believed to be secondary to inflamma-
tion at natural dehiscences of the fallopian canal through
the middle ear cavity. Suppurative or coalescent mastoid-
itis may alter neural conduction through the facial nerve
in its vertical segment in the temporal bone. Interestingly,
the most common head and neck manifestation of Lyme
disease is facial nerve paralysis. HIV-associated facial nerve
paralysis has also been reported.
Parotid gland neoplasms may present with hemifacial
paresis or paralysis, as can paragangliomas involving the
middle ear cavity. Temporal bone malignancy, primary or
metastatic, may also present in a similar fashion. Choles-
teatoma may also erode the fallopian canal, causing paresis
of the facial nerve. A cerebellopontine angle tumor
such as an acoustic neuroma may present with facial weak-
ness as well as with hearing loss, vertigo, and facial
hypesthesia.
Traumatic injury to the facial nerve, either in its intra-
temporal course or after exiting the stylomastoid foramen,
must be excluded. This would include recent surgeries
involving the parotid gland, middle ear, or internal audi-
tory canal as well as trauma violating the tympanic mem-
brane or resulting in a temporal bone fracture.
Inflammatory causes of facial palsy include Sjögren’s
syndrome, amyloidosis, sarcoidosis, and Guillain-Barré
syndrome. Presentation of a patient with bilateral palsies
should raise suspicion of these diagnoses.
Patients with metabolic disorders such as diabetes mel-
litus and preeclampsia have been noted to have a higher
incidence of facial palsy of various etiologies.
Central nervous system insults such as cerebrovascular
accident and multiple sclerosis may present with facial
paralysis. These lesions typically present as an upper motor
neuron lesion pattern without involvement of the upper
face musculature on the affected side.
Diagnostic Approach
An imaging study is indicated if there is no improvement
in facial paresis after one month, hearing loss, multiple
cranial neuropathies, or if there signs of limb paresis or
sensory loss. A CT of the temporal bones is indicated if
trauma is suspected or if an intratemporal facial nerve
tumor is suspected. Magnetic resonance imaging with
gadolinium is the test of choice to rule out a cerebellopon-
131  Bell’s Palsy 927
tine angle tumor, multiple sclerosis, or other structural
lesions. An audiogram with stapedial reflexes should be
obtained if hearing loss is reported to help rule out an
acoustic neuroma.
If a patient has evidence of systemic symptoms such as
fever, weight loss, rash, or a progressive facial weakness
without improvement, a complete blood count with dif-
ferential helps rule out lymphoreticular malignancy. Blood
glucose (or hemoglobin A1C) should be ordered if diabetes
is suspected. Serum antibodies against varicella zoster and
Borrelia burgdorferi should be obtained if these entities
are high on the differential list. Serum calcium and
angiotensin-converting enzyme levels should be ordered if
sarcoidosis is suspected.
Management and Therapy
The management of acute unilateral facial palsy is directed
toward decreasing presumed inflammation influencing the
facial nerve, preventing potential complications, and estab-
lishing prognosis for recovery.
Optimum Treatment
Optimum treatment for Bell’s palsy includes a regimen of
corticosteroids equivalent to 1 mg/kg prednisone daily for
1 week, tapering to off over a second week of therapy. This
has been demonstrated to improve return of facial func-
tion. Antiviral therapy has also been shown to improve
outcome when given in conjunction with corticosteroids,
and a typical dose equivalent to 1000 mg of acyclovir daily
is often used for 7 to 10 days. Early treatment (within 3
days of onset) is necessary for acyclovir-prednisone therapy
to have the greatest effects.
Meticulous eye protection and care is critical in patients
unable to fully close the affected eye (House-Brackmann
grade IV or higher). This should consist of the liberal use
of artificial tears and lubricating ointment multiple times
daily until the protective function of eye closing returns.
In addition, the affected eye should be taped or patched in
the closed position before sleeping to avoid inadvertent
damage or desiccation to the exposed cornea during sleep.
Rarely, a tarsorrhaphy may be required to prevent eye
damage.
Electrical testing can be used as an aid to predict prog-
nosis in acute facial paralysis. Unlike many other nerves,
the facial nerve cannot easily be stimulated proximal to the
presumed site of inflammation or edema. Instead, stimula-
tion of the trunk of the facial nerve as it exits the stylomas-
toid foramen with measurement of compound muscle
action potential amplitude at the muscles of facial expres-
sion has been shown to be helpful in establishing progno-
sis. This test, called electroneurography (ENOG), is only
beneficial between days 3 and 21 after complete loss of
voluntary movements. In patients with more than 90%
degeneration on ENOG compared with the contralateral
928 SECTION XIII  Neurologic Disorders
side and no evidence of motor unit potentials on electro-
myography by day 14 of paralysis, a poorer prognosis for
return of facial function can be given and surgical decom-
pression considered.
The role of surgical decompression of the facial nerve
in acute paralysis has generated much debate. Surgical
decompression undertaken in carefully selected patients
with clearly defined electrical findings has been shown to
improve final outcome of facial nerve function. The
approach for this surgery involves a middle cranial fossa
craniotomy with selected decompression of the perigenic-
ulate region of the facial nerve by an experienced otolar-
yngologist or neurosurgeon. This directed decompression
is focused on the regions of the facial nerve with the most
restrictive bony canal anatomy and has been shown to
improve final House-Brackmann grade of facial nerve
function.
Avoiding Treatment Errors
The best way to avoid treatment errors is to be thorough
in the evaluation of patients with facial palsy, considering
all possible etiologies before placing the patient on an
acyclovir-prednisone regimen. A serious medical condition
or tumor may otherwise be missed.
Recovery
Generally, recovery from paresis or paralysis of the facial
nerve is satisfactory. For patients with poor recovery 3 to
6 months after onset of weakness and no other discover-
able cause, several surgical procedures may help restore
function. For patients with poor recovery of eye-closing
function, upper eyelid gold weight implantation may be
considered to enhance corneal protection. For patients
with poor recovery of the muscles of facial expression, a
variety of reanimation and reinnervation operations have
been developed in recent years.
Future Directions
Although the current evidence linking HSV infection to
Bell’s palsy is strong, our understanding of when and why
the latent infection causes symptoms is poorly understood.
In order to demonstrate that the reactivation of HSV virus
from its latent to lytic state, a study performing reverse
transcriptase polymerase chain reaction aimed at detecting
lytic state-specific messenger ribonucleic acids should be
performed. A recent article has also reported facial palsy
following the administration of the inactivated intranasal
influenza vaccine, indicating that other viruses can be
pathogenic.
Additional Resources
American Academy of Otolaryngology—Head and Neck Surgery. Avail-
able at: http://www.entnet.org. Click on Bell’s Palsy. Accessed October
9, 2006.
This site provides a basic overview of the facial nerve anatomy and function.
It offers a one-page summary of diagnosis, treatment, and prognosis.
Bell’s Palsy Information Site. Available at: http://www.bellspalsy.ws/.
Accessed October 9, 2006.
This website provides the most frequent questions from physicians and
patients, with corresponding answers.
eMedicine: Bell’s Palsy. Available at: http://www.emedicine.com/
EMERG/topic56.htm. Accessed October 9, 2006.
This site provides the physician with a more comprehensive approach to the
diagnosis and treatment of patients with Bell’s palsy.
EVIDENCE
1. Adour KK, Ruboyianes JM, Von Doersten PG, et al: Bell’s palsy
treatment with acyclovir and prednisone compared with predni-
sone alone: A double-blind, randomized, controlled trial. Ann Otol
Rhinol Laryngol 105(5):371-378, 1996.
This trial demonstrated that treatment with acyclovir-prednisone is
statistically more effective in returning volitional muscle motion and in
preventing partial nerve degeneration than placebo-prednisone
treatment.
2. Ahmed A: When is facial paralysis Bell palsy? Current diagnosis
and treatment. Cleve Clin J Med 72(5):398-401, 405, 2005.
This article provides a broad differential diagnosis for facial palsy and
discusses appropriate tests to order as well as treatment options.
3. Alaani A, Hogg R, Saravanappa N, Irving RM: An analysis of
diagnostic delay in unilateral facial paralysis. J Laryngol Otol
119(3):184-188, 2005.
This analysis demonstrates how Bell’s palsy has commonly been mis-
diagnosed when there is an underlying cause for the facial palsy.
4. Gilden DH: Clinical practice: Bell’s palsy. N Engl J Med
351(13):1323-1331, 2004.
This article emphasizes the likely viral etiology of Bell’s palsy: herpes
simplex virus type I. It also provides a detailed diagram of the facial nerve
and physical findings associated with central and peripheral facial
weakness.
5. Linder T, Bossart W, Bodmer D: Bell’s palsy and herpes simplex
virus: Fact or mystery? Otol Neurotol 26(1):109-113, 2005.
This article questions herpes simplex virus as the etiology of all Bell’s
palsy; the authors recommend a study in the future to demonstrate the
identification of an active replicating virus in Bell’s palsy patients to
confirm the causality.
6. Ramsey MJ, DerSimonian R, Holtel MR, Burgess LP: Corticoste-
roid treatment for idiopathic facial nerve paralysis: A meta-
analysis. Laryngoscope 110(3 Pt 1):335-341, 2000.
This meta-analysis indicates that corticosteroid treatment improves
complete facial motor recovery for individuals with complete idiopathic
facial nerve paralysis.